- About
- Home
- Introduction
- Statistics
- Programs
- Dignet
- Gene
- GenePair
- BioSummarAI
- Help & Docs
- Documents
- Help
- FAQs
- Links
- Acknowledge
- Disclaimer
- Contact Us
Gene Information
Gene symbol: TNF
Gene name: tumor necrosis factor
HGNC ID: 11892
Synonyms: TNFSF2, DIF, TNF-alpha
Related Genes
Related Sentences
| # | PMID | Sentence |
| 1 | 26468884 | Despite viral clearance, live RSV reinfections caused weight loss and substantial pulmonary inflammation probably due to high levels of RSV specific IFN-γ+IL4-, IFN-γ-TNF-α+, IFN-γ+TNF-α- effector CD4 and CD8 T cells. |
| 2 | 26468884 | Alum adjuvant in the FI-RSV-A was found to be mainly responsible for inducing high levels of RSV-specific IFN-γ-IL4+, IFN-γ-TNF-α+ CD4+ T cells, and proinflammatory cytokines IL-6 and IL-4 as well as B220+ plasmacytoid and CD4+ dendritic cells, and inhibiting the induction of IFN-γ+CD8 T cells. |
| 3 | 26464379 | Additionally, immunization with rOhr induced high production of IFN-γ as well as proinflammatory cytokines such as TNF, MCP-1, IL-12p70, and IL-6, but a lesser amount of IL-10, suggesting that rOhr predominantly elicited a cell-mediated immune response. |
| 4 | 26458317 | The potent antitumor effect correlated with higher secretion levels of tumor necrosis factor-alpha(TNF-α) and lower levels of interleukin-10(IL-10) concentration in serum. |
| 5 | 26455464 | B cell activating factor (BAFF) is a member of the tumor necrosis factor (TNF) ligand family. |
| 6 | 26440045 | In a model of macrophage-like cells, the CpG NFs proved to be potent immunostimulators by triggering the proliferation of these immune cells, which, in turn, secreted immunostimulatory cytokines, including tumor necrosis factor α, interleukin-6, and interleukin-10. |
| 7 | 26425357 | In the present study, a novel pre-miniproinsulin analogue was designed to have a short 9 residue sequence replacing the 35 residue C-chain, one lysine and one arginine added to the C-terminus of the B-chain in combination with glycine and arginine substitution at A21 and B29, respectively, and a 16-residue fusion partner comprising the pentapeptide sequence (PSDKP) of the N-terminus of human tumor necrosis factor-α (TNF-α), 6 histidine residues for Ni(2+) chelated affinity purification and a pentapeptide ending with methionine for ease of chemical cleavage fused at the N-terminus. |
| 8 | 26379269 | Our data show that combinations of the cytokines IFN-γ, TNF, and IL-17A activated murine pulmonary epithelial cells to inhibit the intracellular growth of the F. tularensis Live Vaccine Strain (LVS) and the highly virulent F. tularensis Schu S4 strain. |
| 9 | 26379269 | Our data show that combinations of the cytokines IFN-γ, TNF, and IL-17A activated murine pulmonary epithelial cells to inhibit the intracellular growth of the F. tularensis Live Vaccine Strain (LVS) and the highly virulent F. tularensis Schu S4 strain. |
| 10 | 26379269 | Although paired combinations of IFN-γ, TNF, and IL-17A all significantly controlled LVS growth, simultaneous treatment with all three cytokines had the greatest effect on LVS growth inhibition. |
| 11 | 26379269 | Although paired combinations of IFN-γ, TNF, and IL-17A all significantly controlled LVS growth, simultaneous treatment with all three cytokines had the greatest effect on LVS growth inhibition. |
| 12 | 26376930 | Production of tumor necrosis factor alpha (TNF-α), gamma interferon, interleukin-17A (IL-17A), IL-10, and IL-4 was measured in CD4(+) effector memory (EM) T cells after 24 h by flow cytometry. |
| 13 | 26376930 | We found the number of IL-17A-producing CD4(+) EM T cells, as well as that of cells simultaneously producing both IL-17A and TNF-α, to be significantly elevated in the Giardia-exposed individuals after 24 h of antigen stimulation. |
| 14 | 26376930 | We conclude that symptomatic Giardia infection in humans induces a CD4(+) EM T cell response of which IL-17A production seems to be an important component. |
| 15 | 26346655 | Class B CpG ODNs loaded on the BNNS-PEI complexes enhanced the production of interleukin-6 and tumor necrosis factor-α from peripheral blood mononuclear cells compared with CpG ODNs directly loaded on BNNS. |
| 16 | 26346655 | Class B CpG ODNs loaded on the BNNS-PEI complexes enhanced the production of interleukin-6 and tumor necrosis factor-α from peripheral blood mononuclear cells compared with CpG ODNs directly loaded on BNNS. |
| 17 | 26346655 | Therefore, BNNS-PEI complexes can be used to enhance the immunostimulatory effect and therapeutic activity of CpG ODNs and the treatment of diseases requiring interleukin-6, tumor necrosis factor-α, and interferon-α. |
| 18 | 26346655 | Therefore, BNNS-PEI complexes can be used to enhance the immunostimulatory effect and therapeutic activity of CpG ODNs and the treatment of diseases requiring interleukin-6, tumor necrosis factor-α, and interferon-α. |
| 19 | 26339315 | One mechanism employed by monocytes for sensing foreign antigens is via toll-like receptors (TLRs)-transmembrane proteins that distinguish classes of foreign pathogens, for example, bacteria (TLR4, 5, and 9) vs. fungi (TLR2) vs. viruses (TLR3, 7, and 8). |
| 20 | 26339315 | Three cytokines, tumor necrosis factor-α, interleukin (IL)-6, and IL-10, were detected using anti-cytokine antibody arrays integrated into each of the six chambers. |
| 21 | 26334519 | In the tumor microenvironment, the combination therapy led to significantly downregulated levels of immunosuppressive factors, such as decreased numbers of myeloid-derived suppressor cells and regulatory T cells (Treg) cells and declined levels of interleukin-6 and chemokine ligand 2-in correlation with increased levels of proinflammatory cytokines, including tumor necrosis factor-α and IFN-γ as well as an elevation in the CD8(+) T-cell population. |
| 22 | 26319741 | A Th1-type immune response was indicated by a high IgG2a/IgG1 ratio of RSV-specific antibodies, strong induction of RSV-specific interferon-gamma and tumor necrosis factor-alpha cytokine producing CD8 Tcells, and low RSV-specific CD4 T-cell induction. |
| 23 | 26291403 | Women exhibited a more profound pro-inflammatory response with significantly higher increases in tumor necrosis factor (TNF)-α and interleukin (IL)-6. |
| 24 | 26283332 | We first showed by using flow cytometric analysis that Ly6C(low) major histocompatibility complex class II-positive chemokine receptor type 2 (CCR2)-positive CD64(+) inflammatory monocytes accumulate in the stomach mucosa during the vaccine-induced reduction of H. felis infection. |
| 25 | 26283332 | We observed that inflammatory monocytes produced tumor necrosis factor alpha and inducible nitric oxide synthase (iNOS), two major antimicrobial factors. |
| 26 | 26268065 | Levels of interleukin (IL)-4, IL-10, IL-12p70, IL-17A and tumor necrosis factor (TNF)-α in serum were higher in the immunized mice compared to those in the adjuvant control group. |
| 27 | 26256060 | Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), which is capable of selectively inducing apoptosis of cancer cells, is a potential targeted drug for cancer therapy. |
| 28 | 26232502 | Activation of NF-κB via tumor necrosis factor (TNF) receptor 1 (TNFR1) in these cells induces proinflammatory cytokine secretion. |
| 29 | 26219397 | We found that POL-P3b upregulated the expression of CD80, CD86, CD83, and major histocompatibility complex class II molecules on DCs, stimulated production of more interleukin (IL)-12, tumor necrosis factor-α, and less IL-10. |
| 30 | 26215441 | In this study, mice were primed with either conventional pVRC-based or suicidal pSC-based DNA vaccines carrying DEC-205-targeted NS3 antigen (DEC-NS3) and boosted with type 5 adenoviral vectors encoding the partial NS3 and core antigens (C44P). |
| 31 | 26215441 | Moreover, priming with a suicidal DNA vaccine (pSC-DEC-NS3), which elicited increased TNF-α-producing CD4+ and CD8+ T-cells against NS3-2 peptides (aa 1245-1461), after boosting, showed increased heterogeneous protective potential compared with priming with a conventional DNA vaccine (pVRC-DEC-NS3). |
| 32 | 26215441 | In conclusion, a suicidal DNA vector (pSC-DEC-NS3) expressing DEC-205-targeted NS3 combined with boosting using an rAd5-based HCV vaccine (rAd5-C44P) is a good candidate for a safe and effective vaccine against HCV infection. |
| 33 | 26214521 | Effective cancer vaccines deliver concentrated antigen to both HLA class I and II molecules of DCs, promoting both CD4 and CD8 T cell responses. |
| 34 | 26214521 | Drugs or physical treatments can mitigate the immunosuppressive cancer microenvironment and include chemotherapeutics, radiation, indoleamine 2,3-dioxygenase (IDO) inhibitors, inhibitors of T cell checkpoints, agonists of selected TNF receptor family members, and inhibitors of undesirable cytokines. |
| 35 | 26202436 | Immunization with Rv1733c SLP elicited gamma interferon-positive/tumor necrosis factor-positive (IFN-γ(+)/TNF(+)) and IFN-γ(+) CD4(+) T cells and Rv1733c-specific antibodies and led to a significant reduction in the bacterial load in the lungs of M. tuberculosis-challenged mice. |
| 36 | 26175894 | A robust immune response to each component of the vaccine with polyfunctional CD4 TH1 cell responses characterized by production of antigen-specific interferon-γ, tumor necrosis factor and interleukin-2 (IL-2), and low levels of IL-5 and IL-10 was induced in immunized mice. |
| 37 | 26175894 | We also demonstrate that CD4 T cells, but not CD8 T cells, are sufficient for protection against L. donovani infection in immunized mice. |
| 38 | 26169275 | In vitro infection of macrophages with live attenuated parasites (compared to that with wild-type [WT] L. donovani parasites) induced significantly higher production of proinflammatory cytokines (tumor necrosis factor alpha [TNF-α], interleukin-12 [IL-12], gamma interferon [IFN-γ], and IL-6), chemokines (monocyte chemoattractant protein 1/CCL-2, macrophage inflammatory protein 1α/CCL-3, and IP-10), reactive oxygen species (ROS), and nitric oxide, while concomitantly reducing anti-inflammatory cytokine IL-10 and arginase-1 activities, suggesting a dominant classically activated/M1 macrophage response. |
| 39 | 26169275 | Similarly, parasitized splenic macrophages from live attenuated parasite-infected mice also demonstrated induction of an M1 macrophage phenotype, indicated by upregulation of IL-1β, TNF-α, IL-12, and inducible nitric oxide synthase 2 and downregulation of genes associated with the M2 phenotype, i.e., the IL-10, YM1, Arg-1, and MRC-1 genes, compared to WT L. donovani-infected mice. |
| 40 | 26169275 | Furthermore, an ex vivo antigen presentation assay showed macrophages from live attenuated parasite-infected mice induced higher IFN-γ and IL-2 but significantly less IL-10 production by ovalbumin-specific CD4(+) T cells, resulting in proliferation of Th1 cells. |
| 41 | 26144899 | Regarding cytokine production, increased IL-6, IL-10, TNF, and IFNγ levels were observed after vaccination. |
| 42 | 26108288 | CD8 T cells predominantly expressed cytokines individually, with pronounced tumor necrosis factor alpha (TNF-α) production by BAL fluid cells. |
| 43 | 26108288 | T-cell memory phenotype analysis revealed that CD4 and CD8 populations isolated from BAL fluid samples were polarized toward an effector memory phenotype, whereas the frequencies of peripheral central memory T cells increased significantly and remained elevated following aerosol vaccination. |
| 44 | 26108288 | Expression patterns of the α4β1 integrin lung homing markers remained consistently high on CD4 and CD8 T cells isolated from BAL fluid and varied on peripheral T cells. |
| 45 | 26101787 | By binding to both TLR1 and TLR2, CU-T12-9 facilitates the TLR1/2 heterodimeric complex formation, which in turn activates the downstream signaling. |
| 46 | 26101787 | Fluorescence anisotropy assays revealed competitive binding to the TLR1/2 complex between CU-T12-9 and Pam3CSK4 with a half-maximal inhibitory concentration (IC50) of 54.4 nM. |
| 47 | 26101787 | Finally, we showed that CU-T12-9 signals through nuclear factor κB (NF-κB) and invokes an elevation of the downstream effectors tumor necrosis factor-α (TNF-α), interleukin-10 (IL-10), and inducible nitric oxide synthase (iNOS). |
| 48 | 26098681 | Inflammatory cytokines and chemokines, including tumor necrosis factor-alpha and chemokine (C-C motif) ligand 2, were reduced by treatment with oseltamivir and the fraction of ivy extract. |
| 49 | 26093203 | The vaccinated fish also showed the significantly increased levels of IgM antibody in serum and cytokines such as inerleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) in kidney, spleen and gills. |
| 50 | 26091761 | The profiles of the proinflammatory cytokines interferon γ, tumor necrosis factor α, interleukin 6 (IL-6), and IL-17A and the regulatory cytokine IL-10 induced by the rSj22.6 plus rSjHSP70 combination were similar to those induced by rSj22.6 emulsified with the ISA206 adjuvant control. |
| 51 | 26057192 | RA is commonly treated with non-steroidal anti-inflammatory drugs (NSAIDs), traditional disease-modifying antirheumatic drugs (DMARDs), glucocorticoids and biologic inhibitors of TNF, IL-1, IL-6, T cells and B cells. |
| 52 | 26054442 | For didactic reasons, we opted by elaborating a summary of safety assessment in accordance with the previous themes, by drug class/mechanism of action (tumor necrosis factor antagonists, T-cell co-stimulation blockers, B-cell depletors and interleukin-6 receptor blockers). |
| 53 | 26041038 | The supernatant was then assayed for gamma interferon (IFN-γ), interleukin-2 (IL-2), tumor necrosis factor alpha (TNF-α), IL-4, IL-6, IL-10, and IL-17A. |
| 54 | 26041038 | In addition, IL-6 concentrations were higher while IL-2 and IFN-γ concentrations were significantly lower in those with nonmeningeal disseminated disease diagnosed within 12 months than in those with acute pneumonia (for all, P < 0.05). |
| 55 | 26035950 | Levels of pro-inflammatory factors viz., tumor necrosis factor-alpha (TNF-α); interferon-gamma (IFN-γ); and macrophage chemo-attractant protein-1 (MAC-1) during disease pathogenesis have been found to be reduced. |
| 56 | 26032420 | Spleen Tyrosine Kinase (Syk) Mediates IL-1β Induction by Primary Human Monocytes during Antibody-enhanced Dengue Virus Infection. |
| 57 | 26032420 | Syk induces elevated IL1B, TNF, and IL6 mRNA by 2 hpi. |
| 58 | 26032420 | Syk mediates elevated IL-1β secretion by activating ERK1/2, and both Syk and ERK1/2 inhibitors ablated ADE-induced IL-1β secretion. |
| 59 | 26032420 | Maturation of pro-IL-1β during ADE requires caspase-1 and NLRP3, but caspase-1 is suboptimally increased by ADE and can be significantly enhanced by a typical inflammasome agonist, ATP. |
| 60 | 26032420 | Importantly, this inflammatory Syk-ERK signaling axis requires DENV immune complexes, because DENV-2 in the presence of serotype-matched anti-DENV-2 mAb, but not anti-DENV-1 mAb, activates Syk, ERK, and IL-1β secretion. |
| 61 | 26032420 | Syk and ERK may serve as new therapeutic targets for interfering with ADE-induced cytokine expression during severe dengue. |
| 62 | 26009966 | The cellular responses were assessed by interferon-γ (IFN-γ) ELISPOT and by intracellular staining (ICS) for the Th1 cytokines IFN-γ, interleukin-2 (IL-2) and tumor necrosis factor-α (TNF-α). |
| 63 | 25965646 | RNA was extracted from PBMCs, and the relative concentration of cytokine messenger RNA (mRNA) transcripts (IFN-β, IFN-γ, IL-12, TNF-α, IL-6, IL-17, or IL-10) relative to transcription of the β-actin gene was determined by real-time polymerase chain reaction. |
| 64 | 25965646 | The median increase in vaccine-stimulated cultures was: IFN-β=334.4-fold; IL-12=46.33-fold; IFN-γ=12.64-fold; IL-6=9.07-fold; IL-17=7.33-fold; IL-10=6.47-fold; and TNF-α=2.36-fold. |
| 65 | 25962477 | The results demonstrated that the prime-boost strategy induced a potent antigen-specific immune response, which was primarily characterized by an enhanced T cell response and increased production of cytokines, including interferon-γ, tumor necrosis factor-α and interleukin-2, in mice. |
| 66 | 25957883 | RT-qPCR results showed that Hsp70C could up-regulate the expression of i) T cell markers: Cluster of Differentiation 8 alpha (CD8α) and CD4, ii) cytokine genes: Interferon gamma (IFNγ), Tumor Necrosis Factor alpha (TNFα) and Interleukin 12 p40 (IL-12/P40), iii) antibody genes: Immunoglobulin M heavy chain (IgMH) and IgTH, and iv) major histocompatibility complex (MHC-I & MHC-II), in the spleen of iAg:Hsp70C group. |
| 67 | 25947145 | BCG vaccination induced an unexpectedly dichotomous immune response in this small, BCG-naive, young-adult cohort: BCG vaccination induced either gamma interferon-positive (IFN-γ(+)) interleukin 2-positive (IL-2(+)) tumor necrosis factor α-positive (TNF-α(+)) polyfunctional CD4(+) T cells concurrent with CD4(+) IL-17A(+) and CD8(+) IFN-γ(+) T cells or, in contrast, virtually absent cytokine responses with induction of CD8(+) regulatory T cells. |
| 68 | 25947145 | Significant induction of polyfunctional CD4(+) IFN-γ(+) IL-2(+) TNF-α(+) T cells and IFN-γ production by peripheral blood mononuclear cells (PBMCs) was confined to individuals with strong immunization-induced local skin inflammation and increased serum C-reactive protein (CRP). |
| 69 | 25947145 | Thus, BCG vaccination either induced a broad proinflammatory T cell response with local inflammatory reactogenicity or, in contrast, a predominant CD8(+) regulatory T cell response with mild local inflammation, poor cytokine induction, and absent polyfunctional CD4(+) T cells. |
| 70 | 25943203 | Using peptide arrays and intracellular cytokine staining, we demonstrated that TDV elicits CD8(+) T cells targeting the nonstructural NS1, NS3, and NS5 proteins of TDV-2. |
| 71 | 25943203 | The cells were characterized by the production of interferon-γ, tumor necrosis factor-α, and to a lesser extent interleukin-2. |
| 72 | 25941591 | The serum level of chromogranin A (CgA), soluble TNF receptors (sTNFR1/2), vascular endothelial growth factor (VEGF), and MIP-1β and MCP-1 chemokines, was determined. |
| 73 | 25941591 | Low level or reduction of CgA and sTNFR and increase of MIP-1β and MCP-1 were found in patients sera. |
| 74 | 25924764 | We identified high responders, intermediate responders, and nonresponders based on detection of interleukin-2 (IL-2), tumor necrosis factor alpha (TNF-α), and gamma interferon (IFN-γ) expressing central (TCM) and effector memory CD4(+) T cells (TEM) 182 days after the first immunization. |
| 75 | 25919308 | This modified method enhanced staining of IL-2 and IL-4, but not IFNγ, tumor necrosis factor alpha (TNFα), or IL-5. |
| 76 | 25872480 | These CD8+ T-cell responses were largely mediated by MF cells coproducing interferon-γ and macrophage inflammatory protein-1β and expressing CD107a with or without tumor necrosis factor-α. |
| 77 | 25845290 | It is noteworthy that an increase in the multi-functional [interferon (IFN)-γ(hi) /tumour necrosis factor (TNF)-α(hi) ] CD4 and CD8 T cells were observed in BCG-primed and Acr1L-boosted (BCG-Acr1L) animals, compared to BCG alone. |
| 78 | 25845290 | Further, substantial expansion of both central memory (CD44(hi) /CD62L(hi) ) and effector memory (CD44(hi) /CD62L(lo) ) populations of CD4 and CD8 T cells was noted. |
| 79 | 25828583 | Receptor-interacting protein kinase (RIP)3 (also called RIPK3) mediates necrotic death by phosphorylating an executioner protein, MLKL, leading to plasma membrane leakage. |
| 80 | 25828583 | Recent investigations reveal a similar mechanism at play in the human alpha-herpesviruses, herpes simplex virus (HSV)1 and HSV2, where RHIM competitor function and caspase 8 suppression are carried out by the virus-encoded large subunit of ribonucleotide reductase (R1). |
| 81 | 25828583 | In human cells, R1 inhibition of caspase 8 prevents TNF-induced apoptosis, but sensitizes to TNF-induced necroptosis. |
| 82 | 25828583 | The RHIM and caspase 8 interaction domains of R1 collaborate to prevent RIP3-dependent steps and enable both herpesviruses to deflect host cell death machinery that would cut short infection. |
| 83 | 25824831 | Tissue macrophage export of iron occurs concurrent with high serum concentrations of interferon gamma (IFN-γ) and interleukin 12 (IL-12). |
| 84 | 25824831 | In individual mice, high concentrations of both proinflammatory (tumor necrosis factor alpha [TNF-α]) and anti-inflammatory (IL-10) cytokines in serum correlate with increased tissue bacterial loads throughout 4 weeks of infection. |
| 85 | 25787136 | T cells were characterized by flow-based analysis of carboxyfluorescein succinimidyl ester (CFSE) dilution and CD4, CD3, CD45RA, CCR7, gamma interferon (IFN-γ), and tumor necrosis factor alpha (TNF-α) expression. |
| 86 | 25787136 | Before the aP preschool booster vaccination, both the proliferated pertussis toxin (PT)-specific CD4(+) and CD8(+) T-cell fractions (CFSE(dim)) were higher in aP- than in wP-primed children. |
| 87 | 25787136 | At present, infant vaccinations with four aP vaccines in the first year of life result in pertussis-specific CD4(+) and CD8(+) effector memory T-cell responses that persist in children until 4 years of age and are higher than those in wP-primed children. |
| 88 | 25785602 | Using knockout mice, we show that VLP-mediated post-exposure protection requires perforin, B cells, macrophages, conventional dendritic cells (cDCs), and either CD4+ or CD8+ T cells. |
| 89 | 25785602 | However, NK cells, IFN-gamma, and TNF-alpha were not required for post-exposure-mediated protection. |
| 90 | 25778401 | Necroptosis is an alternate programmed cell death pathway that is unleashed by caspase-8 compromise and mediated by receptor-interacting protein kinase 3 (RIP3). |
| 91 | 25778401 | Necroptosis is an alternate programmed cell death pathway that is unleashed by caspase-8 compromise and mediated by receptor-interacting protein kinase 3 (RIP3). |
| 92 | 25778401 | Murine cytomegalovirus (CMV) and herpes simplex virus (HSV) encode caspase-8 inhibitors that prevent apoptosis together with competitors of RIP homotypic interaction motif (RHIM)-dependent signal transduction to interrupt the necroptosis. |
| 93 | 25778401 | Murine cytomegalovirus (CMV) and herpes simplex virus (HSV) encode caspase-8 inhibitors that prevent apoptosis together with competitors of RIP homotypic interaction motif (RHIM)-dependent signal transduction to interrupt the necroptosis. |
| 94 | 25778401 | Importantly, human CMV is shown to block necroptosis induced by either TNF or M45 mutant murine CMV in RIP3-expressing human cells. |
| 95 | 25778401 | Importantly, human CMV is shown to block necroptosis induced by either TNF or M45 mutant murine CMV in RIP3-expressing human cells. |
| 96 | 25778401 | Human CMV blocks TNF-induced necroptosis after RIP3 activation and phosphorylation of the mixed lineage kinase domain-like (MLKL) pseudokinase. |
| 97 | 25778401 | Human CMV blocks TNF-induced necroptosis after RIP3 activation and phosphorylation of the mixed lineage kinase domain-like (MLKL) pseudokinase. |
| 98 | 25763999 | Here, we used enzyme-linked immunosorbent assays with anti-CII IgG antibodies, quantified the expression levels of Th1, Th2, and Th3 cytokines, and performed flow cytometric analyses of different T-cell subsets, including Th1, Th2, Th17, Tc, Ts, Treg, and CD4(+)CD29(+)T cells to systemically evaluate humoral and cellular immune responses to pcDNA-CCOL2A1 vaccine in normal rats. |
| 99 | 25763999 | Furthermore, no significant changes were observed in the expression levels of pro-inflammatory cytokines interleukin (IL)-1α, IL-5, IL-6, IL-12(IL-23p40), monocyte chemotactic protein (MCP)-1, macrophage inflammatory protein (MIP)-1α, regulated on activation in normal T-cell expressed and secreted (RANTES), receptor activator for nuclear factor-κB ligand (RANKL), and granulocyte colony-stimulating factor (G-CSF) or anti-inflammatory cytokines IL-4 and IL-10 in vaccinated normal rats relative to that in controls(P > 0.05). |
| 100 | 25763999 | However, transforming growth factor (TGF)-β levels were significantly increased on days 10 and 14, while interferon (IFN)-γ and tumor necrosis factor (TNF)-α levels were significantly decreased on days 28 and 35 after vaccination(P < 0.05). |
| 101 | 25763999 | Similarly, there were no significant differences in the percentages of Tc, Ts, Th1/Th2, and Th17 cells between the 2 groups(P > 0.05), with the exception of Treg cells, which were significantly reduced on days 14 and 21 after vaccination (P < 0.05), and CD4(+)CD29(+)T cells, which were significantly increased on days 7 and 14 after vaccination(P < 0.05).Taken together, these results suggested that pcDNA-CCOL2A1 vaccine did not markedly affect the balance of immune system components in vaccinated normal rats, indicating that this DNA vaccine may have clinical applications in the treatment of RA. |
| 102 | 25762540 | In human melanoma biopsies, Mel-ILP treatment upregulated IL1B, IL8, and IL6 associated with their release in patients' locoregional sera. |
| 103 | 25762540 | Although induction of apoptosis in melanoma cells by melphalan in vitro did not elicit threshold levels of endoplasmic reticulum and reactive oxygen species stress associated with danger signals, such as induction of cell-surface calreticulin, prophylactic immunization and T-cell depletion experiments showed that melphalan administration in vivo could stimulate a CD8(+) T cell-dependent protective antitumor response. |
| 104 | 25762540 | Interestingly, the vaccination effect was potentiated in combination with exogenous calreticulin, but not tumor necrosis factor, a cytokine often combined with Mel-ILP. |
| 105 | 25754202 | PEM did not change the overall numbers of CD4 T cells in BCG-vaccinated animals but resulted in an almost complete loss of antigen-specific cytokine production. |
| 106 | 25754202 | Furthermore, there was a change in cytokine expression characterized by a gradual loss of multifunctional antigen-specific CD4 T cells and an increased proportion of effector cells expressing gamma interferon and tumor necrosis factor alpha (IFN-γ(+) TNF-α(+) and IFN-γ(+) cells). |
| 107 | 25754202 | PEM during M. tuberculosis infection completely blocked the protection afforded by the H56-CAF01 subunit vaccine, and this was associated with a very substantial loss of the interleukin-2-positive memory CD4 T cells promoted by this vaccine. |
| 108 | 25754202 | Similarly, PEM during the vaccination phase markedly reduced the H56-CAF01 vaccine response, influencing all cytokine-producing CD4 T cell subsets, with the exception of CD4 T cells positive for TNF-α only. |
| 109 | 25748337 | Upon PFWE treatment, BM-DCs dose-dependently upregulated the expression of CD40, CD80, CD86 and MHC II and increased the production of IL-12, IL-6 and tumor necrosis factor (TNF)-α but not for IL-10, which is mediated by TLR4 signaling pathway, at least partially. |
| 110 | 25738816 | CD4 T cell immune responses such as interferon-γ and tumor necrosis factor-α secretion are necessary for Chlamydia immunity. |
| 111 | 25738816 | Nine proteins were orthologous T cell antigens between C. trachomatis and C. muridarum and 2 of the nine were Pmps which generated MHC class II binding epitopes at distinct sequences within the proteins. |
| 112 | 25724777 | The analysis of cytokine has revealed that rNdk can strongly induce production of IFN-γ as well as proinflammatory cytokines (TNF, MCP1 and IL-6) but not much IL-10, suggesting rNdk elicited predominantly cell-mediated immune responses. |
| 113 | 25722892 | The increased levels of Hct, interleukin- (IL-) 10, and tumor necrosis factor-alpha (TNF-α) were detected in dengue fever (DF), dengue hemorrhagic fever (DHF) and dengue shock syndrome (DSS) patients as compared with other febrile illnesses (OFIs). |
| 114 | 25722892 | The highest levels of Hct and IL-10 were detected in DSS patients as compared with other groups (P < 0.05) especially on one day before and after defervescence. |
| 115 | 25722892 | The unstimulated and lipopolysaccharide- (LPS-) stimulated monocytes from DSS patients showed the significantly decreased of intracellular IL-1β and TNF-α. |
| 116 | 25722892 | Furthermore, the negative correlations between IL-10 levels and intracellular IL-1β and MFI of CD11b expression in unstimulated and LPS-stimulated monocytes were also detected. |
| 117 | 25722892 | Nevertheless, not only were the relationships between the prominent IL-10 and the suppression of intracellular monocyte secretion, namely, IL-1β, TNF-α, demonstrated but also the effect of vascular leakage was observed. |
| 118 | 25704666 | Samples were analyzed for concentrations of acute phase reactants (haptoglobin, serum amyloid A, fibrinogen and iron), mRNA expression levels of cytokines (interleukin (IL)-1β, IL-4, IL-10, tumor necrosis factor (TNF)-α and interferon (IFN)-γ) in leukocytes, and vaccine-specific antibody titers. |
| 119 | 25704666 | Statistical differences were observed between groups for haptoglobin, fibrinogen, IL-1β, IL-4, and IL-10, but differences were generally small and none of the vaccine titers were different between the groups. |
| 120 | 25697665 | While Braun lipoprotein (Lpp) activates toll-like receptor-2 to initiate an inflammatory cascade, plasminogen activator (Pla) protease facilitates bacterial dissemination in the host. |
| 121 | 25697665 | Importantly, the ability of the Δlpp Δpla double mutant to be phagocytized by macrophages, to stimulate production of tumor necrosis factor-α and interleukin-6, and to activate the nitric oxide killing pathways of the host cells remained unaltered when compared to the WT CO92-infected macrophages. |
| 122 | 25691576 | 5-Azacytidine-induced protein 2 (AZI2) is a TNF receptor (TNFR)-associated factor family member-associated NF-κB activator-binding kinase 1-binding protein that regulates the production of IFNs. |
| 123 | 25691576 | We revealed that the higher longevity of AZI2-deficient osteoclasts is due to an augmented activation of proto-oncogene tyrosine-protein kinase Src (c-Src), which is a critical player in osteoclast survival. |
| 124 | 25691576 | We found that AZI2 inhibits c-Src activity by regulating the activation of heat shock protein 90 (Hsp90), a chaperone involved in c-Src dephosphorylation. |
| 125 | 25691576 | Furthermore, we demonstrated that AZI2 indirectly inhibits c-Src by interacting with the Hsp90 co-chaperone Cdc37. |
| 126 | 25691576 | Strikingly, administration of a c-Src inhibitor markedly prevented bone loss in AZI2 knock-out mice. |
| 127 | 25674983 | During infection, HSV modulates cell death pathways using the large subunit (R1) of ribonucleotide reductase (RR) to suppress apoptosis by binding to and blocking caspase-8. |
| 128 | 25674983 | Here, we demonstrate that HSV-1 and HSV-2 R1 proteins (ICP6 and ICP10, respectively) also prevent necroptosis in human cells by inhibiting the interaction between receptor-interacting protein kinase 1 (RIP1) and RIP3, a key step in tumor necrosis factor (TNF)-induced necroptosis. |
| 129 | 25674983 | We show that suppression of this cell death pathway requires an N-terminal RIP homotypic interaction motif (RHIM) within R1, acting in concert with the caspase-8-binding domain, which unleashes necroptosis independent of RHIM function. |
| 130 | 25644007 | Interleukin 17A (IL-17A)-, gamma interferon (IFN-γ)-, and tumor necrosis factor alpha (TNF-α)-producing lymphocytes were significantly increased in the spleens and lungs of immunized mice. |
| 131 | 25643774 | In the following literature review we present some of the better-known systemic treatment options for melanoma, from conventional chemotherapy, molecular (MAPK inhibitors) and immunomodulatory (interleukin-2, tumor necrosis factor alpha, cytotoxic T lymphocyte antigen-4 and programmed death-1 inhibitors) therapies, to miscellaneous options, among which are angiogenesis inhibitors, apoptosis modulators, vaccines, and radiotherapy. |
| 132 | 25637347 | Interferon γ and Tumor Necrosis Factor Are Not Essential Parameters of CD4+ T-Cell Responses for Vaccine Control of Tuberculosis. |
| 133 | 25594805 | In the aspect of cytokines, the rSFTSV/NSs-vaccinated mice had a 5- to 10-fold increase in interleukin (IL)-2, IL-5, IL-6, IFN-γ, and tumor necrosis factor-α, which probably just had a negative effect on the bodyweight of mice. |
| 134 | 25589549 | Gamma interferon (IFN-γ) produced by CD4(+) T cells and, recently, multifunctional CD4(+) T cells secreting IFN-γ, tumor necrosis factor (TNF), and interleukin-2 (IL-2) have been used in vaccine studies as a measurable immune parameter, reflecting activity of a vaccine and potentially predicting protection. |
| 135 | 25589549 | Gamma interferon (IFN-γ) produced by CD4(+) T cells and, recently, multifunctional CD4(+) T cells secreting IFN-γ, tumor necrosis factor (TNF), and interleukin-2 (IL-2) have been used in vaccine studies as a measurable immune parameter, reflecting activity of a vaccine and potentially predicting protection. |
| 136 | 25589549 | However, accumulating experimental evidence suggests that host resistance against Mycobacterium tuberculosis infection is independent of IFN-γ and TNF secretion from CD4(+) T cells. |
| 137 | 25589549 | However, accumulating experimental evidence suggests that host resistance against Mycobacterium tuberculosis infection is independent of IFN-γ and TNF secretion from CD4(+) T cells. |
| 138 | 25550942 | The results showed that the percentage of CD3(+) CD56(+) CIK cells after treatment increased significantly while the percentage of CD4(+) CD25(+) Treg cells decreased (P < 0.05). |
| 139 | 25550942 | We then studied and identified the mechanisms of the anti-tumor effects of the vaccines by analyzing a series of cytokines that are commonly involved in tumor progression and ascitic development including granulocyte macrophage colony stimulating factor (GM-CSF), interleukin-10 (IL-10), interferon-γ (IFN-γ), tumor necrosis factor-α (TGF-α), tumor necrosis factor-β (TGF-β), Vascular endothelial growth factor (VEGF) and monocyte chemotactic protein-1 (MCP-1). |
| 140 | 25520147 | The CD4 T cell cytokine response (IFN-γ, interleukin-2 [IL-2], interleukin-17A [IL-17A], interleukin-22 [IL-22], granulocyte-macrophage colony-stimulating factor [GM-CSF], and tumor necrosis factor alpha [TNF-α]) and surface marker expression (CD27, CXCR3, and CD154) were then measured. |
| 141 | 25520147 | We found that the proportion of PPD-specific CD4 T cells, defined as CD154(+) TNF-α(+) cells that were negative for CD27 and positive for GM-CSF, gave the strongest discrimination between subjects with latent and those with active TB (area under the receiver operator characteristic [ROC] curve of 0.9277; P < 0.0001). |
| 142 | 25520147 | Also, the proportions and absolute numbers of HBHA-specific CD4 T cells were significantly higher in those with latent TB infection, particularly CD154(+) TNF-α(+) IFN-γ(+) IL-2(+) and CD154(+) TNF-α(+) CXCR3(+). |
| 143 | 25489000 | In mucosal tissues of normal rhesus macaques, we found CD4(+) pDCs to be the subset responsible for most IFN-α and tumor necrosis factor α (TNF-α) production in response to Toll-like receptor (TLR) 7/8 stimulation, compared with relatively anergic CD4(-) pDCs. |
| 144 | 25485483 | The immune associated genes, interleukin-1β (IL-1β), interleukin-6 (IL-6), interleukin 10 (IL-10), tumor necrosis factor-α (TNF-α), ciclo-oxigenase-2 (COX-2), and Mx gene were studied by real-time PCR in head-kidney leucocytes of sea bass after incubation with the extracellular products (ECPs) of the probiotic strain Vagococcus fluvialis L21 and polyinosinic:polycytidylic acid (POLY I:C), at different times (T1.5, T6, T12, T24, T48 and T72). |
| 145 | 25485483 | In general, we can observe how pro-inflammatory cytokines IL-1β, TNF-α, IL-6 and COX-2 studied displayed a strong peak after stimulation with 1.5 h of ECPs of V. fluvialis L21, significant differences (P < 0.05) exist with other periods and with the POLY I: C at the same time. |
| 146 | 25485483 | Similarly to the case of IL-10 also produced a statistically significant (P < 0.05) peak of expression on leukocytes that were stimulated with the ECPs of V. fluvialis L21. |
| 147 | 25479797 | Modulation of the NAS process represents a path toward the development of novel vaccines or drugs, through targets such as myeloid differentiation primary-response protein 88 (MyD88) and tumor necrosis factor (TNF) receptor-associated factor (TRAF) 3 and 6 in Toll-like receptor (TLR)-mediated signaling pathways. |
| 148 | 25448107 | This protection correlated with the accumulation of CD4(+) T cells expressing IL-17(+)TNF(+)IL-2(+). |
| 149 | 25448107 | This protection correlated with the accumulation of CD4(+) T cells expressing IL-17(+)TNF(+)IL-2(+). |
| 150 | 25448107 | In contrast, mice challenged with Mtb 21 days after BCG vaccination exhibited only a mild and transient protection, associated with the accumulation of CD4(+) T cells that were mostly IFN-γ(+)TNF(+) and to a lesser extent IFN-γ(+)TNF(+)IL-2(+). |
| 151 | 25448107 | In contrast, mice challenged with Mtb 21 days after BCG vaccination exhibited only a mild and transient protection, associated with the accumulation of CD4(+) T cells that were mostly IFN-γ(+)TNF(+) and to a lesser extent IFN-γ(+)TNF(+)IL-2(+). |
| 152 | 25443632 | SHARPIN regulates immune signaling and contributes to full transcriptional activity and prevention of cell death in response to TNF in vitro. |
| 153 | 25443632 | SHARPIN regulates immune signaling and contributes to full transcriptional activity and prevention of cell death in response to TNF in vitro. |
| 154 | 25443632 | The inactivating mouse Sharpin cpdm mutation causes TNF-dependent multi-organ inflammation, characterized by dermatitis, liver inflammation, splenomegaly, and loss of Peyer's patches. |
| 155 | 25443632 | The inactivating mouse Sharpin cpdm mutation causes TNF-dependent multi-organ inflammation, characterized by dermatitis, liver inflammation, splenomegaly, and loss of Peyer's patches. |
| 156 | 25443632 | TNFR1-induced apoptosis can proceed through caspase-8 and BID, but reduction in or loss of these players generally did not suppress inflammation, although Casp8 heterozygosity significantly delayed dermatitis. |
| 157 | 25443632 | TNFR1-induced apoptosis can proceed through caspase-8 and BID, but reduction in or loss of these players generally did not suppress inflammation, although Casp8 heterozygosity significantly delayed dermatitis. |
| 158 | 25443632 | Ripk3 or Mlkl deficiency partially ameliorated the multi-organ phenotype, and combined Ripk3 deletion and Casp8 heterozygosity almost completely suppressed it, even restoring Peyer's patches. |
| 159 | 25443632 | Ripk3 or Mlkl deficiency partially ameliorated the multi-organ phenotype, and combined Ripk3 deletion and Casp8 heterozygosity almost completely suppressed it, even restoring Peyer's patches. |
| 160 | 25443632 | Unexpectedly, Sharpin, Ripk3 and Casp8 triple deficiency caused perinatal lethality. |
| 161 | 25443632 | Unexpectedly, Sharpin, Ripk3 and Casp8 triple deficiency caused perinatal lethality. |
| 162 | 25427992 | In particular, T cell subsets seem dysregulated with an increased production of pro-inflammatory cytokines, as IFN-γ and TNF, and chemokines, as CXCL10. |
| 163 | 25376024 | Lm infection stimulated cytokine secretion [interleukin (IL)-12p70, tumor necrosis factor (TNF)-α, and IL-6] and Th-1 skewing of allogeneic naive CD4 T cells by HIV-moDCs, in contrast to the suppressive effects observed by HIV plasma on moDCs on toll-like receptor ligand stimulation. |
| 164 | 25367297 | CD14(+)CD16(+) inflammatory monocytes were induced after vaccination in both young and older adults. |
| 165 | 25367297 | In classical CD14(+)CD16(-) and inflammatory monocytes, production of tumor necrosis factor α and interleukin 6, as measured by intracellular staining, was strongly induced after vaccination. |
| 166 | 25367297 | In purified monocytes, we found age-associated elevation in phosphorylated signal transducer and activator of transcription-3, and decreased serine 359 phosphorylation of the negative IL-10 regulator dual-specificity phosphatase 1. |
| 167 | 25343523 | Murine granulocyte-macrophage colony-stimulating factor expressed from a bicistronic simian immunodeficiency virus-based integrase-defective lentiviral vector does not enhance T-cell responses in mice. |
| 168 | 25343523 | As a prelude to immunization studies in nonhuman primates, we compared in mice the immunogenicity of a simian immunodeficiency virus (SIV)-based integrase (IN)-defective lentiviral vector (IDLV) encoding the model antigen-enhanced green fluorescence protein (eGFP) in the presence or absence of the murine granulocyte-macrophage colony-stimulating factor (mGM-CSF) expressed from an internal ribosomal entry site (IRES) sequence. |
| 169 | 25343523 | Results indicated that the mGM-CSF was unable to improve the magnitude and quality of the immune response against the eGFP transgene in the context of the SIV-based IDLV, as evaluated by enzyme-linked immunosorbent spot (ELISPOT) assays for interferon-γ (IFN-γ) and by intracellular cytokine staining for IFN-γ, interleukin-2 (IL-2), and tumor necrosis factor-alpha (TNF-α). |
| 170 | 25253667 | Interleukin-10- and transforming growth factor β-independent regulation of CD8⁺ T cells expressing type 1 and type 2 cytokines in human lymphatic filariasis. |
| 171 | 25253667 | INF individuals exhibited significant decreases in the frequencies of CD8⁺ T cells expressing tumor necrosis factor alpha (TNF-α), gamma interferon (IFN-γ), and interleukin-22 (IL-22) at baseline and/or in response to filarial antigens, compared with CP and EN individuals. |
| 172 | 25253667 | In contrast, the same individuals exhibited significant increases in the frequencies of CD8⁺ T cells expressing IL-4, IL-5, IL-9, IL-13, and IL-21, compared with CP and/or EN individuals. |
| 173 | 25253667 | Finally, the regulation of these responses appears to be independent of IL-10 and transforming growth factor β (TGF-β), since blockade of IL-10 or TGF-β signaling did not significantly alter the frequencies of type 1 or type 2 cytokine-expressing CD8⁺ T cells. |
| 174 | 25247707 | Here, we found that Env-APRIL signaled through the two receptors, BCMA and TACI. |
| 175 | 25247707 | Thus, in contrast to the 4-helix cytokines IL-21 and GM-CSF, the TNF-superfamily members CD40L and APRIL induced negligible autoantibodies. |
| 176 | 25239487 | The splenocytes assay showed oral WH1fungin could suppress T cells proliferation, down-regulate amounts of activated CD8(+) T cells with the production of tumor necrosis factor (TNF)-α and interferon (IFN)-γ, and increase CD4(+)CD25(+)FOXP3(+) regulator T cells (Tregs). |
| 177 | 25225247 | The results also demonstrated the ability of Fh12 to downregulate the secretion of the proinflammatory and inflammatory cytokines tumor necrosis factor alpha (TNF-α), interleukin-12 (IL-12), and IL-1βB, even after stimulation with lipopolysaccharide (LPS), as well as its ability to stimulate the overexpression of IL-10. |
| 178 | 25208333 | Survival of mice was associated with bacterial clearance, an increased number of splenic leukocytes, and high levels of interleukin-12, interferon γ and tumor necrosis factor α in spleens as well as in sera. |
| 179 | 25203111 | Primary Ad5hr infection suppressed CCL20, TNF and IL-1 mRNA expression in PBMC, and subsequent virus exposures further dampened expression of these pro-inflammatory cytokines. |
| 180 | 25203111 | Primary, but not secondary, Ad5hr inoculation increased the frequency of CXCR3+ CD4+ T cells in blood, while secondary, but not primary, Ad5hr infection transiently increased the frequencies of Ki67+, HLADR+ and CD95+/CCR5+ CD4+ T cells in blood. |
| 181 | 25203111 | Ad5hr infection induced polyfunctional CD4 and CD8+ T cells specific for the Ad5 hexon protein in all of the animals. |
| 182 | 25192808 | A significant upregulation of mRNA expression for interleukin-1β (il-1β) and tumor necrosis factor-α (tnf-α) was also observed in fish treated with antigens combined with ISA763A, which peaked at 3 months PSV. |
| 183 | 25174880 | Here, we compared phenotype and functional characteristics of human monocyte-derived dendritic cells (DCs) generated in the presence of IL-4/GM-CSF (IL4-DCs) and IFNα/GM-CSF (IFN-DCs). |
| 184 | 25174880 | We showed that IFN-DCs displayed semi-mature phenotype and expressed higher level of CD123, TNF-related apoptosis-inducing ligand (TRAIL) and B7-H1 molecules in comparison with IL4-DCs. |
| 185 | 25174880 | LPS-stimulated IFN-DCs were characterized by greater production of Th1/pro-inflammatory (IFN-γ, IL-2, IL-1β, TNF-α, IL-17), Тh2/anti-inflammatory cytokines (IL-10, IL-5), hematopoietic growth factors (G-CSF) and chemokines (MCP-1). |
| 186 | 25174880 | LPS-stimulated IFN-DCs possessed higher direct cytotoxic activity against TRAIL-sensitive tumor cell line Jurkat and similar cytotoxicity against TRAIL-resistant tumor HEp-2 cells. |
| 187 | 25174880 | Besides, IFN-DCs and IL4-DCs equally induced apoptosis of activated CD4(+) and CD8(+) T cells. |
| 188 | 25150071 | Evaluation of the cellular and humoral immunity was performed by measurement of interferon (IFN)-γ, tumor necrosis factor (TNF)-α, lymphocyte proliferation, total IgG and IgG2a in the control and immunized groups. |
| 189 | 25125502 | Whole blood was incubated in the presence of influenza vaccine and dexamethasone to evaluate production of interleukin-6 (IL-6), interleukin-1-beta (IL-1β), tumor necrosis factor-alpha (TNF-α), and interferon-gamma (IFN-γ). |
| 190 | 25125502 | Multiple regression models controlling for age, gender, and grade point average revealed a negative relationship between PSS and GCS for vaccine-stimulated production of IL-1β, IL-6, and TNF-α. |
| 191 | 25117071 | The CD40 ligand is a type I transmembrane protein that belongs to a tumor necrosis factor (TNF) superfamily. |
| 192 | 25117071 | The CD40 ligand is a type I transmembrane protein that belongs to a tumor necrosis factor (TNF) superfamily. |
| 193 | 25117071 | The receptor for ligand is constitutively expressed on cells, TNF family protein: CD40. |
| 194 | 25117071 | The receptor for ligand is constitutively expressed on cells, TNF family protein: CD40. |
| 195 | 25117071 | The role of the CD40/CD40L pathway in the induction of body immunity, in inflammation, or in hemostasis has been well documented, whereas its involvement in neoplastic disease is still under investigation. |
| 196 | 25117071 | The role of the CD40/CD40L pathway in the induction of body immunity, in inflammation, or in hemostasis has been well documented, whereas its involvement in neoplastic disease is still under investigation. |
| 197 | 25117071 | CD40L ligand may potentiate apoptosis of tumor cells by activation of nuclear factor-κB (NF-κB), AP-1, CD95, or caspase-depended pathways and stimulate host immunity to defend against cancer. |
| 198 | 25117071 | CD40L ligand may potentiate apoptosis of tumor cells by activation of nuclear factor-κB (NF-κB), AP-1, CD95, or caspase-depended pathways and stimulate host immunity to defend against cancer. |
| 199 | 25117071 | CD40L enhance release of strongly pro-angiogenic factor, vascular endothelial growth factor (VEGF), and activator of coagulation, TF, the level of which is correlated with tumor metastasis. |
| 200 | 25117071 | CD40L enhance release of strongly pro-angiogenic factor, vascular endothelial growth factor (VEGF), and activator of coagulation, TF, the level of which is correlated with tumor metastasis. |
| 201 | 25114109 | Splenocytes from mice vaccinated with χ10057(pYA5199) produced significant levels of gamma interferon (IFN-γ), tumor necrosis factor alpha (TNF-α), and interleukin-17 (IL-17) after restimulation with LcrV and YpL antigens. |
| 202 | 25081573 | This review specifically assesses the risk of the TNF inhibitors etanercept, adalimumab and infliximab, as well as interleukin-12/23 inhibitor ustekinumab. |
| 203 | 25024382 | Development of a vaccine against pulmonary tuberculosis may require immunization strategies that induce a high frequency of Ag-specific CD4 and CD8 T cells in the lung. |
| 204 | 25024382 | In contrast, aerosolized AERAS-402 alone or following BCG induced potent and stable Ag85A/b-specific CD4 and CD8 effector T cells in bronchoalveolar lavage that largely produced IFN-γ, as well as TNF and IL-2. |
| 205 | 24998644 | Tumor necrosis factor-alpha and interleukin-6 (p's<.001) increased following vaccination, confirming modest increases in inflammation. |
| 206 | 24967273 | The circulating interleukin-(IL-)10 and interferon-(IFN-) γ concentrations were significantly higher in the vitamin D sufficient athletes. |
| 207 | 24967273 | Furthermore, the production of tumour necrosis factor-(TNF-) α, IL-6, IFN-γ, IL-2, and IL-10 by whole blood culture was significantly inhibited by 1, 25(OH)2D3 concentrations of 1000 pmol/L or 10000 pmol/L. |
| 208 | 24955922 | Structural and functional characterization of a novel molluskan ortholog of TRAF and TNF receptor-associated protein from disk abalone (Haliotis discus discus). |
| 209 | 24955922 | Structural and functional characterization of a novel molluskan ortholog of TRAF and TNF receptor-associated protein from disk abalone (Haliotis discus discus). |
| 210 | 24955922 | Structural and functional characterization of a novel molluskan ortholog of TRAF and TNF receptor-associated protein from disk abalone (Haliotis discus discus). |
| 211 | 24955922 | Within the signaling cascade, TNF receptor-associated factor (TRAF) and TNF receptor-associated protein (TTRAP) has been shown to have a crucial role in the modulation of immune signaling in animals. |
| 212 | 24955922 | Within the signaling cascade, TNF receptor-associated factor (TRAF) and TNF receptor-associated protein (TTRAP) has been shown to have a crucial role in the modulation of immune signaling in animals. |
| 213 | 24955922 | Within the signaling cascade, TNF receptor-associated factor (TRAF) and TNF receptor-associated protein (TTRAP) has been shown to have a crucial role in the modulation of immune signaling in animals. |
| 214 | 24955922 | Collectively, these results reinforce the existence of the TNF signaling cascade in mollusks like disk abalone, further implicating the putative regulatory behavior of TTRAP in invertebrate host pathology. |
| 215 | 24955922 | Collectively, these results reinforce the existence of the TNF signaling cascade in mollusks like disk abalone, further implicating the putative regulatory behavior of TTRAP in invertebrate host pathology. |
| 216 | 24955922 | Collectively, these results reinforce the existence of the TNF signaling cascade in mollusks like disk abalone, further implicating the putative regulatory behavior of TTRAP in invertebrate host pathology. |
| 217 | 24951859 | LIGHT, a TNF superfamily member (TNFSF14), is a type II transmembrane protein expressed on activated T cells and immature dendritic cells (DCs). |
| 218 | 24906994 | After incubated with CotC-CsLAP2, the levels of IFN-γ, IL-6, IL-10, IL-17A, and TNF significantly increased in the supernatant of splenocytes isolated from mice orally treated with CotC-CsLAP2 spores, while there was no statistically significant difference of IL-4 level representing Th2 response among the groups. |
| 219 | 24872512 | While monocyte-derived cytokine (tumor necrosis factor alpha [TNF-α], interleukin-1β [IL-1β], and IL-6) production was rarely affected, 30% of all included patients had deficient production of interferon gamma (IFN-γ), IL-17A, or IL-22. |
| 220 | 24872512 | Defective IL-17A and IL-22 production was mainly confined to ID patients with mucocutaneous fungal infections. |
| 221 | 24872512 | Defective IL-17A and IL-22 production was primarily found in patients with fungal infections, while monocyte-derived cytokine production was unaffected. |
| 222 | 24855352 | The PAs were based on epitopes gB409-505 and gD301-309, selected from HSV envelope glycoprotein B (gB) and glycoprotein D (gD), that had their N-terminus modified with hydrophobic moieties containing two C18 hydrocarbon chains. |
| 223 | 24855352 | In particular, interleukin (IL)-23-, IL-6-, IL-8- or macrophage inflammatory protein (MIP)-2-, and tumor necrosis factor (TNF)-α-release increased considerably when cells were treated with the gB-micelles or gD-micelles compared with the production of the same cytokines when the stimulus was the single gB or gD peptide. |
| 224 | 24854144 | This purified protein was able to stimulate the secretion of high levels of gamma interferon and low levels of interleukin-10 and tumor necrosis factor-α in mice splenocytes, suggesting a predominantly Th-1-type T cell response. |
| 225 | 24837764 | The Rv2034 protein indeed was highly immunogenic in HLA-DR3 transgenic mice and induced HLA-DR3 restricted IFN-γ(+)/TNF(+) and IFN-γ(+) CD4(+) T-cells, specific for an epitope encoded in peptide 31-50. |
| 226 | 24837764 | CD4(+) T-cell responses were optimally induced when using TLR9- and TLR3-ligand-adjuvants or CAF09. |
| 227 | 24837764 | Rv2034-specific antibodies were observed following immunization with either TLR2-, TLR3-, TLR4-, TLR5-, TLR7- or TLR9-ligands or CAF09. |
| 228 | 24821972 | Cutting Edge: RIP1 kinase activity is dispensable for normal development but is a key regulator of inflammation in SHARPIN-deficient mice. |
| 229 | 24821972 | Cutting Edge: RIP1 kinase activity is dispensable for normal development but is a key regulator of inflammation in SHARPIN-deficient mice. |
| 230 | 24821972 | Cutting Edge: RIP1 kinase activity is dispensable for normal development but is a key regulator of inflammation in SHARPIN-deficient mice. |
| 231 | 24821972 | Cutting Edge: RIP1 kinase activity is dispensable for normal development but is a key regulator of inflammation in SHARPIN-deficient mice. |
| 232 | 24821972 | RIP1 (RIPK1) kinase is a key regulator of TNF-induced NF-κB activation, apoptosis, and necroptosis through its kinase and scaffolding activities. |
| 233 | 24821972 | RIP1 (RIPK1) kinase is a key regulator of TNF-induced NF-κB activation, apoptosis, and necroptosis through its kinase and scaffolding activities. |
| 234 | 24821972 | RIP1 (RIPK1) kinase is a key regulator of TNF-induced NF-κB activation, apoptosis, and necroptosis through its kinase and scaffolding activities. |
| 235 | 24821972 | RIP1 (RIPK1) kinase is a key regulator of TNF-induced NF-κB activation, apoptosis, and necroptosis through its kinase and scaffolding activities. |
| 236 | 24821972 | Dissecting the balance of RIP1 kinase activity and scaffolding function in vivo during development and TNF-dependent inflammation has been hampered by the perinatal lethality of RIP1-deficient mice. |
| 237 | 24821972 | Dissecting the balance of RIP1 kinase activity and scaffolding function in vivo during development and TNF-dependent inflammation has been hampered by the perinatal lethality of RIP1-deficient mice. |
| 238 | 24821972 | Dissecting the balance of RIP1 kinase activity and scaffolding function in vivo during development and TNF-dependent inflammation has been hampered by the perinatal lethality of RIP1-deficient mice. |
| 239 | 24821972 | Dissecting the balance of RIP1 kinase activity and scaffolding function in vivo during development and TNF-dependent inflammation has been hampered by the perinatal lethality of RIP1-deficient mice. |
| 240 | 24821972 | In this study, we generated RIP1 kinase-dead (Ripk1(K45A)) mice and showed they are viable and healthy, indicating that the kinase activity of RIP1, but not its scaffolding function, is dispensable for viability and homeostasis. |
| 241 | 24821972 | In this study, we generated RIP1 kinase-dead (Ripk1(K45A)) mice and showed they are viable and healthy, indicating that the kinase activity of RIP1, but not its scaffolding function, is dispensable for viability and homeostasis. |
| 242 | 24821972 | In this study, we generated RIP1 kinase-dead (Ripk1(K45A)) mice and showed they are viable and healthy, indicating that the kinase activity of RIP1, but not its scaffolding function, is dispensable for viability and homeostasis. |
| 243 | 24821972 | In this study, we generated RIP1 kinase-dead (Ripk1(K45A)) mice and showed they are viable and healthy, indicating that the kinase activity of RIP1, but not its scaffolding function, is dispensable for viability and homeostasis. |
| 244 | 24821972 | After validating that the Ripk1(K45A) mice were specifically protected against necroptotic stimuli in vitro and in vivo, we crossed them with SHARPIN-deficient cpdm mice, which develop severe skin and multiorgan inflammation that has been hypothesized to be mediated by TNF-dependent apoptosis and/or necroptosis. |
| 245 | 24821972 | After validating that the Ripk1(K45A) mice were specifically protected against necroptotic stimuli in vitro and in vivo, we crossed them with SHARPIN-deficient cpdm mice, which develop severe skin and multiorgan inflammation that has been hypothesized to be mediated by TNF-dependent apoptosis and/or necroptosis. |
| 246 | 24821972 | After validating that the Ripk1(K45A) mice were specifically protected against necroptotic stimuli in vitro and in vivo, we crossed them with SHARPIN-deficient cpdm mice, which develop severe skin and multiorgan inflammation that has been hypothesized to be mediated by TNF-dependent apoptosis and/or necroptosis. |
| 247 | 24821972 | After validating that the Ripk1(K45A) mice were specifically protected against necroptotic stimuli in vitro and in vivo, we crossed them with SHARPIN-deficient cpdm mice, which develop severe skin and multiorgan inflammation that has been hypothesized to be mediated by TNF-dependent apoptosis and/or necroptosis. |
| 248 | 24821972 | Together, these data suggest that RIP1 kinase represents an attractive therapeutic target for TNF-driven inflammatory diseases. |
| 249 | 24821972 | Together, these data suggest that RIP1 kinase represents an attractive therapeutic target for TNF-driven inflammatory diseases. |
| 250 | 24821972 | Together, these data suggest that RIP1 kinase represents an attractive therapeutic target for TNF-driven inflammatory diseases. |
| 251 | 24821972 | Together, these data suggest that RIP1 kinase represents an attractive therapeutic target for TNF-driven inflammatory diseases. |
| 252 | 24821786 | RIP1 suppresses innate immune necrotic as well as apoptotic cell death during mammalian parturition. |
| 253 | 24821786 | The pronecrotic kinase, receptor interacting protein (RIP1, also called RIPK1) mediates programmed necrosis and, together with its partner, RIP3 (RIPK3), drives midgestational death of caspase 8 (Casp8)-deficient embryos. |
| 254 | 24821786 | RIP1 controls a second vital step in mammalian development immediately after birth, the mechanism of which remains unresolved. |
| 255 | 24821786 | Rip1(-/-) mice display perinatal lethality, accompanied by gross immune system abnormalities. |
| 256 | 24821786 | Here we show that RIP1 K45A (kinase dead) knockin mice develop normally into adulthood, indicating that development does not require RIP1 kinase activity. |
| 257 | 24821786 | In the face of complete RIP1 deficiency, cells develop sensitivity to RIP3-mixed lineage kinase domain-like-mediated necroptosis as well as to Casp8-mediated apoptosis activated by diverse innate immune stimuli (e.g., TNF, IFN, double-stranded RNA). |
| 258 | 24821786 | When either RIP3 or Casp8 is disrupted in combination with RIP1, the resulting double knockout mice exhibit slightly prolonged survival over RIP1-deficient animals. |
| 259 | 24821786 | Surprisingly, triple knockout mice with combined RIP1, RIP3, and Casp8 deficiency develop into viable and fertile adults, with the capacity to produce normal levels of myeloid and lymphoid lineage cells. |
| 260 | 24821786 | A single allele of Rip3 is tolerated in Rip1(-/-)Casp8(-/-)Rip3(+/-) mice, contrasting the need to eliminate both alleles of either Rip1 or Rip3 to rescue midgestational death of Casp8-deficient mice. |
| 261 | 24821786 | These observations reveal a vital kinase-independent role for RIP1 in preventing pronecrotic as well as proapoptotic signaling events associated with life-threatening innate immune activation at the time of mammalian parturition. |
| 262 | 24812238 | Taurine reduced the expression of tumor necrosis factor-α mRNA in all 3 rearing patterns, IL-4 mRNA expression in the high-density group, and IL-10 in the low-density group (P < 0.05). |
| 263 | 24799678 | Caspase-8 and RIP kinases regulate bacteria-induced innate immune responses and cell death. |
| 264 | 24799678 | Caspase-8 and RIP kinases regulate bacteria-induced innate immune responses and cell death. |
| 265 | 24799678 | The rapid killing of macrophages induced by Y. pestis, dependent upon type III secretion system effector Yersinia outer protein J (YopJ), is minimally affected by the absence of caspase-1, caspase-11, Fas ligand, and TNF. |
| 266 | 24799678 | The rapid killing of macrophages induced by Y. pestis, dependent upon type III secretion system effector Yersinia outer protein J (YopJ), is minimally affected by the absence of caspase-1, caspase-11, Fas ligand, and TNF. |
| 267 | 24799678 | Here we provide genetic evidence for a receptor-interacting protein (RIP) kinase-caspase-8-dependent macrophage apoptotic death pathway after infection with Y. pestis, influenced by Toll-like receptor 4-TIR-domain-containing adapter-inducing interferon-β (TLR4-TRIF). |
| 268 | 24799678 | Here we provide genetic evidence for a receptor-interacting protein (RIP) kinase-caspase-8-dependent macrophage apoptotic death pathway after infection with Y. pestis, influenced by Toll-like receptor 4-TIR-domain-containing adapter-inducing interferon-β (TLR4-TRIF). |
| 269 | 24799678 | Interestingly, macrophages lacking either RIP1, or caspase-8 and RIP3, also had reduced infection-induced production of IL-1β, IL-18, TNF, and IL-6; impaired activation of the transcription factor NF-κB; and greatly compromised caspase-1 processing. |
| 270 | 24799678 | Interestingly, macrophages lacking either RIP1, or caspase-8 and RIP3, also had reduced infection-induced production of IL-1β, IL-18, TNF, and IL-6; impaired activation of the transcription factor NF-κB; and greatly compromised caspase-1 processing. |
| 271 | 24799678 | Cleavage of the proform of caspase-1 is associated with triggering inflammasome activity, which leads to the maturation of IL-1β and IL-18, cytokines important to host responses against Y. pestis and many other infectious agents. |
| 272 | 24799678 | Cleavage of the proform of caspase-1 is associated with triggering inflammasome activity, which leads to the maturation of IL-1β and IL-18, cytokines important to host responses against Y. pestis and many other infectious agents. |
| 273 | 24799678 | Our results identify a RIP1-caspase-8/RIP3-dependent caspase-1 activation pathway after Y. pestis challenge. |
| 274 | 24799678 | Our results identify a RIP1-caspase-8/RIP3-dependent caspase-1 activation pathway after Y. pestis challenge. |
| 275 | 24799678 | Mice defective in caspase-8 and RIP3 were also highly susceptible to infection and displayed reduced proinflammatory cytokines and myeloid cell death. |
| 276 | 24799678 | Mice defective in caspase-8 and RIP3 were also highly susceptible to infection and displayed reduced proinflammatory cytokines and myeloid cell death. |
| 277 | 24799678 | We propose that caspase-8 and the RIP kinases are key regulators of macrophage cell death, NF-κB and inflammasome activation, and host resistance after Y. pestis infection. |
| 278 | 24799678 | We propose that caspase-8 and the RIP kinases are key regulators of macrophage cell death, NF-κB and inflammasome activation, and host resistance after Y. pestis infection. |
| 279 | 24795357 | We have shown that a vaccine based on alphavirus replicon particles (VRP) activates strong cellular and humoral immunity to tyrosinase-related protein-2 (TRP2) melanoma antigen, providing prophylactic and therapeutic effects in stringent mouse models. |
| 280 | 24795357 | Here, we report that the immunogenicity and efficacy of this vaccine is increased in combination with either antagonist anti-CTL antigen-4 (CTLA-4) or agonist anti-glucocorticoid-induced TNF family-related gene (GITR) immunomodulatory monoclonal antibodies (mAb). |
| 281 | 24795357 | These mAbs had similar adjuvant effects in priming an adaptive immune response against the vaccine-encoded antigen, augmenting, respectively, approximately 4- and 2-fold the TRP2-specific CD8(+) T-cell response and circulating Abs, compared with the vaccine alone. |
| 282 | 24795357 | Furthermore, while both mAbs increased the frequency of tumor-infiltrating CD8(+) T cells, anti-CTLA-4 mAb also increased the quantity of intratumor CD4(+)Foxp3(-) T cells expressing the negative costimulatory molecule programmed death-1 (PD-1). |
| 283 | 24795357 | They also indicate that tumor-infiltrating CD4(+)Foxp3(-)PD-1(+) T cells may affect the outcome of immunomodulatory treatments. |
| 284 | 24788303 | The expression of important pro-inflammatory cytokines (tumor necrosis factor-α, interleukin-6 and interferon-γ), which was quantified using ELISA showed that simvastatin decreased the expression of pro-inflammatory cytokines to an average of 2-fold. |
| 285 | 24788303 | Endocytosis and autophagy processes were examined by detecting Rab and RhoA GTPase protein prenylation and LC3 lipidation using western blotting. |
| 286 | 24760891 | After vaccination with influenza A/PR8 virus-like particle (VLP) vaccine, in vivo and in vitro vaccine antigen-specific IgG isotype antibodies were not detected in MHC-II KO mice, which is quite different from CD4 T cell-deficient mice that induced vaccine-specific IgG antibodies. |
| 287 | 24760891 | Adoptive transfer of fractionated spleen cells from wild-type mice to MHC-II KO mice indicated that CD43(+) cell populations with MHC-II contributed more significantly to producing vaccine-specific IgG antibodies than CD43(-) B220(+) conventional B cell or CD4 T cell populations, as well as conferring protection against lethal infection. |
| 288 | 24760891 | Bone marrow-derived dendritic cells from MHC-II KO mice showed a significant defect in producing interleukin-6 and tumor necrosis factor alpha cytokines. |
| 289 | 24751414 | In addition, the transcription levels of interleukin-1β and tumor necrosis factor-α genes in the spleen and head kidney of r6EPIS-vaccinated fish were significantly increased during the period of immunization and early phase of infection, while the transcription level of interleukin-10 gene was significantly increased from Day 3 to 7 post challenge, compared to the control level. |
| 290 | 24743542 | Whole blood was stimulated for 24 hours and the pro-inflammatory tumor necrosis factor (TNF) and the anti-inflammatory/regulatory interleukin-10 (IL-10) cytokines in culture supernatant were measured by enzyme-linked immunosorbent assay (ELISA). |
| 291 | 24743542 | Gabonese children had a lower pro-inflammatory response to poly(I:C) (TLR3 ligand), but a higher pro-inflammatory response to FSL-1 (TLR2/6 ligand), Pam3 (TLR2/1 ligand) and LPS (TLR4 ligand) compared to Dutch children. |
| 292 | 24733091 | Moreover, protection correlated with high numbers of CD4(+), gamma interferon-positive (IFN-γ(+)), tumor necrosis factor alpha-positive/negative (TNF-α(+/-)), interleukin-10-negative (IL-10(-)) cells and low numbers of CD4(+) IFN-γ(+/-) TNF-α(-) IL-10(+) T cells at 2 weeks postchallenge. |
| 293 | 24713322 | In some cases (e.g., tumor necrosis factor alpha [TNF-α], interleukin 22 [IL-22], and granulocyte-macrophage colony-stimulating factor [GM-CSF]), liver cells exhibited even higher relative gene expression, whereas fewer genes exhibited differential expression in lung cells. |
| 294 | 24690681 | We report that ex-vivo exposure of quiescent or TCR-activated primary human T cells to thimerosal induced a dose-dependent apoptotic cell death associated with depolarization of mitochondrial membrane, generation of reactive oxygen species, cytochrome c release from the mitochondria and caspase-3 activation. |
| 295 | 24690681 | Moreover, exposure to non-toxic concentrations of thimerosal induced cell cycle arrest in G0/G1 phase of TCR-activated T cells, and inhibition of the release of proinflammatory cytokines such as IFN gamma, IL-1 beta, TNF alpha, IL-2, as well as the chemokine MCP1. |
| 296 | 24686064 | These animals had an increasing number of tumor necrosis factor alpha (TNF-α)-producing CD4(+) and CD8(+) T cells than WT CO92-infected mice. |
| 297 | 24671554 | Eagan and Rd LOS had a lower capacity to induce the expression of ICAM-1, CD40, CD58, tumor necrosis factor alpha (TNF-α), and interleukin-1β (IL-1β) compared to LPS. |
| 298 | 24648995 | In this study, we evaluated a TLR9 ligand (CpG oligodeoxynucleotide 1826, CpG) as an adjuvant for a partially protective DNA vaccine encoding a 26-kDa glutathione S-transferase of Schistosoma japonicum (pVAX1-Sj26GST). |
| 299 | 24648995 | Vaccination with pVAX1-Sj26GST in combination with CpG inhibited Treg immunosuppressive function, upregulated the production of interferon (IFN)-γ, tumor necrosis factor (TNF)-α, interleukin (IL)-4, IL-10, IL-2 and IL-6, and decreased CD4+CD8+Foxp3+ expression in vitro, which may contribute to the escape from Treg-mediated suppression during vaccination, allowing expansion of antigen-specific T cells against pathogens. |
| 300 | 24643207 | Here, we demonstrate that combinations of CIM and PZQ as adjuvants for a HBV DNA vaccine, could induce much stronger antigen specific CD4(+) and CD8(+) T cell responses compared either with CIM or PZQ alone. |
| 301 | 24643207 | The synergistic effects of CIM plus PZQ to HBV DNA vaccine were observed on a higher IgG2a/IgG1 ratio, an increase of HBsAg-specific CD4(+) T cells capable of producing IFN-γ or IL-17A and a robust IFN-γ-, IL-17A-, or TNF-α-producing CD8(+) T cells to HBsAg. |
| 302 | 24637787 | In vitro, BMDCs stimulated with Der p underwent cellular maturation and secreted proinflammatory cytokines interleukin (IL)-6 and tumor necrosis factor (TNF)α In contrast, Der p-stimulated BMDCs that were pretreated with LTS61K showed decreased IL-6 and TNFα production and were less mature. |
| 303 | 24637161 | Remarkably, recent studies identified plasma blasts/plasma cells as the main types of activated B cells producing the cytokines interleukin (IL)-10, IL-35, tumor necrosis factor (TNF)-α, IL-17, and GM-CSF in various contexts in mice. |
| 304 | 24632732 | In a PP cell culture system, b240 promoted the production of immunoglobulin A (IgA), interleukin (IL)-6, IL-10, interferon (IFN)-γ, and tumor necrosis factor, but not IL-4, IL-5, B-cell activating factors, IFN-α, IFN-β, and transforming growth factor-β1. |
| 305 | 24632732 | The enhanced IgA production by b240 was attenuated by neutralizing IL-6, a potent IgA-enhancing cytokine. b240 stimulated DCs to produce an elevated amount of IL-6 in a Toll-like receptor (TLR) 2-, but not TLR4- or TLR9-dependent manner. |
| 306 | 24632732 | Finally, we demonstrated that TLR2-mediated IL-6 production from PP DCs in response to b240 activated B cells to produce a large amount of IgA in a DC-B cell co-culture system. |
| 307 | 24611083 | The frequency of IFN-γ+/tumor necrosis factor-α (TNF-α)+CD45RO+CD4+ T-cells upon stimulation with phorbol myristate acetate (PMA)/Ionomycin was higher in 2-3 months old infants who received BCG vaccination at birth compared to those who did not. |
| 308 | 24611083 | The circulating frequency of forkhead box P3 (FoxP3)+ CD45RO+ regulatory CD4+ T-cells also trended lower in these infants. |
| 309 | 24600592 | Anti-Listeria protection was related to the changes in DC maturation caused by these epitopes, with high production of interleukin-12 as well as significant levels of other Th1 cytokines such as monocyte chemotactic protein-1, tumor necrosis factor-α, and interferon-γ, and with the induction of GAPDH1-22-specific CD4(+) and CD8(+) immune responses. |
| 310 | 24600592 | This is believed to be the first study to explore the use of a novel GAPDH antigen as a potential DC-based vaccine candidate for listeriosis, whose efficiency appears to highlight the relevance of vaccine designs containing multiple CD4(+) and CD8(+) epitopes. |
| 311 | 24599530 | Here, we elucidate for the first time the dominant major histocompatibility complex (MHC) class II-presented B. pertussis CD4(+) T cell epitopes, expressed on human monocyte-derived dendritic cells (MDDC) after the processing of whole bacterial cells by use of a platform of immunoproteomics technology. |
| 312 | 24599530 | Pertussis epitopes identified in the context of HLA-DR molecules were derived from two envelope proteins, i.e., putative periplasmic protein (PPP) and putative peptidoglycan-associated lipoprotein (PAL), and from two cytosolic proteins, i.e., 10-kDa chaperonin groES protein (groES) and adenylosuccinate synthetase (ASS). |
| 313 | 24599530 | CD4(+) T cell responsiveness in healthy adults against peptide pools representing epitope regions or full proteins confirmed the immunogenicity of PAL, PPP, groES, and ASS. |
| 314 | 24599530 | Elevated lymphoproliferative activity to PPP, groES, and ASS in subjects within a year after the diagnosis of symptomatic pertussis suggested immunogenic exposure to these proteins during clinical infection. |
| 315 | 24599530 | The PAL-, PPP-, groES-, and ASS-specific responses were associated with secretion of functional Th1 (tumor necrosis factor alpha [TNF-α] and gamma interferon [IFN-γ]) and Th2 (interleukin 5 [IL-5] and IL-13) cytokines. |
| 316 | 24593999 | In contrast, antigen encapsulated into nanoparticles and admixed with free TLR7/8 agonist leads to lower immunogenicity and rapid induction of high levels of inflammatory cytokines in the serum (e.g., TNF-a and IL-6 levels are 50- to 200-fold higher upon injection of free resiquimod (R848) than of nanoparticle-encapsulated R848). |
| 317 | 24579457 | A novel recombinant BCG (BCG-DHTM), that was deficient in urease, expressed with gene encoding the fusion of BCG-derived HSP70 and M. tuberculosis-derived major membrane protein (MMP)-II, was constructed for use as a vaccine against tuberculosis. |
| 318 | 24579457 | BCG-DHTM efficiently activated dendritic cells (DC) to induce cytokine production, including IL-12, TNFalpha and IL-1beta and phenotypic changes. |
| 319 | 24579457 | The DC infected BCG-DHTM was more potent in activation of native T cells of CD4 and CD8 subsets than those infected vector control BCG. |
| 320 | 24579457 | Further, BCG-DHTM seemed to activate native CD4+ T cells and native CD8+ T cells by antigen-specific fashion. |
| 321 | 24579457 | The primary infection of BCG-DHTM in C57BL/6 mice for 12 weeks efficiently produced T cells responsive to in vitro secondary stimulation with MMP-II, HSP70 and H37Rv-derived cytosolic protein and inhibited with multiplication of subsequently challenged M. tuberculosis in lungs at least partially. |
| 322 | 24575378 | In particular, while interleukin (IL)-12, IL-23, and tumor necrosis factor α (TNFα)-producing, migratory DCs developed in sparse cultures, IL-10-producing, non-migratory DCs differentiated in dense cultures. |
| 323 | 24572790 | In vivo depletion of specific immune cell types (CD8(+) T, CD4(+) T and Natural killer (NK)-1.1(+) cells) effectively blocked the protective effect of this combinational vaccine. |
| 324 | 24572790 | Considerably increased levels of interferon (IFN)-γ, tumor necrosis factor (TNF)-α, granulocyte macrophage colony-stimulating factor (GM-CSF) and cytotoxic T lymphocytes (CTLs) were detected with the combination vaccine group compared with other individual treatment groups. |
| 325 | 24568548 | Specific TEM cells differentiated into cells with a KLRG1(High) CD27(Low) CD43(Low) CD183(Low)T-bet(High) Eomes(Low) phenotype and capable to produce simultaneously the antiparasitic mediators IFNγ and TNF. |
| 326 | 24548461 | A rice-based soluble form of a murine TNF-specific llama variable domain of heavy-chain antibody suppresses collagen-induced arthritis in mice. |
| 327 | 24517026 | Since cytokines such as IL-6, TNF-alpha and IFN-Gamma are responsible for the prevention of viral infection, this study aimed to evaluate the effectiveness of HCV core protein as a vaccine. |
| 328 | 24517026 | Since cytokines such as IL-6, TNF-alpha and IFN-Gamma are responsible for the prevention of viral infection, this study aimed to evaluate the effectiveness of HCV core protein as a vaccine. |
| 329 | 24517026 | Since cytokines such as IL-6, TNF-alpha and IFN-Gamma are responsible for the prevention of viral infection, this study aimed to evaluate the effectiveness of HCV core protein as a vaccine. |
| 330 | 24517026 | Since cytokines such as IL-6, TNF-alpha and IFN-Gamma are responsible for the prevention of viral infection, this study aimed to evaluate the effectiveness of HCV core protein as a vaccine. |
| 331 | 24517026 | Since cytokines such as IL-6, TNF-alpha and IFN-Gamma are responsible for the prevention of viral infection, this study aimed to evaluate the effectiveness of HCV core protein as a vaccine. |
| 332 | 24517026 | Ten BALB/c mice were immunized with HCV core protein and after 42 days the splenocytes were isolated and the IL-6 and INF-gamma secretion were measured using ELISpot technique, at the same time TNF-alpha was determined by ELISA in the sera. |
| 333 | 24517026 | Ten BALB/c mice were immunized with HCV core protein and after 42 days the splenocytes were isolated and the IL-6 and INF-gamma secretion were measured using ELISpot technique, at the same time TNF-alpha was determined by ELISA in the sera. |
| 334 | 24517026 | Ten BALB/c mice were immunized with HCV core protein and after 42 days the splenocytes were isolated and the IL-6 and INF-gamma secretion were measured using ELISpot technique, at the same time TNF-alpha was determined by ELISA in the sera. |
| 335 | 24517026 | Ten BALB/c mice were immunized with HCV core protein and after 42 days the splenocytes were isolated and the IL-6 and INF-gamma secretion were measured using ELISpot technique, at the same time TNF-alpha was determined by ELISA in the sera. |
| 336 | 24517026 | Ten BALB/c mice were immunized with HCV core protein and after 42 days the splenocytes were isolated and the IL-6 and INF-gamma secretion were measured using ELISpot technique, at the same time TNF-alpha was determined by ELISA in the sera. |
| 337 | 24517026 | In the present study the IL-6, INF-gamma and TNF-alpha levels were dramatically higher in the immunized mice compared to the control group (respectively, 22.9 +/- 1.26; 18.53 +/- 3.87; 53.96 +/- 4.54 and p < 0.05). |
| 338 | 24517026 | In the present study the IL-6, INF-gamma and TNF-alpha levels were dramatically higher in the immunized mice compared to the control group (respectively, 22.9 +/- 1.26; 18.53 +/- 3.87; 53.96 +/- 4.54 and p < 0.05). |
| 339 | 24517026 | In the present study the IL-6, INF-gamma and TNF-alpha levels were dramatically higher in the immunized mice compared to the control group (respectively, 22.9 +/- 1.26; 18.53 +/- 3.87; 53.96 +/- 4.54 and p < 0.05). |
| 340 | 24517026 | In the present study the IL-6, INF-gamma and TNF-alpha levels were dramatically higher in the immunized mice compared to the control group (respectively, 22.9 +/- 1.26; 18.53 +/- 3.87; 53.96 +/- 4.54 and p < 0.05). |
| 341 | 24517026 | In the present study the IL-6, INF-gamma and TNF-alpha levels were dramatically higher in the immunized mice compared to the control group (respectively, 22.9 +/- 1.26; 18.53 +/- 3.87; 53.96 +/- 4.54 and p < 0.05). |
| 342 | 24517026 | The immunized mice with recombinant HCV core protein showed higher amount of IL-6, INF-gamma and TNF-alpha in the current study. |
| 343 | 24517026 | The immunized mice with recombinant HCV core protein showed higher amount of IL-6, INF-gamma and TNF-alpha in the current study. |
| 344 | 24517026 | The immunized mice with recombinant HCV core protein showed higher amount of IL-6, INF-gamma and TNF-alpha in the current study. |
| 345 | 24517026 | The immunized mice with recombinant HCV core protein showed higher amount of IL-6, INF-gamma and TNF-alpha in the current study. |
| 346 | 24517026 | The immunized mice with recombinant HCV core protein showed higher amount of IL-6, INF-gamma and TNF-alpha in the current study. |
| 347 | 24517026 | Since the level of IL-6, TNF-alpha and IFN-gamma is high in patients with acute HCV infection, thus a vaccine which could stimulate the secretion of these cytokines in advance may have a preventive role. |
| 348 | 24517026 | Since the level of IL-6, TNF-alpha and IFN-gamma is high in patients with acute HCV infection, thus a vaccine which could stimulate the secretion of these cytokines in advance may have a preventive role. |
| 349 | 24517026 | Since the level of IL-6, TNF-alpha and IFN-gamma is high in patients with acute HCV infection, thus a vaccine which could stimulate the secretion of these cytokines in advance may have a preventive role. |
| 350 | 24517026 | Since the level of IL-6, TNF-alpha and IFN-gamma is high in patients with acute HCV infection, thus a vaccine which could stimulate the secretion of these cytokines in advance may have a preventive role. |
| 351 | 24517026 | Since the level of IL-6, TNF-alpha and IFN-gamma is high in patients with acute HCV infection, thus a vaccine which could stimulate the secretion of these cytokines in advance may have a preventive role. |
| 352 | 24511686 | On the other hand, immunization of rabbits with Pmy induced a significant expression of humoral antibodies (IgM, total IgG, IgG1, IgG2 and IgG4) and different cytokines (IL-6, IL-10, L-12 and TNF-alpha). |
| 353 | 24477852 | Diarrheal stools from patients with CDI (CDI-positive diarrheal stools) showed higher relative amounts of the following inflammatory markers than the diarrheal stools from CDI-negative patients (CDI-negative diarrheal stools): C5a, CD40L, granulocyte colony-stimulating factor, I-309, interleukin-13 (IL-13), IL-16, IL-27, monocyte chemoattractant protein 1, tumor necrosis factor alpha, and IL-8. |
| 354 | 24477852 | IL-8 and IL-23 were present in a larger number of CDI-positive diarrheal stools than CDI-negative diarrheal stools. |
| 355 | 24445619 | There was significant upregulation of maturation markers (CD80, CD86, MHC-I, and MHC-II) in argon-helium freeze-thawed lysate-pulsed DCs. |
| 356 | 24445619 | The concentration of interleukin-6 (IL-6), IL-1β, tumor necrosis factor-α, and IL-12 secreted by lysate-pulsed DCs was increased. |
| 357 | 24421047 | Upregulation of the transcription factor T-bet is correlated with the strength of protection against secondary challenge with the live vaccine strain (LVS) of Francisella tularensis. |
| 358 | 24421047 | Lungs of LVS-infected T-bet-KO mice contained fewer lymphocytes and more neutrophils and interleukin-17 than WT mice. |
| 359 | 24421047 | LVS-vaccinated WT or KO mice controlled intracellular bacterial replication in an in vitro coculture system, but cultures with T-bet-KO splenocyte supernatants contained less IFN-γ and increased amounts of tumor necrosis factor alpha. |
| 360 | 24421046 | Macrophages incubated with sera from vaccinated infected mice exhibited M2 surface markers (CD16, CD32, CD200, and CD206), moderate proliferation, a low oxidative/nitrosative burst, and a regulatory/anti-inflammatory cytokine response (interleukin-4 [IL-4] plus IL-10 > tumor necrosis factor alpha [TNF-α]). |
| 361 | 24421046 | In comparison, macrophages incubated with sera from nonvaccinated infected mice exhibited M1 surface markers, vigorous proliferation, a substantial oxidative/nitrosative burst, and a proinflammatory cytokine response (TNF-α ≫ IL-4 plus IL-10). |
| 362 | 24404140 | Addition of properly formulated TLR agonist-containing adjuvants to recombinant protein vaccines enhances the antigen-specific CD4(+) T cell response characterized by IFN-γ and TNF, both of which are critical for the control of TB. |
| 363 | 24404140 | Addition of properly formulated TLR agonist-containing adjuvants to recombinant protein vaccines enhances the antigen-specific CD4(+) T cell response characterized by IFN-γ and TNF, both of which are critical for the control of TB. |
| 364 | 24404140 | Addition of CpG containing DNA to ID93+GLA-SE enhanced the magnitude of the multi-functional TH1 response against ID93 characterized by co-production of IFN-γ, TNF, and IL-2. |
| 365 | 24404140 | Addition of CpG containing DNA to ID93+GLA-SE enhanced the magnitude of the multi-functional TH1 response against ID93 characterized by co-production of IFN-γ, TNF, and IL-2. |
| 366 | 24396135 | Cytokines, including interleukin 6 (IL-6), interleukin 8 (IL-8), gamma interferon (IFN-γ), and tumor necrosis factor alpha (TNF-α), and cell surface antigens, including soluble intercellular adhesion molecule (sICAM) and CD64, are also being increasingly examined for use as nonspecific screening measures for neonatal sepsis. |
| 367 | 24394635 | The knockdown of SOCS1 in BMDCs by PLGA (OVA/SOCS1 siRNA) NPs enhanced pro-inflammatory cytokine (tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), IL-12 and IL-2) expression. |
| 368 | 24394635 | Additionally, PLGA (OVA/SOCS1 siRNA) NP-treated BMDCs could elicit an immune response through cross-presentation in OVA-specific CD8 T cells that express IL-2 cytokine. |
| 369 | 24376119 | We found HIV-1 transgenic osteoclast precursors (OCP) express higher levels of suppressor of cytokine signaling-1 (SOCS-1) and TNF receptor-associated factor 6 (TRAF6) and are resistant to interferon-gamma (IFN-γ) mediated suppression of osteoclast differentiation. |
| 370 | 26015961 | Polyfunctional HIV-1-specific CD8+ T cells, which produce interferon-γ and tumor necrosis factor-α and express the degranulation marker CD107a, were induced. |
| 371 | 24361035 | Also, the level of the cytokines IL-6, TNF-α, IL-2, IFN-γ, IL-4 and IL-5 was quantified during the experimental study. |
| 372 | 24361035 | Also, the level of the cytokines IL-6, TNF-α, IL-2, IFN-γ, IL-4 and IL-5 was quantified during the experimental study. |
| 373 | 24361035 | Moreover, early increases of TNF-alpha and IFN-gamma besides late increase of IFN-gamma were observed. |
| 374 | 24361035 | Moreover, early increases of TNF-alpha and IFN-gamma besides late increase of IFN-gamma were observed. |
| 375 | 24361035 | The analysis of biomarkers network pointed out two relevant strong axes during early stages of dengue fever, a protective axes TNF-alpha/Lymphocytes/Platelets, and a pathological IL-2/IL-6/Viremia/Monocyte/PT bond. |
| 376 | 24361035 | The analysis of biomarkers network pointed out two relevant strong axes during early stages of dengue fever, a protective axes TNF-alpha/Lymphocytes/Platelets, and a pathological IL-2/IL-6/Viremia/Monocyte/PT bond. |
| 377 | 24361035 | Later on, the biomarker network highlighted the interaction IFN-gamma/PLT/DENV-3(IgM;HAI)/PT, and the involvement of type-2 cytokines (IL-4; IL-5). |
| 378 | 24361035 | Later on, the biomarker network highlighted the interaction IFN-gamma/PLT/DENV-3(IgM;HAI)/PT, and the involvement of type-2 cytokines (IL-4; IL-5). |
| 379 | 24337259 | In addition, levels of interleukin (IL)-4, IL-13, interferon (IFN)-γ and tumor necrosis factor (TNF)-α in the ears were assayed. |
| 380 | 24337259 | In addition, BCGE inhibited mast cell infiltration into the ear and elevation of serum histamine, increased IFN-γ level and suppressed IL-4, IL-13 and TNF-α levels in the ears. |
| 381 | 24336457 | Furthermore, an in vitro mechanistic study showed that wolfberry supplementation enhanced maturation and activity of antigen-presenting dendritic cells (DCs) in aged mice, as indicated by phenotypic change in expression of DC activation markers major histocompatibility complex class II, cluster of differentiation (CD) 40, CD80, and CD86, and functional change in DC production of cytokines interleukin-12 and tumor necrosis factor-α as well as DC endocytosis. |
| 382 | 24336457 | Also, adoptive transfer of wolfberry-treated bone marrow DCs (loaded with ovalbumin(323-339)-peptide) promoted antigen-specific T cell proliferation as well as interleukin-4 and interferon-γ production in CD4(+) T cells. |
| 383 | 24325456 | The results showed that N-CMCh nanoparticle enhanced the secretion of cytokines (interleukin [IL]-6, IL-12p70, and tumor necrosis factor-α) and antigen uptake in bone marrow-derived dendritic cells. |
| 384 | 24325456 | This activated antigen-specific Th1 cell responses, including IL-2 and interferon-gamma production and proliferation. |
| 385 | 24325394 | The aryl hydrocarbon receptor antagonist StemRegenin 1 promotes human plasmacytoid and myeloid dendritic cell development from CD34+ hematopoietic progenitor cells. |
| 386 | 24325394 | Here, we show that by inhibiting the aryl hydrocarbon receptor with its antagonist StemRegenin 1 (SR1), clinical-scale numbers of functional BDCA2(+)BDCA4(+) pDCs, BDCA1(+) mDCs, and BDCA3(+)DNGR1(+) mDCs can be efficiently generated from human CD34(+) HPCs. |
| 387 | 24325394 | They secreted high levels of pro-inflammatory cytokines such as interferon (IFN)-α, interleukin (IL)-12, and tumor necrosis factor (TNF)-α and upregulated co-stimulatory molecules and maturation markers following stimulation with Toll-like receptor (TLR) ligands. |
| 388 | 24259557 | Consistent with these results, WBM-fed mice had higher interferon-γ, tumor necrosis factor (TNF)-α, and interleukin (IL)-17A production and unchanged IL-4 production in their splenocytes after polyclonal (anti-CD3/CD28) or antigen-specific stimulation. |
| 389 | 24235222 | Mycoplasma synoviae infection of embryos resulted in intensive upregulation of cytokine and chemokine genes, including interferon (IFN)-γ, IL-1β, IL-6, IL-12p40, IL-16, IL-18, MIP-1β (CCL4), inducible nitric oxide synthase (iNOS), XCL1, and lipopolysaccharide-induced tumor necrosis factor-α factor (LITAF), with different expression profiles in the 4 organs. |
| 390 | 24235222 | Inoculation of lentogenic NDV significantly upregulated IFN-γ, IL-6, and IL-16 genes in spleen and IFN-γ, IL-1β, IL-2, IL-16, IL-21, XCL1, and MIP-1β (CCL4) genes in the thymus, but to a lesser extent than M. synoviae. |
| 391 | 24205068 | Toll-like receptor induced pro-interleukin-1β and interleukin-6 in monocytes are lower in healthy infants compared to adults. |
| 392 | 24205068 | We compared Toll-like receptor (TLR)-induced production of pro-interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α between 2-month-old infants and adults. |
| 393 | 24205068 | TLR 7/8-induced production of pro-IL-1β and IL-6 in monocytes was lower in 2-month-old infants compared to adults. |
| 394 | 24205068 | Lower TLR-induced production of pro-IL-1β and IL-6 in innate immune cells during early infancy likely contributes to suboptimal vaccine responses and infectious diseases susceptibility. |
| 395 | 24198065 | In addition, the molecule latent membrane protein 1 (LMP1), a viral mimic of the TNF superfamily receptor CD40, provides an alternative approach for the design of novel molecular adjuvants. |
| 396 | 24198065 | In addition, the molecule latent membrane protein 1 (LMP1), a viral mimic of the TNF superfamily receptor CD40, provides an alternative approach for the design of novel molecular adjuvants. |
| 397 | 24198065 | Here, we discuss advances in the development of recombinant TNF superfamily ligands as adjuvants for HIV vaccines and as cancer immunotherapy, including the use of LMP1 and LMP1-CD40 chimeric fusion proteins to mimic constitutive CD40 signaling. |
| 398 | 24198065 | Here, we discuss advances in the development of recombinant TNF superfamily ligands as adjuvants for HIV vaccines and as cancer immunotherapy, including the use of LMP1 and LMP1-CD40 chimeric fusion proteins to mimic constitutive CD40 signaling. |
| 399 | 24176499 | CD4(+) and CD8(+) T cell proliferation in response to pertussis toxin and/or filamentous hemagglutinin was detected in 79% and 60% of the children respectively, and interferon-γ or tumor necrosis factor-α producing CD4(+) T cells were detected in 65% and 53% of the children respectively. |
| 400 | 24126533 | In contrast to the functional exhaustion of T cells observed after chronic infection, M. tuberculosis-specific CD8(+) T cells differentiated into either effector (CD127(lo) CD62L(lo)) or effector memory (CD127(hi) CD62L(lo)) cells, but not central memory cells (CD127(hi) CD62L(hi)), with low programmed death 1 (PD-1) expression, even in the presence of high levels of bacteria. |
| 401 | 24126533 | Additionally, M. tuberculosis-specific CD8(+) and CD4(+) T cells produced substantial levels of tumor necrosis factor alpha (TNF-α) and gamma interferon (IFN-γ), but not interleukin 2 (IL-2), upon in vitro restimulation. |
| 402 | 24126533 | Among M. tuberculosis-specific CD8(+) T cells, CD127(hi) effector memory cells displayed slower ongoing turnover but greater survival potential. |
| 403 | 24126533 | However, the effector function of M. tuberculosis-specific CD8(+) CD127(hi) effector memory T cells was inferior to that of canonical CD8(+) CD127(hi) memory T cells generated after acute lymphocytic choriomeningitis virus infection. |
| 404 | 24126524 | In vitro infection of bovine monocytes with Mycoplasma bovis delays apoptosis and suppresses production of gamma interferon and tumor necrosis factor alpha but not interleukin-10. |
| 405 | 24126524 | In vitro infection of bovine monocytes with Mycoplasma bovis delays apoptosis and suppresses production of gamma interferon and tumor necrosis factor alpha but not interleukin-10. |
| 406 | 24126524 | Here, we show that infection of bovine blood monocytes with M. bovis delays spontaneous or tumor necrosis factor alpha (TNF-α)/staurosporine-driven apoptosis, activates the NF-κB p65 subunit, and inhibits caspase-9 activity. |
| 407 | 24126524 | Here, we show that infection of bovine blood monocytes with M. bovis delays spontaneous or tumor necrosis factor alpha (TNF-α)/staurosporine-driven apoptosis, activates the NF-κB p65 subunit, and inhibits caspase-9 activity. |
| 408 | 24089561 | We show that the CX4C virus induces higher levels of type I/III interferon (IFN) in A549 cells, increased IFN-α and tumor necrosis factor alpha (TNF-α) production by human plasmacytoid dendritic cells (pDCs) and monocytes, and increased IFN-γ production in effector/memory T cell subpopulations. |
| 409 | 24089189 | For CD8 T cells, all adjuvants induced a comparable response magnitude, but combining poly I:C with ISCOMs induced a high frequency of CD127(+), IL-2-producing cells with decreased expression of Tbet compared with either adjuvant alone. |
| 410 | 24089189 | For CD4 T cells, combining poly I:C and ISCOMs increased the frequency of multifunctional cells, producing IFN-γ, IL-2, and TNF, and the total magnitude of the response compared with either adjuvant alone. |
| 411 | 24089189 | CD8 or CD4 T cell responses induced by both adjuvants mediated protection against Gag-expressing Listeria monocytogenes or vaccinia viral infections. |
| 412 | 24083082 | Here, we report that the administration of L. monocytogenes-based anticancer vaccines increases the secretion of chemokine (C-X-C motif) ligand 9 (CXCL9), and CXCL10 by tumors, hence favoring the recruitment of T cells bearing the cognate chemokine (C-X-C motif) receptor 3 (CXCR3). |
| 413 | 24083082 | Furthermore, the expression of CXCL9, but not CXCL10, in TC-1 tumors was significantly reduced upon anti-IFNγ antibody treatment. |
| 414 | 24083082 | CXCL9 was highly expressed by TC-1 cells following the administration of IFNγ and tumor necrosis factor α (TNFα), in vitro. |
| 415 | 24083082 | Moreover, the inhibition of CXCL9 in TC-1 cells reduced the proportion of CD8+ T cells infiltrating tumors in vaccinated mice, while increasing that of CD4+ T cells, thus altering T-cell subset distribution. |
| 416 | 24069354 | The viral gene A46R is not required for virus replication in primary chicken embryo fibroblast (CEF) cells and its deletion in NYVAC-C markedly increases TNF, IL-6 and IL-8 secretion by human macrophages. |
| 417 | 24069354 | Analysis of the immune responses elicited in BALB/c mice after DNA prime/NYVAC boost immunization shows that deletion of A46R improves the magnitude of the HIV-1-specific CD4 and CD8 T cell immune responses during adaptive and memory phases, maintains the functional profile observed with the parental NYVAC-C and enhances anti-gp120 humoral response during the memory phase. |
| 418 | 24043884 | The roles of IRF-3 and IRF-7 in innate antiviral immunity against dengue virus. |
| 419 | 24043884 | We investigated the roles of IFN regulatory factor (IRF)-3 and IRF-7 in innate antiviral immunity against dengue virus (DENV). |
| 420 | 24043884 | IFN-α/β was induced similarly in wild-type and Irf-3(-/-) mice post-DENV infection, whereas in the Irf-7(-/-) and Irf-3(-/-)7(-/-) mice, significantly low levels of IFN-α/β expression was observed within 24 hpi. |
| 421 | 24043884 | IFN-stimulated gene induction was also delayed in Irf-3(-/-)7(-/-) mice relative to wild-type and single-deficient mice. |
| 422 | 24043884 | In particular, Cxcl10 and Ifnα2 were rapidly induced independently of both IRF-3 and IRF-7 in the Irf-3(-/-)7(-/-) mice with DENV infection. |
| 423 | 24043884 | Higher levels of serum IFN-γ, IL-6, CXCL10, IL-8, IL-12 p70, and TNF were also observed in Irf-3(-/-)7(-/-) mice 24 hpi, at which time point viral titers peaked and started to be cleared. |
| 424 | 24043884 | Ab-mediated blockade experiments revealed that IFN-γ, CXCL10, and CXCR3 function to restrict DENV replication in Irf-3(-/-)7(-/-) mice. |
| 425 | 24043884 | Additionally, the IFN-stimulated genes Cxcl10, Ifit1, Ifit3, and Mx2 can be induced via an IRF-3- and IRF-7-independent pathway that does not involve IFN-γ signaling for protection against DENV. |
| 426 | 24043884 | Collectively, these results demonstrate that IRF-3 and IRF-7 are redundant, albeit IRF-7 plays a more important role than IRF-3 in inducing the initial IFN-α/β response; only the combined actions of IRF-3 and IRF-7 are necessary for efficient control of early DENV infection; and the late, IRF-3- and IRF-7-independent pathway contributes to anti-DENV immunity. |
| 427 | 24035752 | The transcription levels of inflammatory cytokines such as interleukin (IL)-1β, IL-6 and tumor necrosis factor α were significantly up-regulated in the gills at 3 days following exposure to the bacterin. |
| 428 | 24035752 | There was also a corresponding increase in IL-8 receptor, CD4-1, CD4-2 and CD8α transcript levels in the gills. |
| 429 | 24027025 | Moreover, HbR-DNA immunization stimulated the production of protective cytokines like interferon-γ (IFN-γ), interleukin-12 (IL-12), and tumor necrosis factor-α (TNF-α) with concomitant down-regulation of disease-promoting cytokines like IL-10 and IL-4. |
| 430 | 24027025 | HbR-DNA vaccination also induced a protective response by generating multifunctional CD4(+) and CD8(+) T cells. |
| 431 | 24019532 | Toll-like receptor 3-mediated necrosis via TRIF, RIP3, and MLKL. |
| 432 | 24019532 | Toll-like receptor 3-mediated necrosis via TRIF, RIP3, and MLKL. |
| 433 | 24019532 | Toll-like receptor (TLR) signaling is triggered by pathogen-associated molecular patterns that mediate well established cytokine-driven pathways, activating NF-κB together with IRF3/IRF7. |
| 434 | 24019532 | Toll-like receptor (TLR) signaling is triggered by pathogen-associated molecular patterns that mediate well established cytokine-driven pathways, activating NF-κB together with IRF3/IRF7. |
| 435 | 24019532 | In addition, TLR3 drives caspase 8-regulated programmed cell death pathways reminiscent of TNF family death receptor signaling. |
| 436 | 24019532 | In addition, TLR3 drives caspase 8-regulated programmed cell death pathways reminiscent of TNF family death receptor signaling. |
| 437 | 24019532 | We find that inhibition or elimination of caspase 8 during stimulation of TLR2, TLR3, TLR4, TLR5, or TLR9 results in receptor interacting protein (RIP) 3 kinase-dependent programmed necrosis that occurs through either TIR domain-containing adapter-inducing interferon-β (TRIF) or MyD88 signal transduction. |
| 438 | 24019532 | We find that inhibition or elimination of caspase 8 during stimulation of TLR2, TLR3, TLR4, TLR5, or TLR9 results in receptor interacting protein (RIP) 3 kinase-dependent programmed necrosis that occurs through either TIR domain-containing adapter-inducing interferon-β (TRIF) or MyD88 signal transduction. |
| 439 | 24019532 | TLR3 or TLR4 directly activates programmed necrosis through a RIP homotypic interaction motif-dependent association of TRIF with RIP3 kinase (also called RIPK3). |
| 440 | 24019532 | TLR3 or TLR4 directly activates programmed necrosis through a RIP homotypic interaction motif-dependent association of TRIF with RIP3 kinase (also called RIPK3). |
| 441 | 24019532 | In fibroblasts, this pathway proceeds independent of RIP1 or its kinase activity, but it remains dependent on mixed lineage kinase domain-like protein (MLKL) downstream of RIP3 kinase. |
| 442 | 24019532 | In fibroblasts, this pathway proceeds independent of RIP1 or its kinase activity, but it remains dependent on mixed lineage kinase domain-like protein (MLKL) downstream of RIP3 kinase. |
| 443 | 24019532 | Here, we describe two small molecule RIP3 kinase inhibitors and employ them to demonstrate the common requirement for RIP3 kinase in programmed necrosis induced by RIP1-RIP3, DAI-RIP3, and TRIF-RIP3 complexes. |
| 444 | 24019532 | Here, we describe two small molecule RIP3 kinase inhibitors and employ them to demonstrate the common requirement for RIP3 kinase in programmed necrosis induced by RIP1-RIP3, DAI-RIP3, and TRIF-RIP3 complexes. |
| 445 | 24019532 | Cell fate decisions following TLR signaling parallel death receptor signaling and rely on caspase 8 to suppress RIP3-dependent programmed necrosis whether initiated directly by a TRIF-RIP3-MLKL pathway or indirectly via TNF activation and the RIP1-RIP3-MLKL necroptosis pathway. |
| 446 | 24019532 | Cell fate decisions following TLR signaling parallel death receptor signaling and rely on caspase 8 to suppress RIP3-dependent programmed necrosis whether initiated directly by a TRIF-RIP3-MLKL pathway or indirectly via TNF activation and the RIP1-RIP3-MLKL necroptosis pathway. |
| 447 | 23980113 | Here, we have further characterized vaccine-induced changes in the CD8(+) T cell phenotype and demonstrated significant upregulation of CD11c on CD3(+) CD8b(+) T cells in the liver, spleen, and peripheral blood. |
| 448 | 23980113 | CD11c(+) CD8(+) T cells are predominantly CD11a(hi) CD44(hi) CD62L(-), indicative of antigen-experienced effector cells. |
| 449 | 23980113 | Following in vitro restimulation with malaria-infected hepatocytes, CD11c(+) CD8(+) T cells expressed inflammatory cytokines and cytotoxicity markers, including IFN-γ, tumor necrosis factor alpha (TNF-α), interleukin-2 (IL-2), perforin, and CD107a. |
| 450 | 23980113 | CD11c(-) CD8(+) T cells, on the other hand, expressed negligible amounts of all inflammatory cytokines and cytotoxicity markers tested, indicating that CD11c marks multifunctional effector CD8(+) T cells. |
| 451 | 23980113 | Coculture of CD11c(+), but not CD11c(-), CD8(+) T cells with sporozoite-infected primary hepatocytes significantly inhibited liver-stage parasite development. |
| 452 | 23980113 | Tetramer staining for the immunodominant circumsporozoite protein (CSP)-specific CD8(+) T cell epitope demonstrated that approximately two-thirds of CSP-specific cells expressed CD11c at the peak of the CD11c(+) CD8(+) T cell response, but CD11c expression was lost as the CD8(+) T cells entered the memory phase. |
| 453 | 23980113 | Further analyses showed that CD11c(+) CD8(+) T cells are primarily KLRG1(+) CD127(-) terminal effectors, whereas all KLRG1(-) CD127(+) memory precursor effector cells are CD11c(-) CD8(+) T cells. |
| 454 | 23966552 | The CD3(+) CD4(-) CD8(hi) T cell population was the first and major source of CSFV-specific IFN-γ. |
| 455 | 23966552 | A proportion of these cells showed evidence for cytotoxicity, as evidenced by CD107a mobilization, and coexpressed tumor necrosis factor alpha (TNF-α). |
| 456 | 23966552 | While virus-specific CD4 T cell (CD3(+) CD4(+) CD8α(+)) responses were detected, the dominant response was again from the CD8 T cell population, with the highest numbers of these cells being detected 14 and 7 days after the primary and secondary challenges, respectively. |
| 457 | 23966552 | These CD8 T cells were further characterized as CD44(hi) CD62L(-) and expressed variable levels of CD25 and CD27, indicative of a mixed effector and effector memory phenotype. |
| 458 | 23966552 | The majority of virus-specific IFN-γ(+) CD8 T cells isolated at the peaks of the response after each challenge displayed CD107a on their surface, and subpopulations that coexpressed TNF-α and interleukin 2 (IL-2) were identified. |
| 459 | 23947352 | The contextual role of TNFR family members in CD8(+) T-cell control of viral infections. |
| 460 | 23947352 | The contextual role of TNFR family members in CD8(+) T-cell control of viral infections. |
| 461 | 23947352 | The role of specific TNF receptor (TNFR) family members in antiviral immunity depends on the stage of the immune response and can vary with the virus type and its virulence. |
| 462 | 23947352 | The role of specific TNF receptor (TNFR) family members in antiviral immunity depends on the stage of the immune response and can vary with the virus type and its virulence. |
| 463 | 23947352 | Here, we focus on five members of the TNFR family that are prominently expressed on CD8(+) T cells during viral infections, namely, 4-1BB (CD137), CD27, OX40 (CD134), GITR, and TNFR2. 4-1BB, CD27, OX40, and GITR have primarily prosurvival roles for CD8(+) T cells during viral infection, although under some circumstances 4-1BB, GITR, or CD27 signals can limit immunity. |
| 464 | 23947352 | Here, we focus on five members of the TNFR family that are prominently expressed on CD8(+) T cells during viral infections, namely, 4-1BB (CD137), CD27, OX40 (CD134), GITR, and TNFR2. 4-1BB, CD27, OX40, and GITR have primarily prosurvival roles for CD8(+) T cells during viral infection, although under some circumstances 4-1BB, GITR, or CD27 signals can limit immunity. |
| 465 | 23947352 | Although TNFR2 can be costimulatory under some circumstances, its main role in CD8(+) T-cell responses during viral infection appears to be in contraction of the response. |
| 466 | 23947352 | Although TNFR2 can be costimulatory under some circumstances, its main role in CD8(+) T-cell responses during viral infection appears to be in contraction of the response. |
| 467 | 23947352 | Several TNF family ligands are being explored as adjuvants for viral vaccines, and agonistic antibodies to TNFR family members are being investigated for immunotherapy of chronic viral infection alone and in combination with checkpoint blockade. |
| 468 | 23947352 | Several TNF family ligands are being explored as adjuvants for viral vaccines, and agonistic antibodies to TNFR family members are being investigated for immunotherapy of chronic viral infection alone and in combination with checkpoint blockade. |
| 469 | 23933364 | IL-4 and IL-13 mediated down-regulation of CD8 expression levels can dampen anti-viral CD8⁺ T cell avidity following HIV-1 recombinant pox viral vaccination. |
| 470 | 23933364 | We have shown that mucosal HIV-1 recombinant pox viral vaccination can induce high, avidity HIV-specific CD8(+) T cells with reduced interleukin (IL)-4 and IL-13 expression compared to, systemic vaccine delivery. |
| 471 | 23933364 | Out of a panel of T cell avidity markers tested, only CD8 expression levels were found to be enhanced on, KdGag197-205 (HIV)-specific CD8(+) T cells obtained from IL-13(-/-), IL-4(-/-) and signal transducer and, activator of transcription of 6 (STAT6)(-/-) mice compared to wild-type (WT) controls following, vaccination. |
| 472 | 23933364 | Elevated CD8 expression levels in this instance also correlated with polyfunctionality, (interferon (IFN)-γ, tumour necorsis factor (TNF)-α and IL-2 production) and the avidity of HIVspecific CD8(+) T cells. |
| 473 | 23933364 | IL-13Rα2) vaccines significantly enhanced CD8 expression levels on HIV-specific CD8(+), T cells, which correlated with avidity. |
| 474 | 23933364 | Using anti-CD8 antibodies that blocked CD8 availability on CD8(+), T cells, it was established that CD8 played an important role in increasing HIV-specific CD8(+) T cell avidity and polyfunctionality in IL-4(-/-), IL-13(-/-) and STAT6(-/-) mice compared to WT controls, following vaccination. |
| 475 | 23933364 | Collectively, our data demonstrate that IL-4 and IL-13 dampen CD8 expression levels on anti-viral CD8(+) T cells, which can down-regulate anti-viral CD8(+) T cell avidity and, polyfunctionality following HIV-1 recombinant pox viral vaccination. |
| 476 | 23928481 | Our previous study established that Poly-ICLC is the most potent individual maturation stimulus for human DCs as assessed by an upregulation of CD83 and CD86, induction of interleukin-12 (IL-12), tumor necrosis factor (TNF), interferon gamma-induced protein 10 (IP-10), interleukmin 1 (IL-1), and type I interferons (IFN), and minimal interleukin 10 (IL-10) production. |
| 477 | 23928481 | After incubation, the lymphocytes are washed off and the adherent monocytes are cultured for 5 days in the presence of interleukin-4 (IL-4) and granulocyte macrophage-colony stimulating factor (GM-CSF) to differentiate to immature DCs. |
| 478 | 23897618 | Sustained production of IFN-γ, interleukin-2, and tumor necrosis factor alpha was elicited in both the CD4(+) and CD8(+) T cell compartments. |
| 479 | 23897618 | Notably, antigen-specific CD8(+) granzyme B(+) T cells were observed in NHPs. |
| 480 | 23845817 | Protection is mediated by a strong innate and CD4 Th1, CD8 Tc1 immune response. |
| 481 | 23845817 | Splenocytes from strain RB51 with TLR2 vaccinated mice up-regulated antigen specific interferon-gamma and TNF-alpha production. |
| 482 | 23845817 | Vaccination and challenge resulted in significant increases in activated dendritic cells (DCs), and increased CD4 and CD8 cells in the BAL. |
| 483 | 23836827 | Significantly higher levels of gamma interferon (IFN-γ)/interleukin-2 (IL-2)/tumor necrosis factor (TNF) multifunctional T cells were noted in immunized mice than in control mice. |
| 484 | 23836827 | We also report the first identification of minimal CD8(+) and CD4(+) T cell epitopes on Plasmodium yoelii AMA-1. |
| 485 | 23825193 | We previously reported that sepsis differentially represses transcription and translation of tumor necrosis factor alpha (TNF-α) and interleukin 1β (IL-1β) to reprogram sepsis inflammation. |
| 486 | 23825193 | We showed that phosphorylation-dependent activation of p38 mitogen-activated protein kinase (MAPK) and translation disruption of TNF-α and IL-6 follow increased MAPK phosphatase 1 (MKP-1) expression and that MKP-1 knockdown rephosphorylates p38 and restores the capacity to translate TNF-α and IL-6 mRNAs. |
| 487 | 23825193 | We also observed that the RNA-binding protein motif 4 (RBM4), a p38 MAPK target, accumulates in an unphosphorylated form in the cytosol in endotoxin-adapted cells, suggesting that dephosphorylated RBM4 may function as a translational repressor. |
| 488 | 23825193 | Moreover, MKP-1 knockdown promotes RBM4 phosphorylation, blocks its transfer from the nucleus to the cytosol, and reverses translation repression. |
| 489 | 23825193 | We also found that microRNA 146a (miR-146a) knockdown prevents and miR-146a transfection induces MKP-1 expression, which lead to increases or decreases in TNF-α and IL-6 translation, respectively. |
| 490 | 23825193 | We conclude that a TLR4-, miR-146a-, p38 MAPK-, and MKP-1-dependent autoregulatory pathway regulates the translation of proinflammatory genes during the acute inflammatory response by spatially and temporally modifying the phosphorylation state of RBM4 translational repressor protein. |
| 491 | 23773020 | Murine bone marrow-derived dendritic cells (DCs) stimulated in vitro with ApxIIA#5-expressed on S. cerevisiae upregulated the expression of maturation and activation markers, leading to production of tumor necrosis factor-α, interleukin (IL)-1β, IL-12p70 and IL-10. |
| 492 | 23771216 | Wild-type measles virus infection upregulates poliovirus receptor-related 4 and causes apoptosis in brain endothelial cells by induction of tumor necrosis factor-related apoptosis-inducing ligand. |
| 493 | 23771216 | Wild-type measles virus infection upregulates poliovirus receptor-related 4 and causes apoptosis in brain endothelial cells by induction of tumor necrosis factor-related apoptosis-inducing ligand. |
| 494 | 23771216 | Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), but not Fas ligand, was induced by MV infection. |
| 495 | 23771216 | Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), but not Fas ligand, was induced by MV infection. |
| 496 | 23734306 | Co-stimulatory members of the tumor necrosis factor ligand (TNFL) family may be used in this sense due to their pleiotropic and robust effects on cells of innate, adaptive and regulatory immune responses. |
| 497 | 23720366 | Upregulation of tumor necrosis factor alpha-induced protein 3 mRNA in mild psoriasis vulgaris. |
| 498 | 23716300 | MyD88 and TRIF synergistic interaction is required for TH1-cell polarization with a synthetic TLR4 agonist adjuvant. |
| 499 | 23716300 | Different TLR4 agonists may preferentially signal via MyD88 or TIR-domain-containing adapter inducing IFN-beta (TRIF) to exert adjuvant effects; however, the contribution of MyD88 and TRIF signaling to the induction of polyclonal T(H)1 responses by TLR4 agonist adjuvants has not been studied in vivo. |
| 500 | 23716300 | To determine whether GLA-SE preferentially signals through MyD88 or TRIF, we evaluated the immune response against a candidate tuberculosis (TB) vaccine Ag following immunization of mice lacking either signaling adapter compared with that of wild-type mice. |
| 501 | 23716300 | We find that both MyD88 and TRIF are necessary for GLA-SE to induce a poly-functional T(H)1 immune response characterized by CD4(+) T cells producing IFN-γ, TNF, and IL-2, as well as IgG2c class switching, when paired with the TB vaccine Ag ID93. |
| 502 | 23716300 | We demonstrate that MyD88 and TRIF must be expressed in the same cell for the in vivo T(H)1-skewing adjuvant activity, indicating that these two signaling pathways cooperate on an intracellular level. |
| 503 | 23716300 | Thus engagement of both the MyD88 and TRIF signaling pathways are essential for the effective adjuvant activity of this TLR4 agonist. |
| 504 | 23708293 | The two approaches yielded similar beneficial results in evaluation of the disease activity parameters (stool consistency, weight loss and colon length) as well as VEGF expression and tumor necrosis factor-α (TNF-α). |
| 505 | 23708146 | The immunization of mice with recombinant PE3 protein stimulated the secretion of TNF, IL-6 and IL-2 cytokines and generated strong protective immunity against challenge with live mycobacteria, which was evidenced by decreased viable bacilli in the lungs, histopathological changes and increased survival of PE3 immunized mice. |
| 506 | 23697573 | Blood plasma cytokine concentrations did not differ between the ORS cases and controls for most cytokines measured (interleukin 4 [IL-4], IL-5, IL-10, IL-13, IL-1α, IL-8, tumor necrosis factor alpha [TNF-α], gamma interferon [IFN-γ], and IL-17A). |
| 507 | 23697573 | However, ORS cases had higher levels of IL-10 and IL-3 than the controls at visits 1 and 2, even after all symptoms had subsided. |
| 508 | 23697573 | Persistent higher levels of IL-10 and IL-3 in ORS cases suggest that host factors may have predisposed these individuals to develop ORS following influenza vaccination. |
| 509 | 23681283 | We investigated whether HDAC inhibitors augmented antitumor effect of indoleamine 2,3 dioxygenase (IDO) shRNA. |
| 510 | 23681283 | In addition, OSU-HDAC42 treatment did not alter mRNA expression of IL-12 and tumor necrosis factor-α. |
| 511 | 23638188 | The P domain complexes induced significant central memory CD4(+) T cell phenotypes (CD4(+) CD44(+) CD62L(+) CCR7(+)) and activated polyclonal CD4(+) T cells as shown by production of Interleukin (IL)-2, Interferon (IFN)-γ, and Tumor Necrosis Factor (TNF)-α. |
| 512 | 23638188 | Furthermore, P domain complexes efficiently induced bone marrow-derived dendritic cell (BMDC) maturation, evidenced by up-regulation of co-stimulatory and MHC class II molecules, as well as production of IL-12 and IL-1β. |
| 513 | 23637043 | At 24 h after LPS injection, renal glomerular hypercellularity and hepatocellular injury were observed in both strains, accompanying further elevated serum levels of creatinine and alanine aminotransferase in TRPV1(-/-) mice compared to those in WT mice. |
| 514 | 23637043 | At 6 or 24 h after LPS injection, neutrophil recruitment into kidneys and livers, serum cytokine (tumor necrosis factor alpha [TNF-α], interleukin 1β [IL-1β], IL-6) and renal chemokine (KC, macrophage inflammatory protein 2 [MIP-2]) levels, and renal VCAM-1 and ICAM-1 expression were greater in TRPV1(-/-) mice than WT mice. |
| 515 | 23637043 | In addition, increased plasma calcitonin gene-related peptide (CGRP) levels observed in WT mice 6 h after LPS injection were absent in TRPV1(-/-) mice. |
| 516 | 23631767 | Cytokine production from BMDCs treated with the AuNP-Es revealed that only Rod-E-treated cells produced significant levels of interleukin-1β (IL-1β) and interleukin-18 (IL-18), indicating that Rod-Es activated inflammasome-dependent cytokine secretion. |
| 517 | 23631767 | Meanwhile, Sphere40-Es and Cube-Es both significantly induced inflammatory cytokine production, including tumor necrosis factor-α (TNF-α), IL-6, IL-12, and granulocyte macrophage colony-stimulating factor (GM-CSF). |
| 518 | 23616409 | Stimulation of human macrophages with T. forsythia LPS resulted in the production of the proinflammatory cytokines interleukin-1 (IL-1), IL-6, and tumor necrosis factor alpha in a dose-dependent manner. |
| 519 | 23607482 | No differences were observed in γδ T cells for the same patient in either situation, and a tendency to lower percentages of CD4(+) CD25(hi) T cells was observed under stability. |
| 520 | 23607482 | A significantly lower production of tumour necrosis factor (TNF)-α and a significantly higher production of interleukin (IL)-5 was observed in asthma patients compared to healthy individuals, but no differences could be observed for IL-4, IL-13 or IL-10. |
| 521 | 23595503 | Reduced frequency of a CD14+ CD16+ monocyte subset with high Toll-like receptor 4 expression in cord blood compared to adult blood contributes to lipopolysaccharide hyporesponsiveness in newborns. |
| 522 | 23595503 | To better understand the mechanistic basis for this age-related difference in innate immunity, we compared tumor necrosis factor alpha (TNF-α) production by monocytes from cord blood (CB) and adult blood (AB) in response to LAM (lipoarabinomannan from Mycobacterium tuberculosis, a TLR2 ligand) and LPS (lipopolysaccharide from Escherichia coli, a TLR4 ligand). |
| 523 | 23595503 | LPS or LAM-induced TNF-α production was 5 to 18 times higher in AB than in CB monocytes, whereas interleukin-1α (IL-1α) stimulated similar levels of TNF-α in both groups, suggesting that decreased responses to LPS or LAM in CB are unlikely to be due to differences in the MyD88-dependent signaling pathway. |
| 524 | 23595503 | This impaired signaling was attributable, in part, to lower functional TLR4 expression, especially on CD14(+) CD16(+) monocytes, which are the primary cell subset for LPS-induced TNF-α production. |
| 525 | 23595503 | Importantly, the frequency of CD14(+) CD16(+) monocytes in CB was 2.5-fold lower than in AB (P < 0.01). |
| 526 | 23595503 | CB from Kenyan newborns sensitized to parasite antigens in utero had more CD14(+) CD16(+) monocytes (P = 0.02) and produced higher levels of TNF-α in response to LPS (P = 0.004) than CB from unsensitized Kenyan or North American newborns. |
| 527 | 23595503 | Thus, a reduced CD14(+) CD16(+) activated/differentiated monocyte subset and a correspondingly lower level of functional TLR4 on monocytes contributes to the relatively low TNF-α response to LPS observed in immunologically naive newborns compared to the response in adults. |
| 528 | 23580062 | Key findings of this study are summarized by the following model predictions: i) increased strength and duration of memory protection is associated with higher levels of Tumor Necrosis Factor-[Formula: see text] (TNF) during primary infection; ii) production of TNF, but not of interferon-[Formula: see text], by memory T cells during secondary infection is a major determinant of effective protection; iii) impaired recruitment of CD4+ T cells may promote reactivation of latent TB infections in aging hosts. |
| 529 | 23577175 | The pro-inflammatory cytokines tested Interleukin (IL)-6, IL17A, tumour necrosis factor (TNF)-α did not influence IFN-α responses except TNF-α, which promoted responses induced by FMDV. |
| 530 | 23577175 | The haematopoietic cytokines Fms-related tyrosine kinase 3 ligand (Flt3-L) and granulocyte-macrophage colony-stimulating factor (GM-CSF) had enhancing effects on pDC activation at least in one of the protocols tested. |
| 531 | 23577175 | Interestingly, also the Th2 cytokine IL-4 was an efficient promoter of pDC activity, while IL-10 was the only negative regulator of IFN-α in pDC identified. |
| 532 | 23555269 | Murine models of pneumococcal colonisation show that IL-17A-secreting CD4(+) T-cells (Th-17 cells) are essential for clearance of pneumococci from the nasopharynx. |
| 533 | 23555269 | Pneumococcal-responding IL-17A-secreting CD4(+) T-cells have not been described in the adult human lung and it is unknown whether they can be elicited by carriage and protect the lung from pneumococcal infection. |
| 534 | 23555269 | We showed that human pneumococcal carriage leads to a 17.4-fold (p = 0.007) and 8-fold (p = 0.003) increase in the frequency of cognate IL-17A(+) CD4(+) T-cells in BAL and blood, respectively. |
| 535 | 23555269 | The phenotype with the largest proportion were TNF(+)/IL-17A(+) co-producing CD4(+) memory T-cells (p<0.01); IFNγ(+) CD4(+) memory T-cells were not significantly increased following carriage. |
| 536 | 23555269 | Pneumococci could stimulate large amounts of IL-17A protein from BAL cells in the absence of carriage but in the presence of cognate CD4(+) memory T-cells, IL-17A protein levels were increased by a further 50%. |
| 537 | 23555269 | We conclude that human pneumococcal carriage can increase the proportion of lung IL-17A-secreting CD4(+) memory T-cells that may enhance innate cellular immunity against pathogenic challenge. |
| 538 | 23554897 | Respiratory infection with the attenuated Live Vaccine Strain (LVS) and the highly virulent SchuS4 strain of Ft engenders intense peribronchiolar and perivascular inflammation, but fails to elicit select pro-inflammatory mediators (e.g., TNF, IL-1β, IL-6, IL-12, and IFN-γ) within the first ~72 h. |
| 539 | 23554897 | Respiratory infection with the attenuated Live Vaccine Strain (LVS) and the highly virulent SchuS4 strain of Ft engenders intense peribronchiolar and perivascular inflammation, but fails to elicit select pro-inflammatory mediators (e.g., TNF, IL-1β, IL-6, IL-12, and IFN-γ) within the first ~72 h. |
| 540 | 23554897 | Growth of Ft in Muller-Hinton Broth or on Muller-Hinton-based chocolate agar plates or genetic mutation of Ft was found to compromise the structural integrity of the bacterium thus rendering it capable of aberrantly eliciting pro-inflammatory mediators (e.g., TNF, IL-1β, IL-6, IL-12, and IFN-γ). |
| 541 | 23554897 | Growth of Ft in Muller-Hinton Broth or on Muller-Hinton-based chocolate agar plates or genetic mutation of Ft was found to compromise the structural integrity of the bacterium thus rendering it capable of aberrantly eliciting pro-inflammatory mediators (e.g., TNF, IL-1β, IL-6, IL-12, and IFN-γ). |
| 542 | 23527290 | Preliminary characterisation of tumor necrosis factor alpha and interleukin-10 responses to Chlamydia pecorum infection in the koala (Phascolarctos cinereus). |
| 543 | 23508902 | Peripheral blood lymphocyte counts indicated lymphopenia and inverted ratios of CD4(+) to CD8(+) cells. |
| 544 | 23508902 | Cytokine analysis showed that the levels of serum IL-6, IL-10, and IFN-r continued to increase, whereas the levels of IL-12 and TNFs decreased during the clinical course. |
| 545 | 23508902 | MCP-1 and IP-10 remained at a high level after infection. |
| 546 | 23507086 | Molecular pathways upregulated by MA-CNTs included IL6, CD40, dendritic cell maturation, tumor necrosis factor-(TNF)-α/TNFR1-2, NFKB signaling and T helper 1 chemokine pathways (CXCR3 and CCR5 ligand pathways). |
| 547 | 23507086 | To confirm the results at protein level, the secretion of IL1β, TNFα, IL6 and IL10 by THP1 and primary monocytes was assessed by ELISA, corroborating gene-expression data. |
| 548 | 23493554 | Using an array-based sequencing assay, we identified an autosomal-dominant deficiency in TNF-like weak inducer of apoptosis (TWEAK; TNFSF12) in a kindred with recurrent infection and impaired antibody responses to protein and polysaccharide vaccines. |
| 549 | 23493554 | Using an array-based sequencing assay, we identified an autosomal-dominant deficiency in TNF-like weak inducer of apoptosis (TWEAK; TNFSF12) in a kindred with recurrent infection and impaired antibody responses to protein and polysaccharide vaccines. |
| 550 | 23493554 | This mutation occurs in the sixth exon of TWEAK and results in the amino acid substitution R145C within the conserved TNF-homology domain of the full-length protein. |
| 551 | 23493554 | This mutation occurs in the sixth exon of TWEAK and results in the amino acid substitution R145C within the conserved TNF-homology domain of the full-length protein. |
| 552 | 23493554 | As a result, mutant TWEAK associated with B-cell-activating factor (BAFF) protein and down-regulated the BAFF-mediated activation of the noncanonical NF-κB pathway through inhibition of p100 processing to p52, resulting in inhibition of BAFF-dependent B-cell survival and proliferation. |
| 553 | 23493554 | As a result, mutant TWEAK associated with B-cell-activating factor (BAFF) protein and down-regulated the BAFF-mediated activation of the noncanonical NF-κB pathway through inhibition of p100 processing to p52, resulting in inhibition of BAFF-dependent B-cell survival and proliferation. |
| 554 | 23493554 | As BAFF mediates T-cell-independent isotype switching and B-cell survival, our data implicate TWEAK as a disease-susceptibility gene for a humoral immunodeficiency. |
| 555 | 23493554 | As BAFF mediates T-cell-independent isotype switching and B-cell survival, our data implicate TWEAK as a disease-susceptibility gene for a humoral immunodeficiency. |
| 556 | 23490396 | ELISpot assays for HCV-induced interferon (IFN)-γ and interleukin (IL)-2 production by T lymphocytes, as well as multiplex in vitro cytokine production assays, were performed. |
| 557 | 23490396 | The IFN-γ ELISpot responses involved both CD4 and CD8 T lymphocytes and were comparable in magnitude, but narrower in specificity, in uninfected subjects than in seroconverters. |
| 558 | 23490396 | A subset of seronegative subjects had HCV-induced cytokine production patterns comparable with the seroconverters with increased production of IFN-γ, IL-2 and tumour necrosis factor (TNF)-α and reduced IL-10 in response to nonstructural peptides. |
| 559 | 23486418 | In addition, children with active TB had significantly elevated levels of C-reactive protein, α-2 macroglobulin, and haptoglobin, as well as hemoxygenase 1. |
| 560 | 23486418 | Markers of innate immune activation (lipopolysaccharide [LPS] and lipopolysaccharide-binding protein [LBP]) were significantly lower in ETB than in PTB children. |
| 561 | 23486418 | Although there were no significant differences between the two groups in their levels of cytokines (type 1 [gamma interferon (IFN-γ), tumor necrosis factor α (TNF-α), interleukin 2 (IL-2), and IL-12], type 2 [IL-4, IL-5, IL-13, and IL-33], and most type 17 [IL-17A, IL-22, IL-1β, and IL-6] and type 1 interferons [IFN-α and IFN-β]) or most of the cytokines associated with immune modulation (IL-10 and IL-20), pediatric TB was associated with elevated plasma transforming growth factor β (TGF-β), IL-21, and IL-23 levels. |
| 562 | 23465356 | Alteration in the mRNA concentrations of tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-10 in whole-blood culture at 4h after stimulation with different doses of LPS was observed and determined by quantitative reverse-transcription polymerase chain reaction (qRT-PCR). |
| 563 | 23460531 | The list of antagonist agents acting on repressors under development includes anti-CTLA-4, anti-PD-1, anti-PD-L1 (B7-H1), anti-KIR, and anti-TGF-β. |
| 564 | 23460531 | Agonist antibodies currently being investigated in clinical trials target CD40, CD137 (4-1BB), CD134 (OX40), and glucocorticoid-induced TNF receptor (GITR). |
| 565 | 23439306 | Boosting LVS ΔcapB-primed mice with rLm/iglC significantly enhanced T cell immunity; their splenic T cells secreted significantly more gamma interferon (IFN-γ) and had significantly more cytokine (IFN-γ and/or tumor necrosis factor [TNF] and/or interleukin-2 [IL-2])-producing CD4(+) and CD8(+) T cells upon in vitro IglC stimulation. |
| 566 | 23370464 | TNFSF14 is one of the most important TNF superfamily cytokines playing roles in lymphocyte homeostasis by enhancing effector cell activation and survival, or by cellular elimination through apoptosis. |
| 567 | 23370464 | The obtained results will lay the foundation for future study of human TNFSF14/LTBR signal pathway and relative diseases in O. cuniculus model. |
| 568 | 23364316 | Both PRL-3-targeted cytotoxic T lymphocytes (CTLs) and T-helper type 1 cell immune response (production of high levels of interferon-γ and tumor necrosis factor-α) were found to be involved in the preventive effect. |
| 569 | 23354042 | Clostridium butyricum MIYAIRI 588 shows antitumor effects by enhancing the release of TRAIL from neutrophils through MMP-8. |
| 570 | 23354042 | Recent studies have demonstrated urinary tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) levels to be higher in BCG-responsive patients than non-responders and shown that polymorphonuclear neutrophils (PMNs) migrating to the bladder after BCG instillation release large amounts of TRAIL. |
| 571 | 23354042 | Interestingly, TLR2/4 signaling pathway has been suggested to be important for the release of TRAIL by MMP-8. |
| 572 | 23345580 | After 24 h of incubation, production of tumor necrosis factor alpha (TNF-α), interleukin-1 beta (IL-1β), IL-6, and IL-10 was measured in supernatants by enzyme-linked immunosorbent assay (ELISA). |
| 573 | 23345580 | The combinations of TLR2 and NOD2, TLR5 and NOD2, TLR5 and TLR3, and TLR5 and TLR9 acted as synergistic combinations. |
| 574 | 23345580 | Surprisingly, inhibitory interactions between TLR4 and TLR2, TLR4 and Dectin-1, and TLR2 and TLR9 as well as TLR3 and TLR2 were observed. |
| 575 | 23330678 | To study the immunogenicity of the HIV-1 vif DNA vaccine in inducing the humoral and cellular immune responses and the immunoadjuvant effect of LIGHT, which is a member of TNF superfamily and can stimulate the proliferation of naïve T cells as a co-stimulatory molecule, DNA vaccine plasmid pcDNA-Vif was constructed by inserting HIV-1 vif gene into the downstream of CMV promoter in eukaryotic expression vector pcDNA3.1(+). |
| 576 | 23300801 | On in vitro circumsporozoite protein (CSP) peptide stimulation and intra-cellular cytokine staining of whole blood taken from 407 5-17 month-old children in a phase IIb trial of RTS,S/AS01(E), we identified significantly increased frequencies of two CSP-specific CD4+ T cells phenotypes among RTS,S/AS01(E) vaccinees (IFNγ-IL2+TNF- and IFNγ-IL2+TNF+ CD4+ T cells), and increased frequency of IFNγ-IL2-TNF+ CD4+ T cells after natural exposure. |
| 577 | 23300801 | Furthermore, there was a strongly significant synergistic interaction between CSP-specific IFNγ-IL2-TNF+ CD4+ T cells and anti-CSP antibodies in determining protection against clinical malaria (p = 0.002). |
| 578 | 23291105 | In addition, the expression levels of immune-related genes such as interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), major histocompatibility complexes I and II (MHC I and II), and transforming growth factor-β1 (TGF-β1) were determined in spleen and gills. |
| 579 | 23284789 | Interleukin-15-induced CD56(+) myeloid dendritic cells combine potent tumor antigen presentation with direct tumoricidal potential. |
| 580 | 23284789 | Notwithstanding marked expression of the natural killer (NK) cell marker CD56 on a subset of IL-15 DCs, we found no evidence of a further phenotypic overlap between IL-15 DCs and NK cells. |
| 581 | 23284789 | The cytotoxicity of IL-15 DCs is predominantly mediated by granzyme B and, to a small extent, by tumor necrosis factor-α (TNF-α)-related apoptosis-inducing ligand (TRAIL) but is independent of perforin, Fas ligand and TNF-α. |
| 582 | 23284733 | Furthermore, HCV protein levels in liver tissue also decreased in a CD4 and CD8 T-cell-dependent manner. |
| 583 | 23284733 | We also demonstrated that the onset of chronic hepatitis in CN2-29((+/-))/MxCre((+/-)) mice was mainly attributable to inflammatory cytokines, (tumor necrosis factor) TNF-α and (interleukin) IL-6. |
| 584 | 23267892 | [Prediction of WT1/MUC1 peptide dendritic cell therapy responders by quantification of ex vivo induced mRNA in whole blood]. |
| 585 | 23267892 | To challenge this classic problem, we quantified 17 different leukocyte function-associated mRNAs( IFN-γ,TNFSF1, TNFSF2, TNFSF5, IL-10, TGF β,CTLA4, PD1, FOXP3, GMCSF, VEGF, IL-8, CCL8, CXCL3, and IL-2) in whole blood after ex vivo stimulation with 7 different agents(PHA, HAG, zymosan, IFN-γ,rIL-2, aTCR, and picibanil) to activate various subsets of leukocytes. |
| 586 | 23267892 | The clinical outcomes for WT1 peptide-and/or MUC1 peptide-pulsed dendritic cell therapy for advanced cancer (n=26) were CR+PR, 4 cases; SD, 9 cases; and PD, 13 cases. |
| 587 | 23225417 | We have been successfully performing WT1 vaccination with a 9-mer modified WT1(235) peptide, which has one amino acid substitution (M→Y) at position 2 of 9-mer natural WT1(235) peptide (235-243 a.a.), for close to 700 HLA-A*24:02-positive patients with leukemia or solid tumors. |
| 588 | 23225417 | In this study, we established a modified WT1(235) peptide-specific CTL clone, we isolated T-cell receptor (TCR) genes from it and transduced the TCR genes into CD8(+) T-cells. |
| 589 | 23225417 | The TCR-transduced CD8(+) T-cells produced interferon-γ (IFNγ) and tumor necrosis factor-α (TNFα) in response to stimulation not only with the modified WT1(235) peptide but also with the natural WT1(235) peptide and lysed modified or natural WT1(235) peptide-pulsed target cells and endogenously WT1-expressing leukemia cells in a HLA-A*24:02-restriction manner. |
| 590 | 23221000 | The levels of CD8(+) and γδTcR(+) T cells increased significantly (P < 0.05) in the lamina propria, and M. avium subsp. paratuberculosis-specific tumor necrosis factor alpha (TNF-α) and gamma interferon secretion by lamina propria leukocytes was also significantly (P < 0.05) increased. |
| 591 | 23166298 | Sonic hedgehog-dependent induction of microRNA 31 and microRNA 150 regulates Mycobacterium bovis BCG-driven toll-like receptor 2 signaling. |
| 592 | 23166298 | Interestingly, sustained tumor necrosis factor alpha (TNF-α) secretion by macrophages was essential for robust SHH activation, as TNF-α(-/-) macrophages exhibited compromised ability to activate SHH signaling. |
| 593 | 23166298 | Intriguingly, activated SHH signaling downregulated M. bovis BCG-mediated Toll-like receptor 2 (TLR2) signaling events to regulate a battery of genes associated with divergent functions of M1/M2 macrophages. |
| 594 | 23166298 | Genome-wide expression profiling as well as conventional gain-of-function or loss-of-function analysis showed that SHH signaling-responsive microRNA 31 (miR-31) and miR-150 target MyD88, an adaptor protein of TLR2 signaling, thus leading to suppression of TLR2 responses. |
| 595 | 23132493 | Nevertheless, we found, unexpectedly, that Mycobacterium bovis bacillus Calmette-Guerin (BCG)-vaccinated monkeys exhibited GMM-specific T cell responses that were restricted by CD1c rather than CD1b molecules. |
| 596 | 23132493 | The circulating GMM-specific T cells were detected broadly in both CD4(+) and CD8(+) cell populations, and upon antigenic stimulation, a majority of the GMM-specific T cells produced both gamma interferon (IFN-γ) and tumor necrosis factor alpha (TNF-α), two major host protective cytokines functioning against infection with mycobacteria. |
| 597 | 23103299 | Immunization with the multistage-polyepitope adjuvanted with CpG generated high IgG levels as well as polyfunctional CD4(+) T-cells producing IFN-γ, TNF and IL-2, specific for these HLA-DR3-restricted epitopes. |
| 598 | 23054742 | Expression of tumor necrosis factor alpha-induced protein 3 mRNA in peripheral blood mononuclear cells negatively correlates with disease severity in psoriasis vulgaris. |
| 599 | 23054742 | Expression of tumor necrosis factor alpha-induced protein 3 mRNA in peripheral blood mononuclear cells negatively correlates with disease severity in psoriasis vulgaris. |
| 600 | 23054742 | The tumor necrosis factor alpha-induced protein 3 (TNFAIP3) gene functions in negative-feedback regulation of inflammation, and its single nucleotide polymorphism is associated with psoriasis. |
| 601 | 23054742 | The tumor necrosis factor alpha-induced protein 3 (TNFAIP3) gene functions in negative-feedback regulation of inflammation, and its single nucleotide polymorphism is associated with psoriasis. |
| 602 | 23015647 | Tumor necrosis factor alpha (TNF-α), interleukin 10 (IL-10), and IL-6 were commonly detected at high levels after stimulation with 4/15 latency antigens (Rv0081, Rv2006, Rv2629, and Rv1733c) and were found especially in supernatants of the three strong IFN-γ inducers (Rv2629, Rv1009, and Rv2389c). |
| 603 | 23015647 | IL-8, IL-6, and IL-17 were exclusively detected after stimulation with Rv0574c, Rv2630, Rv1998, Rv054c, and Rv2028c. |
| 604 | 23015647 | The distinct expression levels of IFN-γ, TNF-α, IL-6, and IL-10 in response to specific subsets of M. tuberculosis antigens may be promising for the development of immunodiagnostics. |
| 605 | 22988082 | Here we show that bacille Calmette-Guérin (BCG) vaccination in healthy volunteers led not only to a four- to sevenfold increase in the production of IFN-γ, but also to a twofold enhanced release of monocyte-derived cytokines, such as TNF and IL-1β, in response to unrelated bacterial and fungal pathogens. |
| 606 | 22988018 | To elucidate the potential adjuvant effect of N. farcinica on the induction of T-cell-mediated immune responses, we characterized the cytokines produced by nocardia-exposed DCs and detected substantial amounts of tumor necrosis factor alpha (TNF-α) and interleukin-12 p40 (IL-12p40). |
| 607 | 22986285 | NOD2 (Nucleotide binding oligomerization domain 2), an intracellular pathogen recognition sensor, attenuates two key putative host bacterial killing mechanisms: interfering the production of TNF-alpha and inducing resistance to apoptosis. |
| 608 | 22966165 | We observed that FSME-activated pDCs specifically lysed NK target cells and expressed cytotoxic molecules, such as tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) and granzyme B. |
| 609 | 22956655 | These synthetic mimics of antimicrobial peptides (SMAMPs) specifically reduced cytokine production in response to Staphylococcus aureus and the S. aureus component lipoteichoic acid (LTA), a TLR2 agonist. |
| 610 | 22956655 | These synthetic mimics of antimicrobial peptides (SMAMPs) specifically reduced cytokine production in response to Staphylococcus aureus and the S. aureus component lipoteichoic acid (LTA), a TLR2 agonist. |
| 611 | 22956655 | Anti-inflammatory SMAMPs prevented the induction of tumor necrosis factor (TNF), interleukin 6 (IL-6), and IL-10 in response to S. aureus or LTA, but no other TLR2 ligands. |
| 612 | 22956655 | Anti-inflammatory SMAMPs prevented the induction of tumor necrosis factor (TNF), interleukin 6 (IL-6), and IL-10 in response to S. aureus or LTA, but no other TLR2 ligands. |
| 613 | 22956655 | We show that these SMAMPs bind specifically to LTA in vitro and prevent its interaction with TLR2. |
| 614 | 22956655 | We show that these SMAMPs bind specifically to LTA in vitro and prevent its interaction with TLR2. |
| 615 | 22956655 | Importantly, the SMAMP greatly reduced the induction of TNF and IL-6 in vivo in mice acutely infected with S. aureus while simultaneously reducing bacterial loads dramatically (4 log(10)). |
| 616 | 22956655 | Importantly, the SMAMP greatly reduced the induction of TNF and IL-6 in vivo in mice acutely infected with S. aureus while simultaneously reducing bacterial loads dramatically (4 log(10)). |
| 617 | 22926059 | Like other TNF family members, in vivo and in vitro activity of CD40L requires a homotrimeric configuration, and growing evidence suggests that bioactivity depends on higher-order clustering of CD40. |
| 618 | 22912884 | Furthermore, we show that distinct polyfunctional (interferon-γ(+), tumor necrosis factor(+), and interleukin-2(+)) Salmonella-specific CD4(+) T cell responses develop with respect to magnitude and kinetics. |
| 619 | 22884682 | Therapeutic role of a vaccine targeting RANKL and TNF-α on collagen-induced arthritis. |
| 620 | 22884682 | Targeting tumor necrosis factor-α (TNF-α) and activator of NF-κB ligand (RANKL) has been proved highly successful in rheumatoid arthritis (RA) models and patients. |
| 621 | 22861368 | Multi-parameter flow cytometry was used to delineate CD4(+) T cell populations and phenotypes producing interferon (IFN)-γ, interleukin (IL)-2, tumour necrosis factor (TNF)-α and IL-4. |
| 622 | 22861368 | Based on surface CD69 expression, infants demonstrated activation of vaccine antigen-specific CD4(+) T cells similar to adults. |
| 623 | 22861368 | However, among infants, Boolean combinations of gates suggested that type 1 (Th-1) CD4(+) T cell responses were confined largely to TNF-α(+) IL-2(+) IFN-γ(-) or TNF-α(+) IL-2(-) IFN-γ(-) . |
| 624 | 22861368 | A significantly lower percentage of polyfunctional T helper type 1 (Th1) responses (TNF-α(+) IFN-γ(+) IL-2(+) ) and type 2 (Th2) responses (IL-4) were present in the infants compared to adults. |
| 625 | 22861368 | Moreover, a significantly higher percentage of infants' functional CD4(+) T cells were restricted to CD45RA(-) CCR7(+) CD27(+) phenotype, consistent with early-stage differentiated pertussis-specific memory CD4(+) T cells. |
| 626 | 22855392 | Serum concentrations of interleukin-1 receptor antagonist (IL-1Ra), IL-6, IL-8, IL-10, IL-17, tumor necrosis factor alpha (TNF-α), gamma interferon (IFN-γ), macrophage inflammatory protein-1 alpha (MIP-1α), and monocyte chemotactic protein-1 (MCP-1) were measured on days 0, 1, 2, and 4 and at a control visit. |
| 627 | 22855392 | Overall, the concentrations of IL-6 (P < 0.01), IL-8 (P < 0.01), MCP-1 (P < 0.01), and TNF-α (P < 0.01) were significantly lower on day 2 in the dexamethasone group than in the placebo group. |
| 628 | 22855392 | In patients with CAP caused by an atypical pathogen (Legionella pneumophila, Chlamydophila species, Coxiella burnetii, or Mycoplasma pneumoniae; n = 58), IL-1Ra (P < 0.01), IL-6 (P < 0.01), and MCP-1 (P = 0.03) decreased more rapidly in the dexamethasone group than in the placebo group. |
| 629 | 22829882 | With regard to cytokines, the SAP led to production of interleukin (IL)-2, IL-6, and IL-4. |
| 630 | 22829882 | IFA promoted production of tumor necrosis factor (TNF)-α, interferon (IFN)-γ, IL-6, IL-17, IL-4, and IL-10. |
| 631 | 22829882 | We also observed that MPL induced high production of IL-2, TNF-α, and IFN-γ, in addition to IL-6, IL-17, and IL-10. |
| 632 | 22778396 | Human TOLLIP regulates TLR2 and TLR4 signaling and its polymorphisms are associated with susceptibility to tuberculosis. |
| 633 | 22778396 | Using short hairpin RNA knockdown of TOLLIP in peripheral blood human monocytes, we found that TOLLIP suppresses TNF and IL-6 production after stimulation with TLR2 and TLR4 ligands. |
| 634 | 22778396 | In contrast, secretion of the anti-inflammatory cytokine IL-10 was induced by TOLLIP. |
| 635 | 22761301 | Secretion of interleukin-6 (IL-6) and gamma interferon (IFN-γ) was reduced at 24 h postchallenge, and the induction of tumor necrosis factor alpha (TNF-α) secretion, observed in the first hours postchallenge, was completely abolished at 24 h. |
| 636 | 22761301 | Before challenge and at 12 h postchallenge, vaccinated mice displayed higher numbers of CD4(+) T, CD8(+) T, and B lymphocytes in the lungs. |
| 637 | 22722447 | Lipid bodies do not contain the melanoma-associated antigen MART-1. |
| 638 | 22722447 | However, when a maturation cocktail composed of TNF-alpha, IL-6, IL-1beta and prostaglandin E2 is added to the coculture, the tumor cells clumps disaggregate, dendritic cells remain free in suspension and their ability to efficiently stimulate allogeneic lymphocytes is restored. |
| 639 | 22693228 | There were fewer vaccine-specific CD4(+) and CD8(+) cells in the P. inui-infected animals, compared with uninfected animals. |
| 640 | 22693228 | Of importance, P. inui infection seemed to decrease the number of CD8(+) cells that could proliferate or secrete interferon γ, although the number of CD8(+) cells capable of secreting tumor necrosis factor α following in vitro stimulation was increased. |
| 641 | 22679502 | Typhi antigens in T memory subsets, we developed multiparametric flow cytometry methods to detect up to 6 cytokines/chemokines (IL-10, IL-17A, IL-2, interferon-γ (IFN-γ), tumor necrosis factor-α (TNF-α) and macrophage inflammatory protein-1β (MIP-1β)) simultaneously. |
| 642 | 22679502 | Virtually all of the IL-17A detected was derived from multifunctional CD8+ T cells. |
| 643 | 22679502 | The presence of these multifunctional IL-17A+ CD8+ T cells was confirmed using an unsupervised analysis program, flow cytometry clustering without K (FLOCK). |
| 644 | 22679502 | The presence of IL-17A in multifunctional cells co-producing Tc1 cytokines (IL-2, IFN-γ and TNF-α) may also indicate that the distinction between Tc17 and Tc1 responses in humans is not as clearly delineated as suggested by in vitro experiments and animal models. |
| 645 | 22675156 | Concentrations of interleukin 1β (IL-1β), IL-4, IL-6, CXCL8 (IL-8), IL-10, IL-12p70, IL-17, CCL2 (monocyte chemoattractant protein 1), tumor necrosis factor alpha (TNF-α), and gamma interferon (IFN-γ) were measured by multiplex cytokine array. |
| 646 | 22675156 | When M. tuberculosis-infected macrophages were cocultured with monocyte-depleted peripheral blood mononuclear cells, IFN-γ (P = 0.01), TNF-α (P = 0.04), IL-10 (P < 0.001), and IL-6 (P = 0.03) exhibited similar continua of responses, with uninfected persons producing the lowest levels, followed by extrapulmonary tuberculosis cases, pulmonary tuberculosis controls, and persons with latent M. tuberculosis infection. |
| 647 | 22675156 | A similar pattern was observed with CXCL8 (P = 0.04), IL-10 (P = 0.02), and CCL2 (P = 0.03) when monocyte-depleted peripheral blood mononuclear cells from the four groups were cultured alone. |
| 648 | 22652666 | The TNF family receptors BAFFR and TACI interaction with the cytokines BAFF and APRIL are essential co-stimulatory factors for humoral responses to PS. |
| 649 | 22648753 | Blood samples were obtained weekly to determine serum neutralizing (SN) antibody titers to IBRV, BVDV-1, BVDV-2, and PI-3 and cytokine levels for IL-4, IL-6, TNF-α (tumor necrosis factor-α), and IFN-γ (interferon-gamma). |
| 650 | 22615254 | Nontoxigenic El Tor O1 V. cholerae infection is characterized by the upregulation of interleukin-6 (IL-6), IL-10, and macrophage inflammatory protein 2 alpha in the intestine, indicating an acute innate immune response. |
| 651 | 22615254 | In the absence of neutrophils, the infection spread to the spleen and led to increased systemic levels of IL-1β and tumor necrosis factor alpha, suggesting the decreased survival in neutropenic mice is due to systemic shock. |
| 652 | 22552381 | Antibody blocking of monocyte TLR4 inhibited surface expression, determined by flow cytometry, of the major histocompatibility complex class I, CCR7, CD80, CD83 and CD86 on TAPCells, reduced interleukin (IL)-6 and tumor necrosis factor -α gene expression evaluated by qRT-PCR, and also inhibited the TAPCells-mediated interferon-γ (IFN-γ) secretion of melanoma-specific CD8(+) T cells determined by ELISpot (p < 0.01). |
| 653 | 22552381 | Moreover, CD8(+) T-cell activation capacity was significantly reduced in TAPCells bearing the TLR4 Asp299Gly receptor (p < 0.05). |
| 654 | 22539471 | We evaluated IFN-γ, tumor necrosis factor alpha (TNF-α), and interleukin-10 (IL-10) release in 35 patients with active VL, 54 patients with VL who were cured, 27 patients with other diseases, 52 healthy controls who lived in regions where VL or kala-azar is not endemic (NEHCs [for nonendemic healthy controls]), and 147 healthy controls who lived in regions where kala-azar is endemic (EHCs [for endemic healthy controls]). |
| 655 | 22532670 | Using polychromatic flow cytometry, we measured levels of degranulation, cytokine expression (gamma interferon [IFN-γ], tumor necrosis factor alpha [TNF-α], and interleukin-2 [IL-2]), and the cytolytic mediator granzyme B. |
| 656 | 22532670 | In vivo killing assays revealed that CD8(+) T cells specific for both viruses were equally cytolytic (∼80% target cell lysis after 4 h), consistent with the similar levels of granzyme B and degranulation detected among these cells. |
| 657 | 22508289 | Furthermore, ex vivo polychromatic functional analysis of the CMV-specific T-cells from GBM patients revealed that large proportions of these cells were unable to produce multiple cytokines (macrophage inflammatory protein (MIP)-1β, tumor necrosis factor (TNF)α and interferon (IFN)γ) and displayed limited cytolytic function (CD107a mobilization) following stimulation with CMV peptide epitopes. |
| 658 | 22438548 | The double-stranded RNA bluetongue virus induces type I interferon in plasmacytoid dendritic cells via a MYD88-dependent TLR7/8-independent signaling pathway. |
| 659 | 22438548 | Other inflammatory cytokines, including tumor necrosis factor alpha (TNF-α), interleukin-6 (IL-6), and IL-12p40, were also induced by UV-BTV in primary pDCs. |
| 660 | 22438548 | In contrast, pathways involving the MyD88 adaptor and kinases dsRNA-activated protein kinase (PKR) and stress-activated protein kinase (SAPK)/Jun N-terminal protein kinase (JNK) were implicated. |
| 661 | 22426042 | After challenge, significant increases of IgG and IgG2a antibodies were noted only in the CA4 vaccinated mice that showed extended IDR, higher IFN-γ production by CD8+ and TNF-α production by CD4+ T cells, higher TNF-α secretion and the highest reduction of the parasite load (78%). |
| 662 | 22426042 | Protection generated by the CA4 vaccine was mainly mediated by a CD4+ T cell and a TNF-α driven response with a lower contribution of CD8+ T cells, as confirmed by an in vivo depletion with monoclonal antibodies and by vaccination assays in TNF-α-receptor knock-out mice. |
| 663 | 22425788 | In addition, GLA-SE induced a strong cellular immune response characterized by multi-functional, antigen-specific CD4(+) T cells secreting IL-2, TNF and IFN-γ. |
| 664 | 22425788 | In addition, GLA-SE induced a strong cellular immune response characterized by multi-functional, antigen-specific CD4(+) T cells secreting IL-2, TNF and IFN-γ. |
| 665 | 22425788 | In contrast, mice immunized with SE or R848-SE produced low numbers of antigen-specific CD4(+) T cells, and these T cells secreted IL-2 and TNF, but not IFN-γ. |
| 666 | 22425788 | In contrast, mice immunized with SE or R848-SE produced low numbers of antigen-specific CD4(+) T cells, and these T cells secreted IL-2 and TNF, but not IFN-γ. |
| 667 | 22419388 | Induction of proapoptotic antibodies to triple-negative breast cancer by vaccination with TRAIL death receptor DR5 DNA. |
| 668 | 22419388 | TNF-related apoptosis-inducing ligand receptor 2 [TRAIL-R2 or death receptor 5 (DR5)] is expressed at elevated levels in a broad range of solid tumors to mediate apoptotic signals from TRAIL or agonist antibodies. |
| 669 | 22419388 | Apoptotic cell death induced by anti-DR5 antibody was shown by the cleavage of PARP and caspase-3. |
| 670 | 22412866 | We hypothesized that this immunity depends on polyfunctional memory T cells, i.e., CD4(+) and/or CD8(+) T cells with the capability to simultaneously express several functional markers. |
| 671 | 22412866 | Significant differences were detected between either of the immune donor groups and naïve individuals for secreted levels of IL-5, IL-6, IL-10, IL-12, IL-13, IFN-γ, MCP-1, and MIP-1β. |
| 672 | 22412866 | Expression of IFN-γ, MIP-1β, and CD107a by CD4(+)CD45RO(+) or CD8(+)CD45RO(+) T cells correlated to antigen concentrations. |
| 673 | 22412866 | Notably, IL-2- or TNF-α-secretion was low. |
| 674 | 22379065 | The magnitude of IFN-γ-producing CD8(+) T-cell responses to CMV-specific peptides measured with the QuantiFERON-CMV assay correlated significantly (σ = 0.695; P = <0.001) with that of the total IFN-γ-producing CD8(+) T cells and dual-functional (IFN-γ/tumor necrosis factor alpha [TNF-α] [σ = 0.652; P = <0.001] and IFN-γ/CD107a [σ = 0.690; P = <0.001]) and trifunctional (IFN-γ/TNF-α/CD107a [σ = 0.679; P = >0.001]) CMV-specific CD8(+) T-cell responses, as quantitated by ICS. |
| 675 | 22379065 | In summary, the data indicated that the QuantiFERON-CMV assay is less sensitive than the ICS method for the detection of CMV-specific IFN-γ-producing CD8(+) T-cell responses in the allo-SCT setting. |
| 676 | 22379065 | Nevertheless, it allowed the estimation of the total and polyfunctional CMV-specific IFN-γ-producing CD8(+) T-cell responses in specimens that tested positive by both methods. |
| 677 | 22301691 | Our data indicated that βGM has a higher ability than S. cerevisiae var. boulardii to inhibit Salmonella-induced proinflammatory mRNA (cytokines tumor necrosis factor alpha [TNF-α], interleukin-1α [IL-1α], IL-6, and granulocyte-macrophage colony-stimulating factor [GM-CSF] and chemokines CCL2, CCL20, and CXCL8) and at protein levels (IL-6 and CXCL8). |
| 678 | 22301691 | Additionally, βGM and S. cerevisiae var. boulardii induced some effects on DCs that were not observed on IECs: βGM and S. cerevisiae var. boulardii showed slight upregulation of mRNA for TNF-α, GM-CSF, and CCR7 receptor on porcine monocyte-derived dendritic cells (DCs). |
| 679 | 22301691 | Indeed, the addition of βGM or S. cerevisiae var. boulardii on DCs cocultured with Salmonella showed higher gene expression (mRNA) for TNF-α, GM-CSF, and CXCL8 compared to that of the control with Salmonella. |
| 680 | 22298881 | Identification and immunogenicity of two new HLA-A*0201-restricted CD8+ T-cell epitopes on dengue NS1 protein. |
| 681 | 22298881 | Here, we identified two new HLA-A*0201-restricted CD8(+) T-cell epitopes, DEN-4 NS1(990)(-998) and DEN-4 NS1(997)(-1005) that are conserved in three or four major DEN serotypes, respectively. |
| 682 | 22298881 | Unexpectedly, we found that immunization of HLA-A*0201 transgenic mice with DEN-4 NS1(990)(-998) or DEN-4 NS1(997)(-1005) epitope peptide induced de novo synthesis of tumor necrosis factor (TNF)-α and IFN-γ, two important pro-inflammatory molecules that are hard to be detected directly without in vitro antigenic re-stimulation. |
| 683 | 22298881 | Importantly, we demonstrated that CD8(+) T cells specifically activated by DEN-4 NS1(990)(-998) or DEN-4 NS1(997)(-1005) epitope peptide induced de novo synthesis of perforin. |
| 684 | 22298881 | Furthermore, we observed that DEN-4 NS1(990)(-998) or DEN-4 NS1(997)(-1005)-specific CD8(+) T cells capable of producing large amounts of perforin, TNF-α and IFN-γ preferentially displayed CD27(+)CD45RA(-), but not CD27(-)CD45RA(+), phenotypes. |
| 685 | 22218690 | HCV-specific T cells consisted of both CD4+ and CD8+ T cell subsets; secreted interleukin-2, interferon-γ, and tumor necrosis factor-α; and could be sustained for at least a year after boosting with the heterologous adenoviral vector. |
| 686 | 22190395 | In vivo profiling of 16 inflammatory cytokines in patients infected with the outbreak strain revealed a common profile of a remarkable gamma interferon (IFN-γ) induction together with elevated concentrations of tumor necrosis factor alpha (TNF-α), IL-6, IL-8, IL-10, and IL-15, but not IL-12, which was previously demonstrated as elevated in nontyphoidal Salmonella infections. |
| 687 | 22178730 | An alternative signal 3: CD8⁺ T cell memory independent of IL-12 and type I IFN is dependent on CD27/OX40 signaling. |
| 688 | 22178730 | Type I IFN and IL-12 are well documented to serve as so called "signal 3" cytokines, capable of facilitating CD8(+) T cell proliferation, effector function and memory formation. |
| 689 | 22178730 | We have established a vaccine model system in which the primary CD8(+) T cell response is independent of either IL-12 or type I IFN receptors, but dependent on CD27/CD70 interactions. |
| 690 | 22178730 | We show here that primary and secondary CD8(+) T cell responses are generated in the combined deficiency of IFN and IL-12 signaling. |
| 691 | 22178730 | In contrast, antigen specific CD8(+) T cell responses are compromised in the absence of the TNF receptors CD27 and OX40. |
| 692 | 22178730 | These data indicate that CD27/OX40 can serve the central function as signal 3 mediators, independent of IFN or IL-12, for the generation of CD8(+) T cell immune memory. |
| 693 | 22161305 | The induction of P. berghei circumspor-ozoite protein (CSP)-specific CD8(+) T cells, achieved by a single immunization with a CSP fusion protein, was diminished in L. sigmodontis-infected mice. |
| 694 | 22161305 | This modulation was reflected by reduced frequencies of CSP-specific CD8(+) T cells, reduced CSP-specific IFN-y and TNF-a production, reduced CSP-specific cytotoxicity, and reduced protection against P. berghei challenge infection. |
| 695 | 22161305 | Implementation of a more potent vaccine regime, by first priming with CSP-expressing recombinant live Salmonella prior to CSP fusion protein immunization, restored induction of CSP-specific CD8(+) T cells and conferred almost sterile immunity to P. berghei challenge infection also in L. sigmodontis-infected mice. |
| 696 | 22125550 | Determinations of peripheral blood cytokine and chemokine profiles following individual protein immunizations show that interleukin-2 (IL-2) and IL-4 are elicited by the three confirmed candidates, but unexpectedly interferon-γ and tumor necrosis factor-α are not. |
| 697 | 22096993 | We revealed that immunization with these particles causes a specific induction of Th1-response, characterized by increased levels ofcytokine TNF-alpha and IL-2. |
| 698 | 22072720 | Increased amounts of antigen-specific gamma interferon, interleukin-17A (IL-17A), IL-6, and tumor necrosis factor alpha were produced from splenocytes postvaccination, but no or minimal IL-4, IL-5, or IL-10 was produced, indicating Th1- and Th17-biased T cell responses. |
| 699 | 22038233 | The secretion of TNF, IL-10 and IL-12 was measured by ELISA. |
| 700 | 22038233 | The secretion of TNF, IL-10 and IL-12 was measured by ELISA. |
| 701 | 22038233 | The secretion of TNF, IL-10 and IL-12 was measured by ELISA. |
| 702 | 22038233 | When cultured with HPC-4(TLG) cells, monocytes released a higher amount of TNF, but IL-10 and IL-12 secretion was inhibited. |
| 703 | 22038233 | When cultured with HPC-4(TLG) cells, monocytes released a higher amount of TNF, but IL-10 and IL-12 secretion was inhibited. |
| 704 | 22038233 | When cultured with HPC-4(TLG) cells, monocytes released a higher amount of TNF, but IL-10 and IL-12 secretion was inhibited. |
| 705 | 22038233 | The pre-exposure of monocytes to HPC-4(TLG), but not to HPC-4, cells did not decrease TNF nor increase IL-10 production, thus not leading to monocyte deactivation. |
| 706 | 22038233 | The pre-exposure of monocytes to HPC-4(TLG), but not to HPC-4, cells did not decrease TNF nor increase IL-10 production, thus not leading to monocyte deactivation. |
| 707 | 22038233 | The pre-exposure of monocytes to HPC-4(TLG), but not to HPC-4, cells did not decrease TNF nor increase IL-10 production, thus not leading to monocyte deactivation. |
| 708 | 21984246 | Vaccination site lesions were minimal in all mice vaccinated with HCc PHB beads or recombinant protein, all mixed in the oil-in-water adjuvant Emulsigen, while vaccination with the recombinant protein in complete Freund's adjuvant produced a marked inflammatory reaction at the vaccination site. |
| 709 | 21984246 | Vaccination with the PHB beads produced in L. lactis and displaying HCc antigen produced antigen-specific cellular immune responses with significant release of gamma interferon (IFN-γ) and interleukin-17A (IL-17A) from splenocyte cultures and no significant antigen-specific serum antibody, while the PHB beads displaying HCc but produced in E. coli released IFN-γ and IL-17A as well as the proinflammatory cytokines tumor necrosis factor alpha (TNF-α) and IL-6 and low levels of IgG2c antibody. |
| 710 | 21976223 | Importantly, CCL1 directly regulated the expression of CD18 and CD49b and hence influenced the adhesion capacity of human macrophages. |
| 711 | 21976223 | Finally, CCL1 induced production of proinflammatory cytokines such as tumor necrosis factor alpha (TNF-α) and interleukin-6 (IL-6) and could inhibit LPS-induced cytokine production in a dose-dependent manner. |
| 712 | 21957286 | Of note, the levels of T cell activation, proliferation, and apoptosis were comparable between SIVmnd-1- and SIVmnd-2-infected MNDs and to those observed in uninfected animals, with the only exception being an increase in tumor necrosis factor alpha-producing CD8+ T cells in SIVmnd-2-infected MNDs. |
| 713 | 21956503 | We worked out a protocol to study oxidative stress in human peripheral blood lymphocytes by determining their potency to secrete IFN-gamma, IL-2, IL-4, IL-5, IL-8, and TNF-alpha in response to acute treatment with hydrogen peroxide. |
| 714 | 21956503 | We worked out a protocol to study oxidative stress in human peripheral blood lymphocytes by determining their potency to secrete IFN-gamma, IL-2, IL-4, IL-5, IL-8, and TNF-alpha in response to acute treatment with hydrogen peroxide. |
| 715 | 21956503 | We show that hydrogen peroxide-induced oxidative stress can cause a ∼twofold decrease in the number of lymphocytes secreting the TH1 cytokines IFN-gamma and IL-2, as well as chemokines IL-8 and TNF-alpha. |
| 716 | 21956503 | We show that hydrogen peroxide-induced oxidative stress can cause a ∼twofold decrease in the number of lymphocytes secreting the TH1 cytokines IFN-gamma and IL-2, as well as chemokines IL-8 and TNF-alpha. |
| 717 | 21956503 | However, the number of cells secreting TH2 cytokines IL-4 and IL-5 in hydrogen -peroxide-treated group did not change. |
| 718 | 21956503 | However, the number of cells secreting TH2 cytokines IL-4 and IL-5 in hydrogen -peroxide-treated group did not change. |
| 719 | 21949376 | We generated VLPs that contain Gag-Cre recombinase, Gag-Fcy::Fur, and Gag-human caspase-8 as a proof-of-concept and demonstrated that the encapsidated proteins are active in recipient cells. |
| 720 | 21949376 | In addition, we show that murine IFN-γ and human TNF-related apoptosis-inducing ligand can be displayed on the surface of VLPs, and that these modified VLPs can cause the appropriate response in cells, as evidenced by phosphorylation of STAT1 and induction of cell death, respectively. |
| 721 | 21934655 | Identification of molecular adjuvants to in vivo "modulate " DC to coordinately render improved Th1 and CD8 T cell immunity, and attenuated deleterious Treg effects, is a critical challenge. |
| 722 | 21934655 | This immunization strategy is based on a genetic vaccine encoding both cytomegalovirus (CMV)-driven vaccine Aghsp70 and DC-specific CD11c-driven XBP1s. |
| 723 | 21934655 | The novel targeted vaccine induced durable Th1 and CD8 T cell responses to poorly immunogenic self/tumor antigen (Ag) and attenuated tumor-associated Treg suppressive function. |
| 724 | 21934655 | Bone marrow (BM)-derived DC genetically modified to simultaneously overexpress XBP1s and express Aghsp70 upregulated CD40, CD70, CD86, interleukin (IL)-15, IL-15Rα, and CCR7 expression, and increased IL-6, IL-12, and tumor necrosis factor (TNF)-α production in vitro. |
| 725 | 21908716 | Promastigote infection of macrophages induced the inflammatory mediators TNF, CCL3, and CCL4, whereas amastigote infection was silent and resulted in significantly increased parasite numbers: from 7.1 ± 1.4 (after 3 h) to 20.1 ± 7.9 parasites/cell (after 96 h). |
| 726 | 21889412 | Therefore CMI responses were evaluated in 15 CVID-patients and 15 matched healthy controls (HC) by determining frequencies of interferon (IFN)γ-producing PBMC, and frequencies of IFNγ-, interleukin (IL)-2- and tumour necrosis factor (TNF)α-producing CD4+ and CD8+ T-cells before and after influenza vaccination using IFNγ enzyme-linked immunospot (IFNγ-ELISpot) and flow cytometry. |
| 727 | 21881953 | Dengue virus-specific CD4+ and CD8+ T lymphocytes target NS1, NS3 and NS5 in infected Indian rhesus macaques. |
| 728 | 21881953 | DENV-specific CD4+ and CD8+ T lymphocytes targeted nonstructural (NS) 1, NS3 and NS5 proteins after resolution of peak viremia. |
| 729 | 21881953 | DENV-specific CD4+ cells expressed interferon-gamma (IFN-γ) along with tumor necrosis factor-alpha (TNF-α), interleukin-2 (IL-2), and macrophage inflammatory protein-1 beta (MIP-1β). |
| 730 | 21881953 | In comparison, DENV-specific CD8+ cells expressed IFN-γ in addition to MIP-1β and TNF-α and were positive for the degranulation marker CD107a. |
| 731 | 21881953 | Interestingly, a fraction of the DENV-specific CD4+ cells also stained for CD107a, suggesting that they might be cytotoxic. |
| 732 | 21879287 | In this paper we have studied memory/naïve B cells in the elderly, evaluating surface immunoglobulin expression, production of the pro- and anti-inflammatory cytokines, tumor necrosis factor (TNF)-α and interleukin (IL)-10, and presence of somatic hypermutation, focusing on the IgG(+)IgD(-)CD27(-) double negative (DN) B cells that are expanded in the elderly. |
| 733 | 21879287 | Our results show that naïve B cells from young donors need a sufficiently strong stimulus to be activated "in vitro", while naïve B cells from old subjects are able to produce IL-10 and TNF-α when stimulated "physiologically" (α-CD40/IL-4), suggesting that these cells might play a role in the control of the immuno-inflammatory environment in the elderly. |
| 734 | 21822116 | Serum cytokines [interleukin-2 (IL-2), IL-4, IL-6, interferon gamma, and tumor necrosis factor alpha] were assayed using standardized methodology. |
| 735 | 21795461 | Antigen stimulation of MLN cells from the severely lesioned group resulted in significant upregulation of the mRNA expression of five cytokines, gamma interferon (IFN-γ), interleukin-10 (IL-10), IL-13, IL-17A, and tumor necrosis factor alpha (TNF-α), which have a diverse range of functions, while there was no significant upregulation of these cytokines by the other groups. |
| 736 | 21779319 | Protective immunity induced with the RTS,S/AS vaccine is associated with IL-2 and TNF-α producing effector and central memory CD4 T cells. |
| 737 | 21779319 | The frequency of Plasmodium falciparum circumsporozoite protein (CSP)-specific CD4(+) T cells was significantly higher in protected subjects as compared to non-protected subjects. |
| 738 | 21779319 | Moreover, both the frequencies and the total numbers of IL-2-producing CD4(+) T(E/EM) cells and of CD4(+) T(CM) cells from protected subjects were significantly higher than those from non-protected subjects. |
| 739 | 21779319 | We also demonstrated for the first time that there is a strong association between the frequency of CSP peptide-reactive CD4(+) T cells producing IL-2 and the titers of CSP-specific antibodies in the same individual, suggesting that IL-2 may be acting as a growth factor for follicular Th cells and/or B cells. |
| 740 | 21779319 | The frequencies of CSP peptide-reactive, TNF-α-producing CD4(+) T(E/EM) cells and of CD4(+) T(E/EM) cells secreting both IL-2 and TNF-α were also shown to be higher in protected vs. non-protected individuals. |
| 741 | 21752952 | The purpose of this study was to determine the degree of infiltration of different cell subpopulations (tissue dendritic macrophages, T-helper cells, cytotoxic T lymphocytes, monocytes, neutrophils, and B cells) and the expression of the cytokines interleukin-12 (IL-12) and tumor necrosis factor alpha (TNF-α) in inflamed and noninflamed resected tissues from Crohn's disease (CD) and non-CD patients. |
| 742 | 21745518 | We also detected a concomitant release of interleukin 1 beta (IL-1β) and tumor necrosis factor alpha (TNF-α), but not metalloproteinase (MMP)-9. |
| 743 | 21722716 | A proliferation-inducing ligand (APRIL) is an important member of the tumor necrosis factor (TNF) superfamily. |
| 744 | 21715581 | The levels of six cytokines were measured in 24-h whole-blood assays with these antigens, revealing that gamma interferon (IFN-γ), tumor necrosis factor (TNF), and interleukin-10 (IL-10) were differentially regulated in response to a subset of antigens. |
| 745 | 21710212 | The immunomodulatory activity of the c-di-GMP preparation was confirmed by its potentiating effect on the lipopolysaccharide-induced interleukin 1β, tumor necrosis factor α, and interleukin 6 messenger RNA expression in J774A.1 mouse macrophages. |
| 746 | 21697338 | In a majority of serum samples, interleukin-6 (IL-6), IL-8, IL-10, and tumor necrosis factor alpha were detectable with at least three kits, while IL-1β was clearly detected with only one kit. |
| 747 | 21690242 | In addition, all groups generated a cellular immune response characterized by antigen-specific CD4(+) T cells secreting predominantly interleukin-2 (IL-2) and lesser amounts of tumor necrosis factor (TNF). |
| 748 | 21688261 | TNFRSF25 is a member of the TNF receptor superfamily (TNFRSF) that binds to the TNF-like protein TL1A. |
| 749 | 21688261 | Although recent studies have demonstrated a role for TNFRSF25 in regulating CD4(+) T-cell responses, it remains to be determined if TNFRSF25 functions as a costimulatory receptor for CD8(+) T cells. |
| 750 | 21688261 | Here, we demonstrate that ectopic expression of TL1A on mouse plasmacytomas promotes elimination of tumor cells in a CD8(+) T-cell-dependent manner and renders mice immune to a subsequent challenge with tumor cells. |
| 751 | 21688261 | To gain further insight into the role of TNFRSF25 in CD8(+) T-cell responses, we analyzed the effect of TNFRSF25 triggering on OT-I TCR transgenic T cells. |
| 752 | 21688261 | We demonstrate that TNFRSF25 triggering in vivo with soluble TL1A promotes the proliferation and accumulation of antigen-specific CD8(+) T cells as well as their differentiation into CTLs. |
| 753 | 21688261 | Furthermore, we show that TNFRSF25 also functions as a costimulatory receptor for memory CD8(+) T cells. |
| 754 | 21688261 | Thus, TNFRSF25 triggering enhances the secondary expansion of endogenous antigen-specific memory CD8(+) T cells. |
| 755 | 21688261 | Our data suggest that TNFRSF25 agonists, such as soluble TL1A, could potentially be used to enhance the immunogenicity of vaccines that aim to elicit human anti-tumor CD8(+) T cells. |
| 756 | 21573974 | Differentiated prostatic antigen expression in LNCaP cells following treatment with bispecific antisense oligonucleotides directed against BCL-2 and EGFR. |
| 757 | 21573974 | In LNCaP cells, we initially identified bispecifics that increased the expression of prostate-specific membrane antigen (PSMA) while not affecting secreted prostate-specific antigen (PSA). |
| 758 | 21573974 | In other systems, when induced, IFN-γ promotes cell surface antigen expression, including HLA and receptors for tumor necrosis factor. |
| 759 | 21573974 | This study initially evaluated the inhibition of in vitro propagating LNCaP cells employing mono- and bispecific oligos directed against bcl-2 (the second bispecific binding site was against the epidermal growth factor receptor). |
| 760 | 21573974 | Employing RT-PCR, the expression of non-targeted proteins encoded by mRNA for PSMA, PSA, PAP, and IFN-γ was subsequently valuated. |
| 761 | 21573974 | Employing RT-PCR, the levels of mRNA encoding PSMA were unexpectedly found to be elevated following treatment with the bispecific oligos but not with a monospecific directed solely against bcl-2. |
| 762 | 21573974 | IFN-γ was significantly induced only by bispecific oligos, and PAP expression was similar to PSA. |
| 763 | 21469087 | CD38 identifies a hypo-proliferative IL-13-secreting CD4+ T-cell subset that does not fit into existing naive and memory phenotype paradigms. |
| 764 | 21469087 | Herein, we show that CD38 expression identifies a hypo-proliferative CD4(+) T-cell subset that, following TCR stimulation, retains expression of naive cell surface markers including CD45RA, CD62L and CCR7. |
| 765 | 21469087 | Hypo-proliferation was mediated by reduced CD25 up-regulation upon TCR stimulation compared to CD4(+) CD38(-) cells and lack of responsiveness to exogenous IL-2. |
| 766 | 21469087 | Instead, CD4(+) CD38(+) T cells expressed CD127, and hypo-proliferation was reversed by addition of IL-7, further associated with increased STAT5 phosphorylation. |
| 767 | 21469087 | Activated CD4(+) CD38(+) cells had a bias towards IL-13 secretion, but not other Th2 cytokines such as IL-4 or IL-5. |
| 768 | 21469087 | In comparison, the CD4(+) CD38(-) cells had a clear bias towards secretion of Th1-associated cytokines IFN-γ and TNF. |
| 769 | 21469087 | The existence of such CD4(+) CD38(+) T cells may play an important role in pathologies such as asthma, which are associated with IL-13, but not IL-4 and IL-5. |
| 770 | 21469087 | Coupled with responsiveness to IL-7 but not IL-2, and the involvement of CD38 ligation, our results highlight a unique T-cell subpopulation that does not fit into existing naive and memory cell paradigms. |
| 771 | 21464087 | A miniTUBA dynamic Bayesian network analysis predicted that VTRS1-induced macrophage cell death was mediated by a proinflammatory gene (the tumor necrosis factor alpha [TNF-α] gene), an NF-κB pathway gene (the IκB-α gene), the caspase-2 gene, and several other genes. |
| 772 | 21464087 | Increased production of TNF-α and interleukin 1β (IL-1β) were also detected in the supernatants in VTRS1-infected macrophage cell culture. |
| 773 | 21464087 | VTRS1-induced macrophage cell death was significantly inhibited by a caspase-2 inhibitor but not a caspase-1 inhibitor. |
| 774 | 21450979 | Splenocytes from mice who had received OMPC with the pneumococcal conjugate vaccine produced significantly more interleukin-2 (IL-2), IL-4, IL-6, IL-10, tumor necrosis factor alpha (TNF-α), and gamma interferon (IFN-γ) than splenocytes from mice who received phosphate-buffered saline (PBS) plus the conjugate vaccine. |
| 775 | 21424108 | Targeting IL-12/IL-23 by employing a p40 peptide-based vaccine ameliorates TNBS-induced acute and chronic murine colitis. |
| 776 | 21424108 | Interleukin (IL)-12 and IL-23 both share the p40 subunit and are key cytokines in the pathogenesis of Crohn's disease. |
| 777 | 21424108 | Our results showed the vaccine induced high level and long-lasting specific IgG antibodies to p40, IL-12 and IL-23. |
| 778 | 21424108 | After administrations of TNBS, vaccinated mice had significantly less body weight loss and a significant decrease of inflammatory scores, collagen deposition and expression of p40, IL-12, IL-23, IL-17, TNF, iNOS and Bcl-2 in colon tissues, compared with carrier and saline groups. |
| 779 | 21424108 | In summary, administration of the vaccine induced specific antibodies to IL-12 and IL-23, which was associated with improvement of intestinal inflammation and fibrosis. |
| 780 | 21367980 | The draining lymph node cells and peripheral blood lymphocytes from vaccinated dogs demonstrated gamma interferon (IFN-γ), tumor necrosis factor alpha (TNF-α), and granulocyte-macrophage colony-stimulating factor (GM-CSF) specifically in response to stimulation with Blastomyces antigens. |
| 781 | 21367979 | P313-specific CD4(+) T-cell clones demonstrated (i) stringent LTA peptide specificity; (ii) promiscuous recognition in the context of HLA-DR alleles; (iii) cross recognition of homologous peptides from the polyomavirus simian virus 40 (SV40); (iv) an effector memory phenotype, CD107a expression, and intracellular production of IFN-γ and tumor necrosis factor alpha (TNF-α); (v) cytotoxic activity in a chromium release assay; and (vi) the ability to directly present cognate antigen to autologous T cells. |
| 782 | 21316756 | In addition, Epi-1 modulated the expressions of immune-responsive genes like interleukin (IL)-6, IL-10, MCP-1, tumor necrosis factor-α, interferon-γ and IL-12, and elevated the levels of anti-JEV-neutralizing antibodies in the serum. |
| 783 | 21275454 | Cost effectiveness of interferon-gamma release assay for tuberculosis screening of rheumatoid arthritis patients prior to initiation of tumor necrosis factor-α antagonist therapy. |
| 784 | 21267444 | Poly(I-C) induction of genes involved in alerting the innate immune system to the infectious threat, including TNF-alpha, IL-1 alpha and beta, CCL5 and IL-6, were suppressed by infection with live MPV. |
| 785 | 21244466 | In this study, the secretion of pro-inflammatory cytokines tumor necrosis factor-alpha (TNF-α), interleukin (IL)-6, IL-8 and IL-1β; Th1 cytokines interferon-gamma (IFN-γ), IL-2 and tumor necrosis factor-beta (TNF-β); and Th2 cytokines IL-4, IL-5 and IL-10 by the peripheral blood mononuclear cells (PBMCs) of pulmonary tuberculosis patients was studied. |
| 786 | 21244466 | PBMCs from the majority of patients (53-100%) spontaneously secreted detectable concentrations of all cytokines tested, except for IL2 (29%) and IL-10 (41%). |
| 787 | 21216868 | We investigated the induction and evolution of CD8(+) T cell responses to a WNV envelope epitope, which is a dominant target in naturally infected HLA-A*02-positive individuals. |
| 788 | 21216868 | In the majority of donors, CD8(+) T cells were able to lyse targets expressing WNV envelope protein and produced macrophage inflammatory protein 1ß, interferon γ, and/or tumor necrosis factor α following envelope peptide stimulation. |
| 789 | 21216131 | B cell activating factor belonging to the TNF family (BAFF or BLyS) is a critical B cell survival factor essential for B cell maturation. |
| 790 | 21186260 | Following tuberculin stimulation, activated CD4 T cells were identified by flow-cytometry (CD154 up-regulation, degranulation, interferon γ [IFN-γ], tumor necrosis factor α [TNF-α], and interleukin 2 [IL-2 production). |
| 791 | 21186260 | Interestingly, CD154 up-regulation accounted for ∼80% of activated CD4 T cells in the active TB group but just 40% in the controls, whereas IFN-γ accounted for only ∼50% of activated cells in each group. |
| 792 | 21169550 | Priming with live lactobacilli resulted in diminished granulocyte recruitment, diminished expression of multiple proinflammatory cytokines (CXCL10, CXCL1, CCL2, and TNF), and reduced virus recovery, although we have demonstrated clearly that absolute virus titer does not predict clinical outcome. |
| 793 | 21154120 | Targeted immunomodulatory therapy is focused primarily on the activation of costimulatory receptors (eg, 4-1BB, OX40 and GITR [glucocorticoid-induced TNF receptor-related gene]) or the blockade of co-inhibitory receptors (eg, CTLA-4, PD-1 and PD-L1) on T-cells during activation and/or effector responses. |
| 794 | 21134965 | The mechanism by which DTH responses were induced was elucidated by histologic examination, analysis of activated CD4(+)/CD8(+) T cells, and cytokine mRNA expression at the site of the DTH response. |
| 795 | 21134965 | Ex vivo phenotyping of T cells at the DTH site indicated that this response is mediated by activated CD4(+) and CD8(+) T cells, with increases in gamma interferon and tumor necrosis factor alpha, but not interleukin-10, at the site of the DTH response. |
| 796 | 21106776 | The serum levels of interleukin-2 (IL-2), gamma interferon (IFN-γ), tumor necrosis factor alpha (TNF-α), IL-4, IL-6, and IL-10 of pneumonic plague patients were determined by enzyme-linked immunosorbent assay. |
| 797 | 21098227 | In this study, we demonstrate that the induction of TNF and IL-6 expression by LVS in mouse bone marrow-derived macrophages was markedly enhanced when PI3K activity was inhibited by either of the well-known chemical inhibitors, wortmannin or LY294002. |
| 798 | 21098227 | In this study, we demonstrate that the induction of TNF and IL-6 expression by LVS in mouse bone marrow-derived macrophages was markedly enhanced when PI3K activity was inhibited by either of the well-known chemical inhibitors, wortmannin or LY294002. |
| 799 | 21098227 | The enhanced cytokine expression was accompanied by enhanced activation of p38 MAPK and ERK1/2, both of which were critical for LVS-induced expression of TNF and IL-6. |
| 800 | 21098227 | The enhanced cytokine expression was accompanied by enhanced activation of p38 MAPK and ERK1/2, both of which were critical for LVS-induced expression of TNF and IL-6. |
| 801 | 21098227 | LVS-induced MAPK activation and cytokine production were TLR2- and MyD88- dependent. |
| 802 | 21098227 | LVS-induced MAPK activation and cytokine production were TLR2- and MyD88- dependent. |
| 803 | 21098227 | PI3K/Akt activation was MyD88-dependent, but was surprisingly TLR2-independent. |
| 804 | 21098227 | PI3K/Akt activation was MyD88-dependent, but was surprisingly TLR2-independent. |
| 805 | 21098227 | LVS infection also rapidly induced MAPK phosphatase-1 (MKP-1) expression; PI3K and TLR2 signaling were required. |
| 806 | 21098227 | LVS infection also rapidly induced MAPK phosphatase-1 (MKP-1) expression; PI3K and TLR2 signaling were required. |
| 807 | 21098227 | Peak levels of MKP-1 correlated closely with the decline in p38 MAPK and ERK1/2 phosphorylation. |
| 808 | 21098227 | Peak levels of MKP-1 correlated closely with the decline in p38 MAPK and ERK1/2 phosphorylation. |
| 809 | 21098227 | These data suggest that infection by LVS restrains the TLR2-triggered proinflammatory response via parallel activation of PI3K, leading to enhanced MKP-1 expression, accelerated deactivation of MAPKs, and suppression of proinflammatory cytokine production. |
| 810 | 21098227 | These data suggest that infection by LVS restrains the TLR2-triggered proinflammatory response via parallel activation of PI3K, leading to enhanced MKP-1 expression, accelerated deactivation of MAPKs, and suppression of proinflammatory cytokine production. |
| 811 | 21093495 | Our results showed that the infection of bmDCs with SA14-14-2 resulted in viral replication and upregulation of bmDC maturation marker molecules (CD40, CD80, CD83 and MHC I). |
| 812 | 21093495 | SA14-14-2 infection also stimulated the production of interferon-α (IFN-α), monocyte chemoattractant protein-1 (MCP-1/CCL2), tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) of bmDC. |
| 813 | 21078851 | By analyzing immunized and unimmunized mice, a significant inverse correlation between the levels of interleukin-12p40 (IL-12p40), tumor necrosis factor alpha (TNF), gamma interferon (IFN-γ), and IL-17 gene expression and the number of H. pylori bacteria in the stomachs of individual animals after challenge could be demonstrated. |
| 814 | 21078851 | By analyzing immunized and unimmunized mice, a significant inverse correlation between the levels of interleukin-12p40 (IL-12p40), tumor necrosis factor alpha (TNF), gamma interferon (IFN-γ), and IL-17 gene expression and the number of H. pylori bacteria in the stomachs of individual animals after challenge could be demonstrated. |
| 815 | 21078851 | By analyzing immunized and unimmunized mice, a significant inverse correlation between the levels of interleukin-12p40 (IL-12p40), tumor necrosis factor alpha (TNF), gamma interferon (IFN-γ), and IL-17 gene expression and the number of H. pylori bacteria in the stomachs of individual animals after challenge could be demonstrated. |
| 816 | 21078851 | In a kinetic study, upregulation of TNF, IFN-γ, and IL-17 coincided with vaccine-induced protection at 7 days after H. pylori challenge and was sustained for at least 21 days. |
| 817 | 21078851 | In a kinetic study, upregulation of TNF, IFN-γ, and IL-17 coincided with vaccine-induced protection at 7 days after H. pylori challenge and was sustained for at least 21 days. |
| 818 | 21078851 | In a kinetic study, upregulation of TNF, IFN-γ, and IL-17 coincided with vaccine-induced protection at 7 days after H. pylori challenge and was sustained for at least 21 days. |
| 819 | 21078851 | In vivo neutralization of these cytokines during the effector phase of the immune response revealed a significant role for IL-17, but not for IFN-γ or TNF, in vaccine-induced protection. |
| 820 | 21078851 | In vivo neutralization of these cytokines during the effector phase of the immune response revealed a significant role for IL-17, but not for IFN-γ or TNF, in vaccine-induced protection. |
| 821 | 21078851 | In vivo neutralization of these cytokines during the effector phase of the immune response revealed a significant role for IL-17, but not for IFN-γ or TNF, in vaccine-induced protection. |
| 822 | 21074068 | OX40 and its ligand, OX40L, are key TNF members that augment T-cell expansion, cytokine production, and survival. |
| 823 | 21060869 | The GLA-SE adjuvanted Fluzone vaccine caused no adverse reactions, increased the induction of T helper type 1 (T(H)1)-biased cytokines such as IFNγ, TNF and IL-2, and broadened serological responses against drifted A/H1N1 and A/H3N2 influenza variants. |
| 824 | 21057930 | The output of an ELISpot assay is a formation of colored spots which appear at the sites of cells releasing cytokines, with each individual spot representing a single cytokine-releasing cell.We have shown that hydrogen peroxide-induced oxidative stress was causing ∼twofold decrease in the number of lymphocytes secreting the TH1 cytokines IFN-gamma and IL-2, as well as chemokine IL-8 and cytokine TNF alpha. |
| 825 | 21057930 | The output of an ELISpot assay is a formation of colored spots which appear at the sites of cells releasing cytokines, with each individual spot representing a single cytokine-releasing cell.We have shown that hydrogen peroxide-induced oxidative stress was causing ∼twofold decrease in the number of lymphocytes secreting the TH1 cytokines IFN-gamma and IL-2, as well as chemokine IL-8 and cytokine TNF alpha. |
| 826 | 21057930 | However, the number of cells secreting TH2 cytokines IL-4 and IL-5 in hydrogen peroxide-treated group did not change. |
| 827 | 21057930 | However, the number of cells secreting TH2 cytokines IL-4 and IL-5 in hydrogen peroxide-treated group did not change. |
| 828 | 21057930 | We adopted ELISpot assay for studying oxidative stress in human peripheral blood lymphocytes by analyzing the acute effect of hydrogen peroxide treatment on the frequency of cells secreting IFN-gamma, IL-2, IL-4, IL-5, IL-8, and TNF-alpha. |
| 829 | 21057930 | We adopted ELISpot assay for studying oxidative stress in human peripheral blood lymphocytes by analyzing the acute effect of hydrogen peroxide treatment on the frequency of cells secreting IFN-gamma, IL-2, IL-4, IL-5, IL-8, and TNF-alpha. |
| 830 | 21051638 | Depletion of FAP-expressing cells, which made up only 2% of all tumor cells in established Lewis lung carcinomas, caused rapid hypoxic necrosis of both cancer and stromal cells in immunogenic tumors by a process involving interferon-γ and tumor necrosis factor-α. |
| 831 | 21030562 | We have completed a phase 1 study in which patients with multiple myeloma underwent serial vaccination with the DC/multiple myeloma fusions in conjunction with granulocyte-macrophage colony-stimulating factor. |
| 832 | 21030562 | DCs were generated from adherent mononuclear cells cultured with granulocyte-macrophage colony-stimulating factor, interleukin-4, and tumor necrosis factor-α and fused with myeloma cells obtained from marrow aspirates. |
| 833 | 21030562 | Vaccination resulted in the expansion of circulating CD4 and CD8 lymphocytes reactive with autologous myeloma cells in 11 of 15 evaluable patients. |
| 834 | 20944089 | In mice, this fusion protein-adjuvant combination induced polyfunctional CD4 T helper 1 cell responses characterized by antigen-specific interferon-γ, tumor necrosis factor, and interleukin-2, as well as a reduction in the number of bacteria in the lungs of animals after they were subsequently infected with virulent or multidrug-resistant Mtb strains. |
| 835 | 20944089 | Finally, the fusion protein elicited polyfunctional effector CD4 and CD8 T cell responses in BCG-vaccinated or Mtb-exposed human peripheral blood mononuclear cells. |
| 836 | 20926697 | Simultaneous measurement of antigen-stimulated interleukin-1 beta and gamma interferon production enhances test sensitivity for the detection of Mycobacterium bovis infection in cattle. |
| 837 | 20926697 | In order to identify cytokines that may be useful as candidates for inclusion in diagnostic tests for Mycobacterium bovis infection in cattle, we compared the levels of gamma interferon (IFN-γ), interleukin 1β (IL-1β), IL-4, IL-10, IL-12, macrophage inflammatory protein 1β (MIP-1β), and tumor necrosis factor alpha (TNF-α) in whole-blood cultures from tuberculosis (TB) reactor animals or TB-free controls following stimulation with M. bovis-specific antigens (purified protein derivative from M. bovis [PPD-B] or ESAT-6/CFP-10). |
| 838 | 20921283 | These pathogenic T cells initiated a cytokine storm characterized by high levels of tumor necrosis factor (TNF) and interleukin 6 (IL-6), and depletion of T cells or blockade of these inflammatory cytokines prevented the lethal disease. |
| 839 | 20921283 | These pathogenic T cells initiated a cytokine storm characterized by high levels of tumor necrosis factor (TNF) and interleukin 6 (IL-6), and depletion of T cells or blockade of these inflammatory cytokines prevented the lethal disease. |
| 840 | 20921283 | Furthermore, we identify a potential strategy (blockade of TNF and IL-6) for treatment of transplant recipients who have acute complications of viral infection. |
| 841 | 20921283 | Furthermore, we identify a potential strategy (blockade of TNF and IL-6) for treatment of transplant recipients who have acute complications of viral infection. |
| 842 | 20870934 | CD4+ T cells are not required for the induction of dengue virus-specific CD8+ T cell or antibody responses but contribute to protection after vaccination. |
| 843 | 20870934 | The DENV-specific CD4(+) T cells expressed intracellular IFN-γ, TNF, IL-2, and CD40L, and killed peptide-pulsed target cells in vivo. |
| 844 | 20870934 | Consistent with this observation, CD4(+) T cell depletion did not affect the DENV-specific IgG or IgM Ab titers or their neutralizing activity, or the DENV-specific CD8(+) T cell response. |
| 845 | 20838241 | Vaccinations targeting extracellular superoxide dismutase 1 (SOD1) mutants are beneficial in mouse models of amyotrophic lateral sclerosis (ALS). |
| 846 | 20838241 | Vaccinations targeting extracellular superoxide dismutase 1 (SOD1) mutants are beneficial in mouse models of amyotrophic lateral sclerosis (ALS). |
| 847 | 20838241 | The vaccines potentiated TH2 deviation in the spinal cord as determined by the ratio of interleukin-4 to interferon-γ (IFNγ) or tumor necrosis factor and induced C1q deposition around motor neurons. |
| 848 | 20838241 | The vaccines potentiated TH2 deviation in the spinal cord as determined by the ratio of interleukin-4 to interferon-γ (IFNγ) or tumor necrosis factor and induced C1q deposition around motor neurons. |
| 849 | 20838241 | On the other hand, the sera from G93A SOD1-vaccinated mice showed higher IFNγ or tumor necrosis factor and yielded a lower IgG1/IgG2c ratio than the sera from WT-apo-vaccinated mice. |
| 850 | 20838241 | On the other hand, the sera from G93A SOD1-vaccinated mice showed higher IFNγ or tumor necrosis factor and yielded a lower IgG1/IgG2c ratio than the sera from WT-apo-vaccinated mice. |
| 851 | 20837698 | The inhibitor of apoptosis proteins (IAPs) have recently been shown to modulate nuclear factor κB (NF-κB) signaling downstream of tumor necrosis factor (TNF) family receptors, positioning them as essential survival factors in several cancer cell lines, as indicated by the cytotoxic activity of several novel small molecule IAP antagonists. |
| 852 | 20826612 | The concentrations of several chemoattractants for neutrophils (CXCL1, CXCL2, CXCL3, CXCL8, and C5a) increased in milk after challenge, and the highest increases followed challenge with the combination of MDP and LTA. |
| 853 | 20826612 | Nucleotide-binding oligomerization domain 2 (NOD2), a major sensor of MDP, was expressed (mRNA) in bovine mammary tissue and by bMEpC in culture. |
| 854 | 20826612 | The production of interleukin-8 (IL-8) following the stimulation of bMEpC by LTA and MDP was dependent on the activation of NF-κB. |
| 855 | 20826612 | LTA-induced IL-8 production did not depend on platelet-activating factor receptor (PAFR), as the PAFR antagonist WEB2086 was without effect. |
| 856 | 20826612 | Although the levels of expression of the inflammatory cytokines tumor necrosis factor alpha (TNF-α) and IL-1β were increased by LTA and MDP at the mRNA level, no protein could be detected in the bMEpC culture supernatant. |
| 857 | 20826612 | Overall, this study indicates that the TLR2 and NOD2 pathways could cooperate to trigger an innate immune response to S. aureus mastitis. |
| 858 | 20816019 | The immunological consequences of the treatment were evaluated with plasma- and serum-levels of inflammatory and non-inflammatory markers (the following 10 cytokines: GM-CSF, INF-gamma, IL-1beta, IL-2, IL-4, IL-5, IL-6, IL-8, IL-10, and TNF-alpha, and in addition the inflammatory chemokines MIP-1beta, Eotaxin and IP-10) and biomarkers CEA and TIMP-1. |
| 859 | 20816019 | The immunological consequences of the treatment were evaluated with plasma- and serum-levels of inflammatory and non-inflammatory markers (the following 10 cytokines: GM-CSF, INF-gamma, IL-1beta, IL-2, IL-4, IL-5, IL-6, IL-8, IL-10, and TNF-alpha, and in addition the inflammatory chemokines MIP-1beta, Eotaxin and IP-10) and biomarkers CEA and TIMP-1. |
| 860 | 20816019 | These analyses showed that the vaccine induced increasing levels of Th1 cytokines such as GM-CSF, TNF-alpha, IFN-gamma, and IL-2 in patients achieving stable disease. |
| 861 | 20816019 | These analyses showed that the vaccine induced increasing levels of Th1 cytokines such as GM-CSF, TNF-alpha, IFN-gamma, and IL-2 in patients achieving stable disease. |
| 862 | 20816019 | Patients with progressive disease had increasing levels of CEA and TIMP-1, while patients achieving stable disease maintained relatively stable levels. |
| 863 | 20816019 | Patients with progressive disease had increasing levels of CEA and TIMP-1, while patients achieving stable disease maintained relatively stable levels. |
| 864 | 20811496 | Production of TNF-alpha, IL-12(p40) and IL-17 can discriminate between active TB disease and latent infection in a West African cohort. |
| 865 | 20810726 | Syncytia were also evident, along with significant basolateral secretion of proinflammatory chemokines, including IP-10, RANTES, tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL), interleukin 6 (IL-6), and IL-8. |
| 866 | 20808670 | On days 3 or 7 of DC culture, TNF-alpha (T), TNF-alpha and LPS (TL) or OPA were employed as maturation stimulators. |
| 867 | 20738198 | All tachyzoite and antigen preparations at high doses stimulated high levels of interleukin (IL) -12, interferon (IFN) -gamma, and tumor necrosis factor (TNF) -alpha, except for heat-killed tachyzoites and sNcAg, which induced moderate level of IL-12 and very low levels of IFN-gamma and TNF-alpha. |
| 868 | 20738198 | All tachyzoite and antigen preparations at high doses stimulated high levels of interleukin (IL) -12, interferon (IFN) -gamma, and tumor necrosis factor (TNF) -alpha, except for heat-killed tachyzoites and sNcAg, which induced moderate level of IL-12 and very low levels of IFN-gamma and TNF-alpha. |
| 869 | 20738198 | In general, whole N. caninum tachyzoites were more effective in inducing IL-12, IFN-gamma, and TNF-alpha than the lysate antigen preparations. |
| 870 | 20738198 | In general, whole N. caninum tachyzoites were more effective in inducing IL-12, IFN-gamma, and TNF-alpha than the lysate antigen preparations. |
| 871 | 20738198 | It appears that the heat-killed N. caninum tachyzoites were less potent in eliciting IFN-gamma or IL-10, but more effective in inducing IL-4. |
| 872 | 20738198 | It appears that the heat-killed N. caninum tachyzoites were less potent in eliciting IFN-gamma or IL-10, but more effective in inducing IL-4. |
| 873 | 20720206 | We show that a rapid increase in parasite biomass is strongly associated with the induction of ECM, mediated by IFN-gamma and lymphotoxin alpha, whereas TNF and IL-10 limit this process. |
| 874 | 20720206 | Crucially, we discovered that host CD4(+) and CD8(+) T cells promote parasite accumulation in vital organs, including the brain. |
| 875 | 20719985 | These new HHV-8 epitopes activated monofunctional and polyfunctional CD8(+) T cells that produced various combinations of gamma interferon, interleukin 2, tumor necrosis factor alpha, macrophage inhibitory protein 1β, and cytotoxic degranulation marker CD107a in healthy HHV-8-seropositive individuals. |
| 876 | 20719985 | We were also able to detect HHV-8-specific CD8(+) T cells in peripheral blood samples using HLA A*0201 pentamer complexes for one gB epitope, one K8.1 epitope, two LANA-1 epitopes, and one K12 epitope. |
| 877 | 20686664 | Our results indicate that both the HCV TCR-transduced CD4(+) and CD8(+) T cells recognized the HCV NS3:1073-1081 peptide-loaded targets and HCV(+) hepatocellular carcinoma cells (HCC) in a polyfunctional manner with cytokine (IFN-gamma, IL-2, and TNF-alpha) production as well as cytotoxicity. |
| 878 | 20686664 | Tumor cell recognition by HCV TCR transduced CD8(-) Jurkat cells and CD4(+) PBL-derived T cells indicated this TCR was CD8-independent, a property consistent with other high affinity TCRs. |
| 879 | 20668555 | Extended LTA, TNF, LST1 and HLA gene haplotypes and their association with rubella vaccine-induced immunity. |
| 880 | 20661301 | In vivo, A172 modulated the transcription of the TNF-alpha, IFN-gamma and Il-1beta genes and, given intramuscularly, protected mice from a lethal dose of A170 (18/20). |
| 881 | 20660192 | The DNA/DNA vaccine induced humoral responses comparable to those induced by a single inoculation with rAd5-GP, as well as CD4(+) and CD8(+) cellular immune responses, with skewing toward CD4(+) T-cell activity against MARV GP. |
| 882 | 20660192 | Across vaccine groups, CD8(+) T-cell subset dominance comprising cells exhibiting a tumor necrosis factor alpha (TNF-alpha) and gamma interferon (IFN-gamma) double-positive functional phenotype was associated with an absence or low frequency of clinical symptoms, suggesting that both the magnitude and functional phenotype of CD8(+) T cells may determine vaccine efficacy against infection by MARV Angola. |
| 883 | 20660136 | Because of the potential importance of HLA-E-restricted CD8(+) responses in resistance to Salmonella infection, we characterized these responses and investigated their kinetics of appearance and persistence in volunteers immunized orally with the licensed attenuated Ty21a strain typhoid vaccine. |
| 884 | 20660136 | Because of the potential importance of HLA-E-restricted CD8(+) responses in resistance to Salmonella infection, we characterized these responses and investigated their kinetics of appearance and persistence in volunteers immunized orally with the licensed attenuated Ty21a strain typhoid vaccine. |
| 885 | 20660136 | An ex vivo multicolor staining panel including antibodies to CD107a and -b, interleukin-2, gamma interferon (IFN-gamma), and tumor necrosis factor alpha (TNF-alpha) was used to functionally assess memory T-cell subsets by flow cytometry. |
| 886 | 20660136 | An ex vivo multicolor staining panel including antibodies to CD107a and -b, interleukin-2, gamma interferon (IFN-gamma), and tumor necrosis factor alpha (TNF-alpha) was used to functionally assess memory T-cell subsets by flow cytometry. |
| 887 | 20660136 | The majority of HLA-E-restricted CD8(+) cells 28 to 56 days after immunization coexpressed CD107, IFN-gamma, and TNF-alpha, showing characteristic features of multifunctional T cells. |
| 888 | 20660136 | The majority of HLA-E-restricted CD8(+) cells 28 to 56 days after immunization coexpressed CD107, IFN-gamma, and TNF-alpha, showing characteristic features of multifunctional T cells. |
| 889 | 20660136 | In summary, the multifunctionality and longevity of the HLA-E-restricted CD8 responses observed in this study highlight their significance in adaptive immunity to S. |
| 890 | 20660136 | In summary, the multifunctionality and longevity of the HLA-E-restricted CD8 responses observed in this study highlight their significance in adaptive immunity to S. |
| 891 | 20660136 | Finally, this is the first demonstration, in either animals or humans, of the presence of long-term multifunctional HLA-E-restricted CD8(+) cells after immunization. |
| 892 | 20660136 | Finally, this is the first demonstration, in either animals or humans, of the presence of long-term multifunctional HLA-E-restricted CD8(+) cells after immunization. |
| 893 | 20640189 | Dual induction of TREM2 and tolerance-related transcript, Tmem176b, in amyloid transgenic mice: implications for vaccine-based therapies for Alzheimer's disease. |
| 894 | 20640189 | In the present study we examined, in a transgenic model of amyloid pathology, the expression of two molecules previously implicated in decreasing the severity of autoimmune responses: TREM2 (triggering receptor expressed on myeloid cells 2) and the intracellular tolerance-associated transcript, Tmem176b (transmembrane domain protein 176b). |
| 895 | 20640189 | Tmem176b expression was highest in the inner zone of amyloid plaques, whereas TREM2 expression was highest in the outer zone. |
| 896 | 20640189 | Induced expression of TREM2 occurred co-incident with detection of thioflavine-S-positive amyloid deposits. |
| 897 | 20640189 | Transfection studies revealed that expression of TREM2 correlated negatively with motility, but correlated positively with the ability of microglia to stimulate CD4(+) T-cell proliferation, TNF (tumour necrosis factor) and CCL2 (chemokine ligand 2) production, but not IFNgamma (interferon gamma) production. |
| 898 | 20640189 | TREM2 expression also showed a positive correlation with amyloid phagocytosis in unactivated cells. |
| 899 | 20640189 | However, activating cells with LPS (lipopolysaccharide), but not IFNgamma, reduced the correlation between TREM2 expression and phagocytosis. |
| 900 | 20640189 | Taken together, these data suggest that, in vivo, Tmem176b(+) cells in closest apposition to amyloid may be the least able to clear amyloid. |
| 901 | 20631336 | Moreover, the levels of interleukin 1 (IL-1), IL-6, tumor necrosis factor alpha (TNF-alpha), and alpha interferon (IFN-alpha) in peripheral blood were upregulated 7 days postinoculation with HuN4, which was earlier than in the HuN4-F112 group. |
| 902 | 20625487 | Fifty six genes such as TNF, NFKB1, IL2, IL6, and MAPK8 were ranked among the top 25 by at least one of the centrality methods in one or both networks. |
| 903 | 20624887 | Using a model wherein mice are vaccinated with bacille Calmette-Guérin after Mtb infection, we show that repeated vaccination results in increased IL-17, tumor necrosis factor, IL-6, and MIP-2 expression, influx of granulocytes/neutrophils, and lung tissue damage. |
| 904 | 20624887 | This pathological response is abrogated in mice deficient in the gene encoding IL-23p19 or in the presence of IL-17-blocking antibody. |
| 905 | 20610663 | Since Toll-like receptor 2 (TLR2), TLR4, and TLR9 activation have been involved in HIV-1 recrudescence, we sought to determine the role of these TLRs in HIV-1 reactivation induced by the periodontal pathogens Fusobacterium nucleatum and Porphyromonas gingivalis using BF24 monocytes/macrophages stably transfected with the HIV-1 promoter driving chloramphenicol acetyltransferase (CAT) expression and THP89GFP cells, a model of HIV-1 latency. |
| 906 | 20610663 | We demonstrated that TLR9 activation by F. nucleatum and TLR2 activation by both bacteria appear to be involved in HIV-1 reactivation; however, TLR4 activation had no effect. |
| 907 | 20610663 | Moreover, the autocrine activity of tumor necrosis factor alpha (TNF-alpha) but not interleukin-1beta (IL-1beta) produced in response to bacteria could impact viral reactivation. |
| 908 | 20610663 | The transcription factors NF-kappaB and Sp1 appear to be positively regulating HIV-1 reactivation induced by these oral pathogens. |
| 909 | 20610663 | These results suggest that oral Gram-negative bacteria (F. nucleatum and P. gingivalis) associated with oral and systemic chronic inflammatory disorders enhance HIV-1 reactivation in monocytes/macrophages through TLR2 and TLR9 activation in a mechanism that appears to be transcriptionally regulated. |
| 910 | 20607036 | Here, we report that PDT can induce IL-1 and IL-6 and reduce TNF-alpha expression from DCs. |
| 911 | 20600501 | Immunization of A/J or C57BL/6 mice with J-LEAPS heteroconjugates containing an epitope from the HSV-1 glycoprotein D (JgD) or an epitope from the HIV gag protein (JH) emulsified with Seppic ISA51 induced increased levels of IL-12p70 by day 3 and increased levels of interferon gamma (IFN-gamma) on days 10 and 24. |
| 912 | 20600501 | Interestingly, levels of IL-10, TNF-alpha, and IL-6 did not change. |
| 913 | 20600501 | Bone marrow (BM) cells became CD86 and CD11c positive within 48 h of treatment with JgD or JH. |
| 914 | 20580469 | In bone marrow-derived macrophages the B. abortusDeltawbkC mutants were attenuated, could not reach a replicative niche and induced higher levels of IL-12 and TNF-alpha when compared to parental smooth strains. |
| 915 | 20574911 | At the end of the 14-d exposure period, bronchoalveolar lavage (BAL) fluids were recovered, cytokines (interleukin [IL]-1beta, IL-6, keratinocyte-derived chemokine [KC], and tumor necrosis factor [TNF]) in BAL were measured by enzyme-linked immunosorbent assay (ELISA), and leukocytes in BAL were counted. |
| 916 | 20574911 | At the end of the 14-d exposure period, bronchoalveolar lavage (BAL) fluids were recovered, cytokines (interleukin [IL]-1beta, IL-6, keratinocyte-derived chemokine [KC], and tumor necrosis factor [TNF]) in BAL were measured by enzyme-linked immunosorbent assay (ELISA), and leukocytes in BAL were counted. |
| 917 | 20574911 | Likewise, the group that was exposed to the highest level of SBD had significantly higher levels of IL-1beta, KC, and TNF than controls and some other groups. |
| 918 | 20574911 | Likewise, the group that was exposed to the highest level of SBD had significantly higher levels of IL-1beta, KC, and TNF than controls and some other groups. |
| 919 | 20543102 | TNF-alpha secreted by the CD4 T cells was identified as the key effector molecule. |
| 920 | 20530206 | Using two distinct vaccine platforms, we evaluate the influence of interleukin (IL) 10 production on the magnitude, quality, and protective capacity of CD4(+) T cell responses in the mouse model of Leishmania major infection. |
| 921 | 20530206 | Using two distinct vaccine platforms, we evaluate the influence of interleukin (IL) 10 production on the magnitude, quality, and protective capacity of CD4(+) T cell responses in the mouse model of Leishmania major infection. |
| 922 | 20530206 | Multiparameter flow cytometry was used to delineate the CD4(+) T cell production of interferon (IFN) gamma, IL-2, tumor necrosis factor (TNF), and IL-10 (or combinations thereof) after vaccination. |
| 923 | 20530206 | Multiparameter flow cytometry was used to delineate the CD4(+) T cell production of interferon (IFN) gamma, IL-2, tumor necrosis factor (TNF), and IL-10 (or combinations thereof) after vaccination. |
| 924 | 20530206 | Immunization with a high dose of adenovirus (ADV) expressing leishmanial proteins (MML-ADV) elicited a limited proportion of multifunctional IFN-gamma(+)IL-2(+)TNF(+) Th1 cells, a high frequency of IL-10-producing CD4(+) T cells, and did not protect against subsequent challenge. |
| 925 | 20530206 | Immunization with a high dose of adenovirus (ADV) expressing leishmanial proteins (MML-ADV) elicited a limited proportion of multifunctional IFN-gamma(+)IL-2(+)TNF(+) Th1 cells, a high frequency of IL-10-producing CD4(+) T cells, and did not protect against subsequent challenge. |
| 926 | 20530206 | In contrast, after immunization with MML protein and CpG (MML + CpG), IL-10 limited the production of IL-12 by DCs in vivo, thereby decreasing the generation of multifunctional Th1 cells. |
| 927 | 20530206 | In contrast, after immunization with MML protein and CpG (MML + CpG), IL-10 limited the production of IL-12 by DCs in vivo, thereby decreasing the generation of multifunctional Th1 cells. |
| 928 | 20519386 | Rheumatic disease was associated with a prolific infiltrate of monocytes, macrophages, and NK cells and the production of monocyte chemoattractant protein 1 (MCP-1), tumor necrosis factor alpha (TNF-alpha), and gamma interferon (IFN-gamma). |
| 929 | 20508727 | In addition, IDLV immunization induced high frequency of polyfunctional CD8+ T cells able to simultaneously produce IFNgamma, TNFalpha, and IL2. |
| 930 | 20490763 | F.t. infection up-regulated IL-12 p40 production and down-regulated TNF-alpha production by stimulated macrophages; on the other hand, F.t. infection did not affect the production of IL-8, IL-6, MCP-5, and RANTES by stimulated macrophages. |
| 931 | 20488263 | This FMIA simultaneously detects innate (IL-1 beta, IL-8, IFN-alpha, TNF-alpha, IL-12), regulatory (IL-10), Th1 (IFN-gamma) and Th2 (IL-4) cytokines. |
| 932 | 20484568 | High levels of interleukin-10 (IL-10), gamma interferon (IFN-gamma), and tumor necrosis factor alpha (TNF-alpha) were associated with poor outcome, since detected concentrations were highest in patients with fatal outcome and lowest in patients with moderate disease course. |
| 933 | 20484568 | High levels of interleukin-10 (IL-10), gamma interferon (IFN-gamma), and tumor necrosis factor alpha (TNF-alpha) were associated with poor outcome, since detected concentrations were highest in patients with fatal outcome and lowest in patients with moderate disease course. |
| 934 | 20484568 | This consequently triggers increased production of IFN-gamma and TNF-alpha, cytokines mediating vascular dysfunction, disseminated intravascular coagulation, organ failure, and shock. |
| 935 | 20484568 | This consequently triggers increased production of IFN-gamma and TNF-alpha, cytokines mediating vascular dysfunction, disseminated intravascular coagulation, organ failure, and shock. |
| 936 | 20471443 | Incorporation of CD40 ligand into SHIV virus-like particles (VLP) enhances SHIV-VLP-induced dendritic cell activation and boosts immune responses against HIV. |
| 937 | 20471443 | Engagement of CD40 with CD40L induces dendritic cell (DC) maturation and activation, thereby promoting immune responses. |
| 938 | 20471443 | We found that CD83, CD40, and CD86 were significantly up-regulated and significantly increased cytokines production were observed after hCD40L/SHIV-VLP treatment in human CD14(+) monocyte-derived DCs as compared to SHIV-VLP treatment. |
| 939 | 20471443 | Mice immunized with mCD40L/SHIV-VLP showed more than a two-fold increase in HIV Env-specific IgG antibody production, an increase in SIV Gag and HIV Env-specific IFN-gamma and IL-4 producing cells, and an increase in HIV Env-specific cytotoxic activity compared to that in SHIV-VLP immunized mice. |
| 940 | 20471443 | Furthermore, multifunctional CD4(+) Th1 cells, which simultaneously produce IFN-gamma, IL-2 and TNF-alpha triple cytokines, and CD8(+) T-cells, which produce IFN-gamma were elevated in the mCD40L/SHIV-VLP immunized group. |
| 941 | 20471443 | Therefore, incorporation of CD40L into VLP may represent a novel strategy to develop effective HIV vaccines. |
| 942 | 20463601 | Depletion of natural killer (NK) cells, but not of CD8 or CD4 T cells, in the splenocytes from DC (without MC38 lysate-pulse or LPS treatment thereafter)-inoculated mice decreased the cytotoxic activity. |
| 943 | 20463601 | MC38 cells pretreated with 5-FU exhibited enhanced expression of procaspase 8 and efficiently underwent apoptosis by TNF-alpha with activation of caspase 8. |
| 944 | 20457786 | Although animals infected with the sigE mutant had low bacillary loads, their lungs showed significantly higher production of the protective factors gamma interferon (IFN-gamma), tumor necrosis factor alpha (TNF-alpha), inducible nitric oxide synthase (iNOS), and beta-defensins than those of animals infected with the parental or complemented mutant strain. |
| 945 | 20457264 | Polychromatic flow cytometry was used to examine CD4(+) T cells for levels of interferon (IFN)-γ, tumor necrosis factor (TNF)-α, and CD154 (CD40 ligand) expression after stimulation with inactivated flu virus. |
| 946 | 20457264 | CD4(+) T cell expression of CD154 and cytokine responses were significantly reduced in HCT recipients compared to healthy adults. |
| 947 | 20457264 | A lack of B cell reconstitution and dysfunctional CD4 T cell costimulation (as marked by low CD154 expression) is associated with low NAb levels postvaccination in HCT patients. |
| 948 | 20450288 | The cytokine measurement profile of IFN-gamma, TNF-alpha, IL-2, IL-4 and IL-10 in culture supernatants of cells primed with peptide antigens in microparticles co-encapsulating CpG ODN showed higher levels of IFN- gamma followed by TNF-alpha and IL-2, with relatively low levels of IL-4 and IL-10. |
| 949 | 20445007 | The current studies used the Toll-like receptor 2 (TLR2) agonist palmitoyl(3)-cysteine-serine-lysine(4) (PAM) or the TLR4 agonist lipopolysaccharide (LPS) to stimulate human whole blood and determine whether postponing the addition of the GC dexamethasone (DEX) limits its ability to decrease cytokine production. |
| 950 | 20445007 | The current studies used the Toll-like receptor 2 (TLR2) agonist palmitoyl(3)-cysteine-serine-lysine(4) (PAM) or the TLR4 agonist lipopolysaccharide (LPS) to stimulate human whole blood and determine whether postponing the addition of the GC dexamethasone (DEX) limits its ability to decrease cytokine production. |
| 951 | 20445007 | Twenty-four hours after stimulation, tumor necrosis factor (TNF), interleukin-1beta (IL-1beta), IL-6, and IL-8 levels were measured, in addition to the cytokine inhibitors IL-1 soluble receptor II (SRII), IL-1 receptor antagonist, and TNF SRII. |
| 952 | 20445007 | Twenty-four hours after stimulation, tumor necrosis factor (TNF), interleukin-1beta (IL-1beta), IL-6, and IL-8 levels were measured, in addition to the cytokine inhibitors IL-1 soluble receptor II (SRII), IL-1 receptor antagonist, and TNF SRII. |
| 953 | 20445007 | PAM stimulation also induced IL-1beta, IL-6, and IL-8. |
| 954 | 20445007 | PAM stimulation also induced IL-1beta, IL-6, and IL-8. |
| 955 | 20445007 | Delaying the addition of DEX until 6 h after LPS stimulation failed to decrease TNF or IL-6. |
| 956 | 20445007 | Delaying the addition of DEX until 6 h after LPS stimulation failed to decrease TNF or IL-6. |
| 957 | 20445007 | In contrast, delayed DEX addition significantly suppressed PAM-induced IL-1beta, IL-6, or IL-8 and also suppressed LPS-induced IL-1beta and IL-8. |
| 958 | 20445007 | In contrast, delayed DEX addition significantly suppressed PAM-induced IL-1beta, IL-6, or IL-8 and also suppressed LPS-induced IL-1beta and IL-8. |
| 959 | 20435931 | Knockdown of CD40, CD80, and CD86, prior to loading DCs with the arthritogenic Ag collagen II, led to a population of cells that could effectively suppress onset of collagen-induced arthritis. |
| 960 | 20435931 | Disease suppression was associated with inhibition of collagen II-specific Ab production and suppression of T cell recall responses. |
| 961 | 20435931 | Downregulation of IL-2, IFN-gamma, TNF-alpha, and IL-17 and increased FoxP3(+) cells with regulatory activity were observed in collagen-induced arthritis mice treated with siRNA-transfected DCs. |
| 962 | 20435929 | Polyfunctional CD4(+) and CD8(+) T cell responses to tuberculosis antigens in HIV-1-infected patients before and after anti-retroviral treatment. |
| 963 | 20435929 | We assessed polyfunctional (IFN-gamma(+)IL-2(+)TNF-alpha(+)) T cell responses to TB Ags in three groups of HIV-1-infected patients dependent on their TB status, CD4 counts, and anti-retroviral exposure. |
| 964 | 20435929 | We found that although the proportion of IFN-gamma cells in response to TB Ags was higher in patients with low CD4 counts, the responding cells changed from a polyfunctional CD4(+) to a monofunctional CD8(+) response. |
| 965 | 20434553 | Splenocytes were separated for detection of lymphocyte proliferation in responses to concanavalin A (Con A), lipopolysaccharide (LPS) and OVA, and mRNA expression of Th1 cytokines (IFN-gamma and IL-12), Th2 cytokines (IL-10 and IL-5) and transcription factors T-bet/GATA-3 (Th1/Th2 switcher). |
| 966 | 20434553 | In addition, up-regulated T-bet/GATA-3 together with significantly increased mRNA expression of IL-4, IL-10, IFN-gamma and IL-12 by splenocytes, as well as the proliferative responses of splenocytes to Con A, LPS and OVA were observed in paclitaxel-adjuvanted groups. |
| 967 | 20434553 | Incubation of a murine macrophage-like cell line with paclitaxel significantly increased TNF-alpha and -10 released from the cells and expression of microRNAs such as miR-155, miR-147, miR-146a and miR-132. |
| 968 | 20430958 | Virally infected and matured human dendritic cells activate natural killer cells via cooperative activity of plasma membrane-bound TNF and IL-15. |
| 969 | 20430958 | Virally infected and matured human dendritic cells activate natural killer cells via cooperative activity of plasma membrane-bound TNF and IL-15. |
| 970 | 20430958 | Virally infected and matured human dendritic cells activate natural killer cells via cooperative activity of plasma membrane-bound TNF and IL-15. |
| 971 | 20430958 | We found that adenovirus transduction and lipopolysaccharide/interferon-gamma-induced maturation increased expression of transmembrane tumor necrosis factor (TNF) and trans-presented (trans) interleukin-15 (IL-15) on DCs, leading to enhanced NK cell activation without enhancing DC susceptibility to NK cell-mediated killing. |
| 972 | 20430958 | We found that adenovirus transduction and lipopolysaccharide/interferon-gamma-induced maturation increased expression of transmembrane tumor necrosis factor (TNF) and trans-presented (trans) interleukin-15 (IL-15) on DCs, leading to enhanced NK cell activation without enhancing DC susceptibility to NK cell-mediated killing. |
| 973 | 20430958 | We found that adenovirus transduction and lipopolysaccharide/interferon-gamma-induced maturation increased expression of transmembrane tumor necrosis factor (TNF) and trans-presented (trans) interleukin-15 (IL-15) on DCs, leading to enhanced NK cell activation without enhancing DC susceptibility to NK cell-mediated killing. |
| 974 | 20430958 | This crosstalk enhanced NK cell CD69 expression, interferon-gamma secretion, proliferation, and antitumor activities, with Ad.DCs being significantly more effective than immature DCs, but less effective than mDCs. |
| 975 | 20430958 | This crosstalk enhanced NK cell CD69 expression, interferon-gamma secretion, proliferation, and antitumor activities, with Ad.DCs being significantly more effective than immature DCs, but less effective than mDCs. |
| 976 | 20430958 | This crosstalk enhanced NK cell CD69 expression, interferon-gamma secretion, proliferation, and antitumor activities, with Ad.DCs being significantly more effective than immature DCs, but less effective than mDCs. |
| 977 | 20430958 | The Ad.DC and mDC crosstalk with NK cells was largely prevented by physical separation of DCs and NK cells, and neutralization of total TNF and IL-15, but not by selective sequestration of soluble TNF. |
| 978 | 20430958 | The Ad.DC and mDC crosstalk with NK cells was largely prevented by physical separation of DCs and NK cells, and neutralization of total TNF and IL-15, but not by selective sequestration of soluble TNF. |
| 979 | 20430958 | The Ad.DC and mDC crosstalk with NK cells was largely prevented by physical separation of DCs and NK cells, and neutralization of total TNF and IL-15, but not by selective sequestration of soluble TNF. |
| 980 | 20427631 | The CMV pp65 peptide pool and the superantigen Staphylococcus enterotoxin B (SEB) induced higher proportions of CD8+ effector T cells expressing gamma interferon (IFN-gamma), tumor necrosis factor alpha (TNF-alpha), and granulocyte-macrophage colony-stimulating factor in the oldest study group, while only SEB induced increased responses in the middle-aged study group. |
| 981 | 20427631 | The CMV pp65 peptide pool and the superantigen Staphylococcus enterotoxin B (SEB) induced higher proportions of CD8+ effector T cells expressing gamma interferon (IFN-gamma), tumor necrosis factor alpha (TNF-alpha), and granulocyte-macrophage colony-stimulating factor in the oldest study group, while only SEB induced increased responses in the middle-aged study group. |
| 982 | 20427631 | Notably, CMV-specific multiple cytokine expression patterns revealed higher proportions of IFN-gamma- and TNF-alpha-coexpressing CD8+ T cells exclusively in the oldest study group. |
| 983 | 20427631 | Notably, CMV-specific multiple cytokine expression patterns revealed higher proportions of IFN-gamma- and TNF-alpha-coexpressing CD8+ T cells exclusively in the oldest study group. |
| 984 | 20427631 | These qualitative differences were absent in SEB-induced CD8+ effector T cells, although quantitative differences were detected. |
| 985 | 20427631 | These qualitative differences were absent in SEB-induced CD8+ effector T cells, although quantitative differences were detected. |
| 986 | 20427628 | We found that only interleukin 12 (IL-12), not other costimulants, increased IFN-gamma production in WBA while maintaining M. leprae peptide specificity, as evidenced by lack of increase of IFN-gamma in control samples stimulated with IL-12 alone. |
| 987 | 20427628 | The IL-12-induced increase in IFN-gamma was mainly mediated by CD4+ T cells that did not produce IL-2 or tumor necrosis factor (TNF). |
| 988 | 20427628 | Although not statistically significantly, macrophage inflammatory protein 1beta (MIP-1beta) and macrophage c protein 1 (MCP-1) levels specific for M. leprae peptide tended to be increased by IL-12. |
| 989 | 20427628 | IP-10 production was also found to be a useful marker of M. leprae peptide responses, but its production was enhanced by IL-12 nonspecifically. |
| 990 | 20421877 | Tumor necrosis factor negative bone marrow-derived dendritic cells exhibit deficient IL-10 expression. |
| 991 | 20421877 | Tumor necrosis factor negative bone marrow-derived dendritic cells exhibit deficient IL-10 expression. |
| 992 | 20421877 | Analysis of DC activated by addition of the mycobacterial vaccine strain Bacillus Calmette-Guérin showed that of the effector molecules studied only interleukin-10 expression was significantly reduced in TNF-negative (B6.TNF(-/-)) DC. |
| 993 | 20421877 | Analysis of DC activated by addition of the mycobacterial vaccine strain Bacillus Calmette-Guérin showed that of the effector molecules studied only interleukin-10 expression was significantly reduced in TNF-negative (B6.TNF(-/-)) DC. |
| 994 | 20419805 | The genotyping for TNF (-308), TGFB1 (+869, +915), IL-10 (-1082, -819, -592), IL-6 (-174), and IFNG (+874) was accomplished by the PCR-SSP technique. |
| 995 | 20419158 | Escape of HIV-1-infected dendritic cells from TRAIL-mediated NK cell cytotoxicity during NK-DC cross-talk--a pivotal role of HMGB1. |
| 996 | 20419158 | We first addressed the question of the mechanisms involved in iDC editing, and we show that cognate NK-iDC interaction triggers apoptosis via the TNF-related apoptosis-inducing ligand (TRAIL)-Death Receptor 4 (DR4) pathway and not via the perforin pathway. |
| 997 | 20419158 | This resistance occurs despite normal amounts of TRAIL released by NK cells and comparable DR4 expression on DC(HIV). |
| 998 | 20419158 | High-mobility group box 1 (HMGB1), an alarmin and a key mediator of NK-DC cross-talk, was found to play a pivotal role in NK-dependent upregulation of c-FLIP and c-IAP2 in DC(HIV). |
| 999 | 20419158 | Finally, we demonstrate that restoration of DC(HIV) susceptibility to NK-induced TRAIL killing can be obtained either by silencing c-FLIP and c-IAP2 by specific siRNA, or by inhibiting HMGB1 with blocking antibodies or glycyrrhizin, arguing for a key role of HMGB1 in TRAIL resistance and DC(HIV) survival. |
| 1000 | 20418899 | Here, we investigated the antitumor effect of adenovirus-mediated gene transfer of LIGHT, the tumor-necrosis factor (TNF) superfamily member also known as TNFSF14, in the murine A20 B-cell lymphoma. |
| 1001 | 20418899 | LIGHT gene modification resulted in upregulated expression of Fas and the accessory molecule--intercellular adhesion molecule-1 (ICAM-1) on A20 cells and led to enhanced A20 cell apoptosis. |
| 1002 | 20418899 | LIGHT-modified A20 cells effectively stimulated the proliferation of T lymphocytes and interferon (IFN)-gamma production in vitro. |
| 1003 | 20418899 | This adenovirus-mediated LIGHT therapy induced substantial splenic natural killer (NK) and cytotoxic T lymphocyte (CTL) activity, enhanced tumor infiltration by inflammatory cells and increased chemokine expression of CC chemokine ligand 21 (CCL21), IFN-inducible protein-10 (IP-10) and monokine induced by IFN-gamma (Mig) from tumor tissues. |
| 1004 | 20410285 | In analyzing the role of type I IFNs in immunity to FPV, we show that they are critical to the secretion of a number of innate and proinflammatory cytokines, including type I IFNs themselves as well as interleukin-12 (IL-12), tumor necrosis factor-alpha (TNF-alpha), IL-6, and IL-1beta, and that deficiency leads to enhanced virus-mediated antigen expression. |
| 1005 | 20410263 | In this study, we demonstrate that the bulk memory cytotoxic T lymphocytes (CTLs) established by seasonal influenza viruses from healthy individuals who have not been exposed to pdmH1N1 can directly lyse pdmH1N1-infected target cells and produce gamma interferon (IFN-gamma) and tumor necrosis factor alpha (TNF-alpha). |
| 1006 | 20410263 | These M1(58-66)-specific CTLs showed an effector memory phenotype and expressed CXCR3 and CCR5 chemokine receptors. |
| 1007 | 20404924 | Further, circulating levels of IFN-gamma, TNF-alpha, IL-10, IL-6, IL-4 and IL-2 were analysed in VL patients (n = 29) by Cytometric Bead Array to evaluate correlation with parasitic load. |
| 1008 | 20362206 | Hepatitis B virus (HBV)-derived DRB1*0101-restricted CD4 T-cell epitopes help in the development of HBV-specific CD8+ T cells in vivo. |
| 1009 | 20362206 | The preS2 epitope favored a well-balanced response with CD4+ and CD8+ T cells producing IFN-gamma, IL-2 and TNF-alpha. |
| 1010 | 20357059 | In this study, we assessed the immunizing activity of a recombinant modified vaccinia Ankara (MVA) construct (MVA/IL-15/5Mtb) which overexpresses five Mycobacterium tuberculosis antigens (antigen 85A, antigen 85B, ESAT6, HSP60, and Mtb39), as well as the molecular adjuvant interleukin-15 (IL-15). |
| 1011 | 20357059 | In this study, we assessed the immunizing activity of a recombinant modified vaccinia Ankara (MVA) construct (MVA/IL-15/5Mtb) which overexpresses five Mycobacterium tuberculosis antigens (antigen 85A, antigen 85B, ESAT6, HSP60, and Mtb39), as well as the molecular adjuvant interleukin-15 (IL-15). |
| 1012 | 20357059 | At 16 months, when the Mycobacterium bovis BCG and MVA/IL-15/5Mtb vaccine-induced protection was essentially equivalent, the protective responses after a tuberculous challenge were associated with elevated levels of gamma interferon (IFN-gamma), IL-17F, Cxcl9, and Cxcl10. |
| 1013 | 20357059 | At 16 months, when the Mycobacterium bovis BCG and MVA/IL-15/5Mtb vaccine-induced protection was essentially equivalent, the protective responses after a tuberculous challenge were associated with elevated levels of gamma interferon (IFN-gamma), IL-17F, Cxcl9, and Cxcl10. |
| 1014 | 20357059 | Long-term memory after immunization with the E6-85-MVA/IL-15/5Mtb combination regimen was associated with the induction of monofunctional CD4 and CD8 IFN-gamma-producing T cells and multifunctional CD4 and CD8 T cells expressing IFN-gamma/tumor necrosis factor alpha (TNF-alpha), TNF-alpha/IL-2, and IFN-gamma/TNF-alpha/IL-2. |
| 1015 | 20357059 | Long-term memory after immunization with the E6-85-MVA/IL-15/5Mtb combination regimen was associated with the induction of monofunctional CD4 and CD8 IFN-gamma-producing T cells and multifunctional CD4 and CD8 T cells expressing IFN-gamma/tumor necrosis factor alpha (TNF-alpha), TNF-alpha/IL-2, and IFN-gamma/TNF-alpha/IL-2. |
| 1016 | 20357059 | In contrast, BCG-induced protection was characterized by fewer CD4 and CD8 monofunctional T cells expressing IFN-gamma and only IFN-gamma/TNF-alpha and IFN-gamma/TNF-alpha/IL-2 expressing multifunctional T (MFT) cells. |
| 1017 | 20357059 | In contrast, BCG-induced protection was characterized by fewer CD4 and CD8 monofunctional T cells expressing IFN-gamma and only IFN-gamma/TNF-alpha and IFN-gamma/TNF-alpha/IL-2 expressing multifunctional T (MFT) cells. |
| 1018 | 20332049 | Expression of co-stimulatory molecules (CD40, CD80, CD86, and MHC-II) and cytokines (IL-12p40, TNF-alpha, and IFN-gamma) was increased in BMDC treated with LT-IIa-B(5). |
| 1019 | 20308630 | Gene expression analysis using tumor-derived RNA demonstrated that imiquimod induced high levels of IL-10 in addition to TNF-alpha and IFN-gamma. |
| 1020 | 20308630 | Elevated serum IL-10 appeared to be derived from IL-10 and dual cytokine secreting (IFN-gamma(+) and IL-10(+)) CD4(+) T cells rather than CD4(+)CD25(+)Foxp3(+) T regulatory cells, which were also induced by imiquimod treatment. |
| 1021 | 20308630 | Blockade of IL-10, but not TGF-beta, enhanced the antitumor effect of imiquimod by significantly prolonging survival in treated mice. |
| 1022 | 20231414 | YopJ/P kills macrophages and dendritic cells, reduces their production of tumor necrosis factor alpha (TNF-alpha) and interleukin-12 (IL-12), and promotes systemic colonization in mouse models of intestinal Yersinia infection. |
| 1023 | 20231414 | Surprisingly, YopJ-promoted cytotoxicity and systemic colonization were associated with significant increases in neutrophils in spleens and the proinflammatory cytokines IL-18 and gamma interferon (IFN-gamma) in serum samples of mice vaccinated with Y. pseudotuberculosis. |
| 1024 | 20231405 | Chlamydia muridarum T-cell antigens formulated with the adjuvant DDA/TDB induce immunity against infection that correlates with a high frequency of gamma interferon (IFN-gamma)/tumor necrosis factor alpha and IFN-gamma/interleukin-17 double-positive CD4+ T cells. |
| 1025 | 20231405 | Chlamydia muridarum T-cell antigens formulated with the adjuvant DDA/TDB induce immunity against infection that correlates with a high frequency of gamma interferon (IFN-gamma)/tumor necrosis factor alpha and IFN-gamma/interleukin-17 double-positive CD4+ T cells. |
| 1026 | 20231405 | Chlamydia muridarum T-cell antigens formulated with the adjuvant DDA/TDB induce immunity against infection that correlates with a high frequency of gamma interferon (IFN-gamma)/tumor necrosis factor alpha and IFN-gamma/interleukin-17 double-positive CD4+ T cells. |
| 1027 | 20231405 | The results demonstrate that mice immunized with the DDA/TDB formulation induced the strongest gamma interferon (IFN-gamma) and interleukin-17 (IL-17) responses, characterized by the highest frequency of IFN-gamma/tumor necrosis factor alpha (TNF-alpha) and IFN-gamma/IL-17 double-positive CD4(+) T cells. |
| 1028 | 20231405 | The results demonstrate that mice immunized with the DDA/TDB formulation induced the strongest gamma interferon (IFN-gamma) and interleukin-17 (IL-17) responses, characterized by the highest frequency of IFN-gamma/tumor necrosis factor alpha (TNF-alpha) and IFN-gamma/IL-17 double-positive CD4(+) T cells. |
| 1029 | 20231405 | The results demonstrate that mice immunized with the DDA/TDB formulation induced the strongest gamma interferon (IFN-gamma) and interleukin-17 (IL-17) responses, characterized by the highest frequency of IFN-gamma/tumor necrosis factor alpha (TNF-alpha) and IFN-gamma/IL-17 double-positive CD4(+) T cells. |
| 1030 | 20231405 | In conclusion, a Chlamydia vaccine based on the recombinant proteins PmpG-1, PmpE/F-2, and MOMP delivered in a DDA/TDB adjuvant conferred protection against infection that correlated with IFN-gamma/TNF-alpha and IFN-gamma/IL-17 double-positive CD4(+) T cells. |
| 1031 | 20231405 | In conclusion, a Chlamydia vaccine based on the recombinant proteins PmpG-1, PmpE/F-2, and MOMP delivered in a DDA/TDB adjuvant conferred protection against infection that correlated with IFN-gamma/TNF-alpha and IFN-gamma/IL-17 double-positive CD4(+) T cells. |
| 1032 | 20231405 | In conclusion, a Chlamydia vaccine based on the recombinant proteins PmpG-1, PmpE/F-2, and MOMP delivered in a DDA/TDB adjuvant conferred protection against infection that correlated with IFN-gamma/TNF-alpha and IFN-gamma/IL-17 double-positive CD4(+) T cells. |
| 1033 | 20224419 | Whole Peripheral blood mononuclear cells or CD8(+) cell-depleted peripheral blood mononuclear cells from previously tetanus toxoid (TT)-immunized individuals were activated with TT plus IL-2, and cell proliferation, cytokine production, and in vitro HIV-1 replication were measured. |
| 1034 | 20224419 | Whole Peripheral blood mononuclear cells or CD8(+) cell-depleted peripheral blood mononuclear cells from previously tetanus toxoid (TT)-immunized individuals were activated with TT plus IL-2, and cell proliferation, cytokine production, and in vitro HIV-1 replication were measured. |
| 1035 | 20224419 | Although the IL-1beta and tumour necrosis factor alpha (TNF-alpha) production were higher in cultures from aged HIV-1-infected patients, a dramatic damage on the interferon gamma (IFN-gamma) release was observed, when compared with younger patients. |
| 1036 | 20224419 | Although the IL-1beta and tumour necrosis factor alpha (TNF-alpha) production were higher in cultures from aged HIV-1-infected patients, a dramatic damage on the interferon gamma (IFN-gamma) release was observed, when compared with younger patients. |
| 1037 | 20224419 | CD8(+) T lymphocytes depletion reduced IL-1beta and TNF-alpha release in the older groups, however, it did not significantly alter their IFN-gamma production. |
| 1038 | 20224419 | CD8(+) T lymphocytes depletion reduced IL-1beta and TNF-alpha release in the older groups, however, it did not significantly alter their IFN-gamma production. |
| 1039 | 20224419 | Furthermore, the neutralization of endogenous IL-10 did not change the IFN-gamma deficiency in older AIDS patients. |
| 1040 | 20224419 | Furthermore, the neutralization of endogenous IL-10 did not change the IFN-gamma deficiency in older AIDS patients. |
| 1041 | 20221274 | The PBSCs were cultured in the X-VIVO 20 medium supplemented with the Flt-3 Ligand (FL), GM-CSF, IL-4 and TNF-alpha for 12 days. |
| 1042 | 20219877 | Furthermore, the immunization of mice with gamma-PGA NPs carrying ovalbumin (OVA) as an antigen significantly induced antigen-specific CD8(+) T cells and antigen-specific production of interleukin-2, tumor necrosis factor alpha, and gamma interferon from the cells. |
| 1043 | 20219876 | To begin to understand the surprising survival of macrophage-specific lipopolysaccharide-induced tumor necrosis factor alpha factor-deficient (macLITAF(-/-)) animals after a lethal dose of lipopolysaccharide (LPS), as reported earlier, the present follow-up study focuses on the role of LITAF in the regulation of inflammatory cytokines secreted in response to lethal or sublethal doses of LPS administered to wild-type (WT) and macLITAF(-/-) mice. |
| 1044 | 20219876 | To begin to understand the surprising survival of macrophage-specific lipopolysaccharide-induced tumor necrosis factor alpha factor-deficient (macLITAF(-/-)) animals after a lethal dose of lipopolysaccharide (LPS), as reported earlier, the present follow-up study focuses on the role of LITAF in the regulation of inflammatory cytokines secreted in response to lethal or sublethal doses of LPS administered to wild-type (WT) and macLITAF(-/-) mice. |
| 1045 | 20219876 | A time course study of kinase expression in peritoneal macrophages revealed increased phosphorylation of prosurvival kinases Akt, Erk1/2, and ribosomal S6 kinase (RSK) in macLITAF(-/-) mice compared to that in WT mice (n = 8), confirming their role in LPS-mediated diseases. macLITAF(-/-) mice (n = 8) survived a lethal dose of LPS plus d-galactosamine (d-GalN), expressing lower serum levels of pro- and anti-inflammatory cytokines than the WT levels. |
| 1046 | 20219876 | A time course study of kinase expression in peritoneal macrophages revealed increased phosphorylation of prosurvival kinases Akt, Erk1/2, and ribosomal S6 kinase (RSK) in macLITAF(-/-) mice compared to that in WT mice (n = 8), confirming their role in LPS-mediated diseases. macLITAF(-/-) mice (n = 8) survived a lethal dose of LPS plus d-galactosamine (d-GalN), expressing lower serum levels of pro- and anti-inflammatory cytokines than the WT levels. |
| 1047 | 20219876 | Our results demonstrate that LITAF deficiency in vivo affects cytokines other than TNF-alpha and influences the balance between the pro- and anti-inflammatory cytokines, which protects the animals from the deleterious effects of an LPS-induced inflammatory response, resulting in a beneficial host regulation of inflammatory cytokines and in enhanced survival. |
| 1048 | 20219876 | Our results demonstrate that LITAF deficiency in vivo affects cytokines other than TNF-alpha and influences the balance between the pro- and anti-inflammatory cytokines, which protects the animals from the deleterious effects of an LPS-induced inflammatory response, resulting in a beneficial host regulation of inflammatory cytokines and in enhanced survival. |
| 1049 | 20219669 | Differences in cytokines production were found for IL-10, IL-4, TNF-alpha, and Arginase-1, which, in some conditions, resulted higher in r-BCG as compared to wt BCG-immunised mice. |
| 1050 | 20217072 | IL-6 secretion was co-directionally associated (p < or = 0.01) with five intronic SNPs in the TNFRSF1B gene in an allele dose-related manner, while five promoter/intronic SNPs in the IL12B gene were associated with variations in IL-6 secretion. |
| 1051 | 20217072 | IL-6 secretion was co-directionally associated (p < or = 0.01) with five intronic SNPs in the TNFRSF1B gene in an allele dose-related manner, while five promoter/intronic SNPs in the IL12B gene were associated with variations in IL-6 secretion. |
| 1052 | 20217072 | TNFA haplotype AAACGGGGC (t-statistic = 3.32) and IL12B promoter haplotype TAG (t-statistic = 2.66) were associated with higher levels of (p < or = 0.01) rubella-IgG and IL-6 secretion, respectively. |
| 1053 | 20217072 | TNFA haplotype AAACGGGGC (t-statistic = 3.32) and IL12B promoter haplotype TAG (t-statistic = 2.66) were associated with higher levels of (p < or = 0.01) rubella-IgG and IL-6 secretion, respectively. |
| 1054 | 20217072 | We identified individual SNPs/haplotypes in TNFA/TNFRSF1B and IL12B genes that appear to modulate immunity to rubella vaccination. |
| 1055 | 20217072 | We identified individual SNPs/haplotypes in TNFA/TNFRSF1B and IL12B genes that appear to modulate immunity to rubella vaccination. |
| 1056 | 20213733 | To elucidate the potential role of T cells in sequential flavivirus infection, we characterized cross-reactive CD4+ and CD8+ T-cell responses between attenuated and pathogenic Japanese encephalitis virus (JEV) and pathogenic West Nile virus (WNV). |
| 1057 | 20213733 | However, there was a virus-dependent, peptide variant-independent pattern of cytokine secretion; the IFNgamma+-to-IFNgamma+TNFalpha+ CD8+ T-cell ratio was greater in JEV- than in WNV-infected mice. |
| 1058 | 20213733 | Patterns of killer cell lectin-like receptor G1 (KLRG1) and CD127 expression differed by virus type, with a rapid expansion and contraction of short-lived effector cells in JEV infection and persistence of high levels of short-lived effector cells in WNV infection. |
| 1059 | 20213311 | Treponema denticola suppresses expression of human beta-defensin-2 in gingival epithelial cells through inhibition of TNFalpha production and TLR2 activation. |
| 1060 | 20213311 | Treponema denticola suppresses expression of human beta-defensin-2 in gingival epithelial cells through inhibition of TNFalpha production and TLR2 activation. |
| 1061 | 20213311 | Treponema denticola suppresses expression of human beta-defensin-2 in gingival epithelial cells through inhibition of TNFalpha production and TLR2 activation. |
| 1062 | 20213311 | Treponema denticola suppresses expression of human beta-defensin-2 in gingival epithelial cells through inhibition of TNFalpha production and TLR2 activation. |
| 1063 | 20213311 | Treponema denticola suppresses expression of human beta-defensin-2 in gingival epithelial cells through inhibition of TNFalpha production and TLR2 activation. |
| 1064 | 20213311 | We previously reported that Treponema denticola, a periodontal pathogen, suppressed the expression of human beta-defensins (HBDs) and IL-8 in human gingival epithelial cells. |
| 1065 | 20213311 | We previously reported that Treponema denticola, a periodontal pathogen, suppressed the expression of human beta-defensins (HBDs) and IL-8 in human gingival epithelial cells. |
| 1066 | 20213311 | We previously reported that Treponema denticola, a periodontal pathogen, suppressed the expression of human beta-defensins (HBDs) and IL-8 in human gingival epithelial cells. |
| 1067 | 20213311 | We previously reported that Treponema denticola, a periodontal pathogen, suppressed the expression of human beta-defensins (HBDs) and IL-8 in human gingival epithelial cells. |
| 1068 | 20213311 | We previously reported that Treponema denticola, a periodontal pathogen, suppressed the expression of human beta-defensins (HBDs) and IL-8 in human gingival epithelial cells. |
| 1069 | 20213311 | Time courses of suppression revealed that T. denticola suppressed HBD-2 expression only at late time points, which was accompanied with the suppression of TNFalpha production. |
| 1070 | 20213311 | Time courses of suppression revealed that T. denticola suppressed HBD-2 expression only at late time points, which was accompanied with the suppression of TNFalpha production. |
| 1071 | 20213311 | Time courses of suppression revealed that T. denticola suppressed HBD-2 expression only at late time points, which was accompanied with the suppression of TNFalpha production. |
| 1072 | 20213311 | Time courses of suppression revealed that T. denticola suppressed HBD-2 expression only at late time points, which was accompanied with the suppression of TNFalpha production. |
| 1073 | 20213311 | Time courses of suppression revealed that T. denticola suppressed HBD-2 expression only at late time points, which was accompanied with the suppression of TNFalpha production. |
| 1074 | 20213311 | Neutralization of TNFalpha with an antibody abrogated the suppressive effect of T. denticola on HBD-2. |
| 1075 | 20213311 | Neutralization of TNFalpha with an antibody abrogated the suppressive effect of T. denticola on HBD-2. |
| 1076 | 20213311 | Neutralization of TNFalpha with an antibody abrogated the suppressive effect of T. denticola on HBD-2. |
| 1077 | 20213311 | Neutralization of TNFalpha with an antibody abrogated the suppressive effect of T. denticola on HBD-2. |
| 1078 | 20213311 | Neutralization of TNFalpha with an antibody abrogated the suppressive effect of T. denticola on HBD-2. |
| 1079 | 20213311 | Knock-down of toll-like receptor (TLR) 2 via RNA interference reversed the suppressive effect of T. denticola on the expression of HBD-3, but not on the production of TNFalpha. |
| 1080 | 20213311 | Knock-down of toll-like receptor (TLR) 2 via RNA interference reversed the suppressive effect of T. denticola on the expression of HBD-3, but not on the production of TNFalpha. |
| 1081 | 20213311 | Knock-down of toll-like receptor (TLR) 2 via RNA interference reversed the suppressive effect of T. denticola on the expression of HBD-3, but not on the production of TNFalpha. |
| 1082 | 20213311 | Knock-down of toll-like receptor (TLR) 2 via RNA interference reversed the suppressive effect of T. denticola on the expression of HBD-3, but not on the production of TNFalpha. |
| 1083 | 20213311 | Knock-down of toll-like receptor (TLR) 2 via RNA interference reversed the suppressive effect of T. denticola on the expression of HBD-3, but not on the production of TNFalpha. |
| 1084 | 20213311 | Collectively, T. denticola suppresses the expression of HBD-2 in gingival epithelial cells by inhibiting the TLR2 axis and TNFalpha production, which may contribute to the pathogenesis of periodontitis by T. denticola. |
| 1085 | 20213311 | Collectively, T. denticola suppresses the expression of HBD-2 in gingival epithelial cells by inhibiting the TLR2 axis and TNFalpha production, which may contribute to the pathogenesis of periodontitis by T. denticola. |
| 1086 | 20213311 | Collectively, T. denticola suppresses the expression of HBD-2 in gingival epithelial cells by inhibiting the TLR2 axis and TNFalpha production, which may contribute to the pathogenesis of periodontitis by T. denticola. |
| 1087 | 20213311 | Collectively, T. denticola suppresses the expression of HBD-2 in gingival epithelial cells by inhibiting the TLR2 axis and TNFalpha production, which may contribute to the pathogenesis of periodontitis by T. denticola. |
| 1088 | 20213311 | Collectively, T. denticola suppresses the expression of HBD-2 in gingival epithelial cells by inhibiting the TLR2 axis and TNFalpha production, which may contribute to the pathogenesis of periodontitis by T. denticola. |
| 1089 | 20207993 | By contrast, the Peyer's patch (PP) was the dominant IgA CSR site in both CD40(-/-) and wild type (WT) mice, and they both hosted similar levels of mRNA expression for B cell activating factor of the TNF family, a proliferation inducing ligand, and inducible NO synthase, potential switch-factors for IgA. |
| 1090 | 20207993 | These findings reconcile that IgA CSR can occur in PP in the absence of GC with the fact that CD40(-/-) mice host near normal levels of IgA plasma cells in the LP. |
| 1091 | 20200188 | The objective of this study was to investigate the effects of glucose-based peritoneal dialysis (PD) fluids and icodextrin-based PD fluids on the expression of Toll-like receptor 2 (TLR2)/TLR4 and subsequent ligand-induced mitogen-activated protein kinase (MAPK) and NF-kappaB signaling and tumor necrosis factor alpha (TNF-alpha) and interleukin-1beta (IL-1beta) mRNA expression in human peritoneal mesothelial cells (HPMCs). |
| 1092 | 20200188 | The objective of this study was to investigate the effects of glucose-based peritoneal dialysis (PD) fluids and icodextrin-based PD fluids on the expression of Toll-like receptor 2 (TLR2)/TLR4 and subsequent ligand-induced mitogen-activated protein kinase (MAPK) and NF-kappaB signaling and tumor necrosis factor alpha (TNF-alpha) and interleukin-1beta (IL-1beta) mRNA expression in human peritoneal mesothelial cells (HPMCs). |
| 1093 | 20200188 | The objective of this study was to investigate the effects of glucose-based peritoneal dialysis (PD) fluids and icodextrin-based PD fluids on the expression of Toll-like receptor 2 (TLR2)/TLR4 and subsequent ligand-induced mitogen-activated protein kinase (MAPK) and NF-kappaB signaling and tumor necrosis factor alpha (TNF-alpha) and interleukin-1beta (IL-1beta) mRNA expression in human peritoneal mesothelial cells (HPMCs). |
| 1094 | 20200188 | The objective of this study was to investigate the effects of glucose-based peritoneal dialysis (PD) fluids and icodextrin-based PD fluids on the expression of Toll-like receptor 2 (TLR2)/TLR4 and subsequent ligand-induced mitogen-activated protein kinase (MAPK) and NF-kappaB signaling and tumor necrosis factor alpha (TNF-alpha) and interleukin-1beta (IL-1beta) mRNA expression in human peritoneal mesothelial cells (HPMCs). |
| 1095 | 20200188 | TLR2/TLR4 expression was determined by real-time PCR, Western blotting, and an immunofluorescence assay. |
| 1096 | 20200188 | TLR2/TLR4 expression was determined by real-time PCR, Western blotting, and an immunofluorescence assay. |
| 1097 | 20200188 | TLR2/TLR4 expression was determined by real-time PCR, Western blotting, and an immunofluorescence assay. |
| 1098 | 20200188 | TLR2/TLR4 expression was determined by real-time PCR, Western blotting, and an immunofluorescence assay. |
| 1099 | 20200188 | In addition, cells were pretreated with different PD solutions and then incubated with Pam3CSK4 or lipopolysaccharide (LPS), and the degrees of MAPK and NF-kappaB activation were reflected by detecting the phosphorylation levels of extracellular signal-regulated kinase 1/2 (ERK1/2), c-Jun N-terminal kinase (JNK), p38, and p65, using a Western blot method. |
| 1100 | 20200188 | In addition, cells were pretreated with different PD solutions and then incubated with Pam3CSK4 or lipopolysaccharide (LPS), and the degrees of MAPK and NF-kappaB activation were reflected by detecting the phosphorylation levels of extracellular signal-regulated kinase 1/2 (ERK1/2), c-Jun N-terminal kinase (JNK), p38, and p65, using a Western blot method. |
| 1101 | 20200188 | In addition, cells were pretreated with different PD solutions and then incubated with Pam3CSK4 or lipopolysaccharide (LPS), and the degrees of MAPK and NF-kappaB activation were reflected by detecting the phosphorylation levels of extracellular signal-regulated kinase 1/2 (ERK1/2), c-Jun N-terminal kinase (JNK), p38, and p65, using a Western blot method. |
| 1102 | 20200188 | In addition, cells were pretreated with different PD solutions and then incubated with Pam3CSK4 or lipopolysaccharide (LPS), and the degrees of MAPK and NF-kappaB activation were reflected by detecting the phosphorylation levels of extracellular signal-regulated kinase 1/2 (ERK1/2), c-Jun N-terminal kinase (JNK), p38, and p65, using a Western blot method. |
| 1103 | 20200188 | TNF-alpha and IL-1beta mRNA expression was measured by real-time PCR. |
| 1104 | 20200188 | TNF-alpha and IL-1beta mRNA expression was measured by real-time PCR. |
| 1105 | 20200188 | TNF-alpha and IL-1beta mRNA expression was measured by real-time PCR. |
| 1106 | 20200188 | TNF-alpha and IL-1beta mRNA expression was measured by real-time PCR. |
| 1107 | 20200188 | Glucose-based peritoneal dialysis fluids suppressed the expression of TLR2 and TLR4 proteins in HPMCs. |
| 1108 | 20200188 | Glucose-based peritoneal dialysis fluids suppressed the expression of TLR2 and TLR4 proteins in HPMCs. |
| 1109 | 20200188 | Glucose-based peritoneal dialysis fluids suppressed the expression of TLR2 and TLR4 proteins in HPMCs. |
| 1110 | 20200188 | Glucose-based peritoneal dialysis fluids suppressed the expression of TLR2 and TLR4 proteins in HPMCs. |
| 1111 | 20200188 | Challenge of cells with either Pam3CSK4 or LPS resulted in impaired TNF-alpha and IL-1beta production. |
| 1112 | 20200188 | Challenge of cells with either Pam3CSK4 or LPS resulted in impaired TNF-alpha and IL-1beta production. |
| 1113 | 20200188 | Challenge of cells with either Pam3CSK4 or LPS resulted in impaired TNF-alpha and IL-1beta production. |
| 1114 | 20200188 | Challenge of cells with either Pam3CSK4 or LPS resulted in impaired TNF-alpha and IL-1beta production. |
| 1115 | 20200188 | Moreover, reduced TLR2 and TLR4 levels in glucose-based peritoneal dialysis solution-treated mesothelial cells were accompanied by reduced p42/44 (ERK1/2), JNK, p38 MAPK, and NF-kappaB p65 phosphorylation upon TLR ligand engagement. |
| 1116 | 20200188 | Moreover, reduced TLR2 and TLR4 levels in glucose-based peritoneal dialysis solution-treated mesothelial cells were accompanied by reduced p42/44 (ERK1/2), JNK, p38 MAPK, and NF-kappaB p65 phosphorylation upon TLR ligand engagement. |
| 1117 | 20200188 | Moreover, reduced TLR2 and TLR4 levels in glucose-based peritoneal dialysis solution-treated mesothelial cells were accompanied by reduced p42/44 (ERK1/2), JNK, p38 MAPK, and NF-kappaB p65 phosphorylation upon TLR ligand engagement. |
| 1118 | 20200188 | Moreover, reduced TLR2 and TLR4 levels in glucose-based peritoneal dialysis solution-treated mesothelial cells were accompanied by reduced p42/44 (ERK1/2), JNK, p38 MAPK, and NF-kappaB p65 phosphorylation upon TLR ligand engagement. |
| 1119 | 20200188 | No significant changes in MAPK and NF-kappaB signaling and TNF-alpha and IL-1beta mRNA expression were observed in icodextrin-based PD solution-treated mesothelial cells. |
| 1120 | 20200188 | No significant changes in MAPK and NF-kappaB signaling and TNF-alpha and IL-1beta mRNA expression were observed in icodextrin-based PD solution-treated mesothelial cells. |
| 1121 | 20200188 | No significant changes in MAPK and NF-kappaB signaling and TNF-alpha and IL-1beta mRNA expression were observed in icodextrin-based PD solution-treated mesothelial cells. |
| 1122 | 20200188 | No significant changes in MAPK and NF-kappaB signaling and TNF-alpha and IL-1beta mRNA expression were observed in icodextrin-based PD solution-treated mesothelial cells. |
| 1123 | 20200188 | Glucose-based PD solution, but not icodextrin-based PD solution, downregulates expression of TLR2/TLR4 by human peritoneal mesothelial cells and triggers hyporesponsiveness to pathogen-associated molecular patterns. |
| 1124 | 20200188 | Glucose-based PD solution, but not icodextrin-based PD solution, downregulates expression of TLR2/TLR4 by human peritoneal mesothelial cells and triggers hyporesponsiveness to pathogen-associated molecular patterns. |
| 1125 | 20200188 | Glucose-based PD solution, but not icodextrin-based PD solution, downregulates expression of TLR2/TLR4 by human peritoneal mesothelial cells and triggers hyporesponsiveness to pathogen-associated molecular patterns. |
| 1126 | 20200188 | Glucose-based PD solution, but not icodextrin-based PD solution, downregulates expression of TLR2/TLR4 by human peritoneal mesothelial cells and triggers hyporesponsiveness to pathogen-associated molecular patterns. |
| 1127 | 20194720 | B cells are required for optimal CD4+ and CD8+ T cell tumor immunity: therapeutic B cell depletion enhances B16 melanoma growth in mice. |
| 1128 | 20194720 | Effector-memory and IFN-gamma-or TNF-alpha-secreting CD4(+) and CD8(+) T cell induction was significantly impaired in B cell-depleted mice with tumors. |
| 1129 | 20181442 | The highly elevated expression of the pro-inflammatory cytokine tumour necrosis factor-alpha (TNFalpha) and low-level expression of interferon-gamma (IFNgamma) that are detected in C. abortus-infected placentas have been implicated in the pathogenesis of OEA. |
| 1130 | 20181442 | The highly elevated expression of the pro-inflammatory cytokine tumour necrosis factor-alpha (TNFalpha) and low-level expression of interferon-gamma (IFNgamma) that are detected in C. abortus-infected placentas have been implicated in the pathogenesis of OEA. |
| 1131 | 20181442 | The highly elevated expression of the pro-inflammatory cytokine tumour necrosis factor-alpha (TNFalpha) and low-level expression of interferon-gamma (IFNgamma) that are detected in C. abortus-infected placentas have been implicated in the pathogenesis of OEA. |
| 1132 | 20181442 | The highly elevated expression of the pro-inflammatory cytokine tumour necrosis factor-alpha (TNFalpha) and low-level expression of interferon-gamma (IFNgamma) that are detected in C. abortus-infected placentas have been implicated in the pathogenesis of OEA. |
| 1133 | 20181442 | Since mouse studies have contributed significantly to our understanding of the immunological responses to chlamydial infections and serve as a good model for rapidly assessing candidate vaccines for OEA, we investigated local expression of TNFalpha and IFNgamma in infected mice. |
| 1134 | 20181442 | Since mouse studies have contributed significantly to our understanding of the immunological responses to chlamydial infections and serve as a good model for rapidly assessing candidate vaccines for OEA, we investigated local expression of TNFalpha and IFNgamma in infected mice. |
| 1135 | 20181442 | Since mouse studies have contributed significantly to our understanding of the immunological responses to chlamydial infections and serve as a good model for rapidly assessing candidate vaccines for OEA, we investigated local expression of TNFalpha and IFNgamma in infected mice. |
| 1136 | 20181442 | Since mouse studies have contributed significantly to our understanding of the immunological responses to chlamydial infections and serve as a good model for rapidly assessing candidate vaccines for OEA, we investigated local expression of TNFalpha and IFNgamma in infected mice. |
| 1137 | 20181442 | Immunostaining for C. abortus was significantly greater in placenta compared to liver (P<0.001), whereas local IFNgamma expression was lower and TNFalpha expression was absent in the placenta compared with the liver across all time points. |
| 1138 | 20181442 | Immunostaining for C. abortus was significantly greater in placenta compared to liver (P<0.001), whereas local IFNgamma expression was lower and TNFalpha expression was absent in the placenta compared with the liver across all time points. |
| 1139 | 20181442 | Immunostaining for C. abortus was significantly greater in placenta compared to liver (P<0.001), whereas local IFNgamma expression was lower and TNFalpha expression was absent in the placenta compared with the liver across all time points. |
| 1140 | 20181442 | Immunostaining for C. abortus was significantly greater in placenta compared to liver (P<0.001), whereas local IFNgamma expression was lower and TNFalpha expression was absent in the placenta compared with the liver across all time points. |
| 1141 | 20181442 | Serum concentrations of both IFNgamma and TNFalpha increased throughout pregnancy in infected mice. |
| 1142 | 20181442 | Serum concentrations of both IFNgamma and TNFalpha increased throughout pregnancy in infected mice. |
| 1143 | 20181442 | Serum concentrations of both IFNgamma and TNFalpha increased throughout pregnancy in infected mice. |
| 1144 | 20181442 | Serum concentrations of both IFNgamma and TNFalpha increased throughout pregnancy in infected mice. |
| 1145 | 20174562 | Tetramer analysis further showed that up to 16.8% of all circulating CD3(+)CD8(+) T cells were specific for the single HLA-B*3501-restricted epitope Gn(465-473) years after the acute infection. |
| 1146 | 20174562 | Remarkably, Gn(465-473)-specific cells readily secreted IFN-gamma, granzyme B and TNF-alpha but not IL-2 upon stimulation and showed a 'revertant' CD45RA(+)CD27(-)CD28(-)CCR7(-)CD127(-) effector memory phenotype, thereby resembling a phenotype seen in other latent virus infections. |
| 1147 | 20172447 | The results showed that both HIFU-ablated tumour and tumour lysate could significantly increase the number of mature DCs and the secretion of IL-12 and IFN-gamma (p<0.001). |
| 1148 | 20172447 | Cytotoxocity and TNF-alpha and IFN-gamma secretion of cytotoxic T lymphocytes against H22 cells were significantly higher in HIFU-ablated tumour group than that in tumour lysate group (p<0.01). |
| 1149 | 20160101 | PD-1 and CTLA-4 combination blockade expands infiltrating T cells and reduces regulatory T and myeloid cells within B16 melanoma tumors. |
| 1150 | 20160101 | Vaccination with irradiated B16 melanoma cells expressing either GM-CSF (Gvax) or Flt3-ligand (Fvax) combined with antibody blockade of the negative T-cell costimulatory receptor cytotoxic T-lymphocyte antigen-4 (CTLA-4) promotes rejection of preimplanted tumors. |
| 1151 | 20160101 | Despite CTLA-4 blockade, T-cell proliferation and cytokine production can be inhibited by the interaction of programmed death-1 (PD-1) with its ligands PD-L1 and PD-L2 or by the interaction of PD-L1 with B7-1. |
| 1152 | 20160101 | Here, we show that the combination of CTLA-4 and PD-1 blockade is more than twice as effective as either alone in promoting the rejection of B16 melanomas in conjunction with Fvax. |
| 1153 | 20160101 | Combination PD-1 and CTLA-4 blockade increases effector T-cell (Teff) infiltration, resulting in highly advantageous Teff-to-regulatory T-cell ratios with the tumor. |
| 1154 | 20160101 | The fraction of tumor-infiltrating Teffs expressing CTLA-4 and PD-1 increases, reflecting the proliferation and accumulation of cells that would otherwise be anergized. |
| 1155 | 20160101 | IFN-gamma production increases in both the tumor and vaccine draining lymph nodes, as does the frequency of IFN-gamma/TNF-alpha double-producing CD8(+) T cells within the tumor. |
| 1156 | 20160101 | These results suggest that combination blockade of the PD-1/PD-L1- and CTLA-4-negative costimulatory pathways allows tumor-specific T cells that would otherwise be inactivated to continue to expand and carry out effector functions, thereby shifting the tumor microenvironment from suppressive to inflammatory. |
| 1157 | 20159051 | Four weeks later, the ConA-, LPS-, and OVA-induced splenocyte proliferation, OVA-specific antibodies levels (IgG, IgG1, and IgG2a) in serum, IL-2, and TNF-alpha were significantly enhanced by PCS at a high dose compared to that induced by Quil A. |
| 1158 | 20156531 | Among the combinations of several immune-modulating factors with known effects on DC maturation, we found that stepwise DC maturation with cytokine cocktail (TNF-alpha+IL-6+IL-1 beta+PGE(2)) followed by poly(I:C) stimulation enhanced the production of IL-12 with strong allostimulatory capacity. |
| 1159 | 20156531 | While there were no significant differences between DC matured by simultaneous or sequential activation by cytokine cocktail and poly(I:C) in expression of markers and costimulatory molecules of mature DCs, the delivery of inflammatory signal prior to poly(I:C) results in sustained interleukin-12 expression with reduced IL-10 than DC matured by simultaneous stimulation. |
| 1160 | 20156531 | This sequential stimulation significantly increased migratory capacity in response to CCL21 and CXCL12 compared to DC matured with cytokine cocktail. |
| 1161 | 20156531 | Furthermore, these DCs retained their responsiveness to CD40L stimulation in secondary IL-12 production and efficiently generated autologous antigen-specific effector T cells as evidenced by ELISPOT assay. |
| 1162 | 20149524 | Members of the TNF ligand superfamily and the TNFR superfamily contribute to this costimulatory molecule signaling. |
| 1163 | 20149524 | Infection of DCs with Ad-tPSMA-IRES-m4-1BBL induced tPSMA-specific proliferative responses and up-regulated CD80 and CD86 s signaling molecules. |
| 1164 | 20145551 | We observed that BMDC, matured with a cytokine cocktail (tumor necrosis factor-alpha, interleukin-beta, interleukin-6, prostaglandin E2), strongly expressed CCR7. |
| 1165 | 20139272 | Therapeutic glucocorticoid-induced TNF receptor-mediated amplification of CD4+ T cell responses enhances antiparasitic immunity. |
| 1166 | 20139272 | Therapeutic glucocorticoid-induced TNF receptor-mediated amplification of CD4+ T cell responses enhances antiparasitic immunity. |
| 1167 | 20139272 | This required CD4(+) T cells, TNF, and IFN-gamma, but crucially, was independent of regulatory T (Treg) cells. |
| 1168 | 20139272 | This required CD4(+) T cells, TNF, and IFN-gamma, but crucially, was independent of regulatory T (Treg) cells. |
| 1169 | 20132994 | Diminished CD4+/CD25+ T cell and increased IFN-gamma levels occur in dogs vaccinated with Leishmune in an endemic area for visceral leishmaniasis. |
| 1170 | 20132994 | Cytokines IFN-gamma, IL-4 and TNF-alpha were measured in culture supernatant and CD4+/CD25+ and CD8+/CD25+ T cell presence was determined. |
| 1171 | 20132994 | Analysis of the data indicated that the vaccine conferred humoral responses (100%) against both antigens and cellular immunity to FML (85%) and total antigen (80%), the supernatant of cultured cells stimulated with TAg and FML showed an increase in IFN-gamma (P<0.05), and the vaccine reduced CD4+/CD25+ T cell presence compared to that observed before vaccination. |
| 1172 | 20130130 | Peripheral blood mononuclear cells (PBMCs) from healthy donor women were stimulated in vitro with HPV-16 VLPs (2.5 microg/ml) in the presence of E2 and P4 administered either alone or in combination; and lymphoproliferation, cytokine production, transcription factor expression, and steroid hormone receptor expression were analyzed. |
| 1173 | 20130130 | Peripheral blood mononuclear cells (PBMCs) from healthy donor women were stimulated in vitro with HPV-16 VLPs (2.5 microg/ml) in the presence of E2 and P4 administered either alone or in combination; and lymphoproliferation, cytokine production, transcription factor expression, and steroid hormone receptor expression were analyzed. |
| 1174 | 20130130 | HPV-16 VLPs significantly increased the levels of lymphoproliferation, proinflammatory cytokine (gamma interferon [IFN-gamma], interleukin-1beta [IL-1beta], IL-2, IL-6, IL-8, IL-12p70, IL-17, tumor necrosis factor alpha [TNF-alpha]) production, anti-inflammatory cytokine (IL-1ra, IL-10) production, and the expression of Eralpha and Erbeta but decreased the levels of Foxp3 expression and production of transforming growth factor beta (TGF-beta). |
| 1175 | 20130130 | HPV-16 VLPs significantly increased the levels of lymphoproliferation, proinflammatory cytokine (gamma interferon [IFN-gamma], interleukin-1beta [IL-1beta], IL-2, IL-6, IL-8, IL-12p70, IL-17, tumor necrosis factor alpha [TNF-alpha]) production, anti-inflammatory cytokine (IL-1ra, IL-10) production, and the expression of Eralpha and Erbeta but decreased the levels of Foxp3 expression and production of transforming growth factor beta (TGF-beta). |
| 1176 | 20130130 | Exposure of PBMCs to E2 and P4 either alone or in combination significantly decreased the levels of lymphoproliferation and production of proinflammatory cytokines (IFN-gamma, IL-12p70, TNF-alpha) but increased the levels of production of IL-10 and TGF-beta and the expression of Foxp3 in response to HPV-16 VLPs. |
| 1177 | 20130130 | Exposure of PBMCs to E2 and P4 either alone or in combination significantly decreased the levels of lymphoproliferation and production of proinflammatory cytokines (IFN-gamma, IL-12p70, TNF-alpha) but increased the levels of production of IL-10 and TGF-beta and the expression of Foxp3 in response to HPV-16 VLPs. |
| 1178 | 20124603 | These DNA were evaluated for their ability to stimulate IL-12, TNF-alpha, IL-10, IFN-gamma and ROS production from spleenocytes as well as NO production from peritoneal macrophages. |
| 1179 | 20124603 | These DNA were evaluated for their ability to stimulate IL-12, TNF-alpha, IL-10, IFN-gamma and ROS production from spleenocytes as well as NO production from peritoneal macrophages. |
| 1180 | 20124603 | It was observed that TNF-alpha was induced in days 1,3,5 by all Brucella strains DNAs and E. coli DNA, IL-10 only was induced in day 1, IFN- gamma was induced only in day 5 and IL-12 not induced. |
| 1181 | 20124603 | It was observed that TNF-alpha was induced in days 1,3,5 by all Brucella strains DNAs and E. coli DNA, IL-10 only was induced in day 1, IFN- gamma was induced only in day 5 and IL-12 not induced. |
| 1182 | 20121698 | The following firm conclusions can be drawn: multiple TLRs activate innate immunity upon RSV infection; TLR4 can influence TLR2 expression, suggesting that optimal induction of multiple signaling pathways is required to elicit protective, rather than deleterious innate immune responses following infection; in mice, TLR4, TLR2/-6, and TLR7 have immune-stimulating properties, while TLR3 activation occurs later and appears to downregulate immune responses; in humans, polymorphism studies have demonstrated an important role for TLR4-signaling; and activation of TLR-signaling leads to antiviral cytokine production, such as TNF-a and IFNs. |
| 1183 | 20121696 | Two families of receptors, the CD28 family and the tumor necrosis factor receptor (TNFR) family, have been found to be major players in providing costimulation to CD8+ T cells. |
| 1184 | 20121696 | Programmed death-1 (PD-1), another member of the CD28 family, may contribute to functional defects of helpless memory CD8+ T cells. |
| 1185 | 20121696 | Members of the TNFR family, such as CD27, 4-1BB, CD40, TRAIL (tumor necrosis factor-related apoptosis-inducing ligand), and OX40, have also been implicated in the survival, generation, maintenance, and quality of virus-specific memory CD8+T cells. |
| 1186 | 20121696 | The delivery of costimulatory molecules such as CD28, 4-1BB, and OX40 can help boost the generation and function of virus-specific memory CD8+ T cells. |
| 1187 | 20117947 | The results showed a robust rubella-specific inflammatory cytokine response characterized by high median [inter-quartile range (IQR)] secretion levels (in pg/mL) of IL-6 [3681.0 (3160.0, 4052.0)], GM-CSF [28.0 (23.6, 32.6)], and TNF-alpha [29.7 (-7.0, 89.2)]. |
| 1188 | 20117947 | We also detected modest levels of rubella-specific secretion of Th1 cytokines IL-2 and IFN-gamma, while IL-12p40 was undetectable. |
| 1189 | 20117947 | Age at vaccination, enrollment, and time elapsed between last vaccination and enrollment was significantly associated with the outcome of IL-2, IL-6, and IFN-gamma secretion. |
| 1190 | 20100933 | We used multicolor flow cytometry and intracellular cytokine staining of myeloid DCs (mDCs) and plasmacytoid DCs (pDCs) and found substantial decreases in older compared with young individuals in TNF-alpha, IL-6, and/or IL-12 (p40) production in mDCs and in TNF-alpha and IFN-alpha production in pDCs in response to TLR1/2, TLR2/6, TLR3, TLR5, and TLR8 engagement in mDCs and TLR7 and TLR9 in pDCs. |
| 1191 | 20099887 | Likewise, siRNA-mediated knockdown of LycPrxIV increased the expression of TNF-alpha and CC chemokine, and downregulated the expression of IL-10. |
| 1192 | 20097864 | Multiple immune-effector molecules play a role in antimicrobial immunity mediated by memory CD8 T cells, including IFN-gamma, perforin, TRAIL, Fas ligand, and TNF-alpha. |
| 1193 | 20097864 | Multiple immune-effector molecules play a role in antimicrobial immunity mediated by memory CD8 T cells, including IFN-gamma, perforin, TRAIL, Fas ligand, and TNF-alpha. |
| 1194 | 20097864 | Multiple immune-effector molecules play a role in antimicrobial immunity mediated by memory CD8 T cells, including IFN-gamma, perforin, TRAIL, Fas ligand, and TNF-alpha. |
| 1195 | 20097864 | Our studies reveal that endogenous memory CD8 T cell-mediated protection against both parasite species is, in part, dependent on IFN-gamma, whereas perforin was only critical in protection against P. yoelii. |
| 1196 | 20097864 | Our studies reveal that endogenous memory CD8 T cell-mediated protection against both parasite species is, in part, dependent on IFN-gamma, whereas perforin was only critical in protection against P. yoelii. |
| 1197 | 20097864 | Our studies reveal that endogenous memory CD8 T cell-mediated protection against both parasite species is, in part, dependent on IFN-gamma, whereas perforin was only critical in protection against P. yoelii. |
| 1198 | 20097864 | We further show that neutralization of TNF-alpha in immunized mice markedly reduces memory CD8 T cell-mediated protection against both parasite species. |
| 1199 | 20097864 | We further show that neutralization of TNF-alpha in immunized mice markedly reduces memory CD8 T cell-mediated protection against both parasite species. |
| 1200 | 20097864 | We further show that neutralization of TNF-alpha in immunized mice markedly reduces memory CD8 T cell-mediated protection against both parasite species. |
| 1201 | 20097864 | Thus, our studies identify IFN-gamma and TNF-alpha as important components of the noncytolytic pathways that underlie memory CD8 T cell-mediated immunity against liver stage Plasmodium infection. |
| 1202 | 20097864 | Thus, our studies identify IFN-gamma and TNF-alpha as important components of the noncytolytic pathways that underlie memory CD8 T cell-mediated immunity against liver stage Plasmodium infection. |
| 1203 | 20097864 | Thus, our studies identify IFN-gamma and TNF-alpha as important components of the noncytolytic pathways that underlie memory CD8 T cell-mediated immunity against liver stage Plasmodium infection. |
| 1204 | 20097110 | Interferon (IFN)-α, interleukin (IL)-6, IL-1 and tumour necrosis factor (TNF)-α peaked in BALF 24-30h PI, when virus titres and the severity of clinical signs were maximal. |
| 1205 | 20097110 | Whereas IFN-γ and IL-12, but not IL-18, increased in tandem in BALF, serum cytokine concentrations were either undetectable or were up to 100-fold lower. |
| 1206 | 20097110 | The APP C-reactive protein (CRP) and haptoglobin peaked 24h later than the cytokines and reached higher levels in serum than in BALF. |
| 1207 | 20097110 | Lung virus titres tightly correlated with BALF IFN-α, IL-6, IL-1, TNF-α, IFN-γ and IL-12, as well as with serum IL-6, IFN-α and IFN-γ. |
| 1208 | 20097110 | Signs of disease correlated with the same cytokines in BALF and serum, as well as with BALF LBP and serum CRP. |
| 1209 | 20092022 | A virosomal formulated Her-2/neu multi-peptide vaccine induces Her-2/neu-specific immune responses in patients with metastatic breast cancer: a phase I study. |
| 1210 | 20092022 | We have previously shown in mice that vaccination with three Her-2-peptides representing B-cell epitopes of the extracellular domain of Her-2/neu induces Her-2/neu-specific IgG antibodies with strong anti-tumor activity in vitro and in vivo. |
| 1211 | 20092022 | Cellular immune responses, as measured by in vitro production of IL-2, IFN-c, and TNF-a of PBMCs showed a marked increase after vaccination in the majority of vaccinees. |
| 1212 | 20092022 | Notably, the number of CD4+CD25+Foxp3+T regulatory cells, which were significantly increased compared to healthy controls prior to vaccination, was markedly reduced following vaccination. |
| 1213 | 20087927 | There was a synergistic increase in cytokine production (TNF-alpha, IL-6, IL-10, and IFN-beta) in BM-DCs, together with an increase in the expression of co-stimulatory molecules (CD86 and CD40) in response to co-treatment with poly(I:C) and zymosan. |
| 1214 | 20087927 | The results of the current study suggest that one of the mechanisms by which zymosan enhances the adjuvant activity of poly(I:C) is through increased cytokine production by DCs involving the synergistic activation of poly(I:C)-induced TLR3- and zymosan-induced TLR2-mediated signaling pathways. |
| 1215 | 20074669 | Most interestingly, CEL-2000 therapy modulated serum cytokine levels with an increase in IL-12p70 and IL-10, which are not seen with etanercept therapy, and reduced IL-17 and TNF-alpha, also seen with etanercept, among other cytokines studied. |
| 1216 | 20072623 | After in vitro stimulation, spleen cells of immunized mice produce high levels of Th1 cytokines and show a prominent mRNA expression of the Th1 transcription factor T-bet, in detriment of the Th2 transcription factor GATA-3. |
| 1217 | 20072623 | Following R. equi challenge, a high H2O2, NO, IL-12, and IFN-gamma content is detected in the organs of immunized mice. |
| 1218 | 20072623 | On the other hand, TNF-alpha and IL-4 levels are markedly lower in the organs of vaccinated mice, compared with the non-vaccinated ones. |
| 1219 | 20072623 | A greater incidence of CD4+ and CD8+ T cells and B lymphocytes is verified in vaccinated mice. |
| 1220 | 20072623 | However, there is no difference between vaccinated and non-vaccinated mice in terms of the frequency of CD4+CD25+Foxp3+ T cells. |
| 1221 | 20056331 | Changes in the levels of rabbit interleukin (IL)-2, IL-4, IL-6, IL-10, tumor necrosis factor-alpha (TNFalpha), and interferon-gamma (IFNgamma) mRNA were determined. |
| 1222 | 20056331 | Changes in the levels of rabbit interleukin (IL)-2, IL-4, IL-6, IL-10, tumor necrosis factor-alpha (TNFalpha), and interferon-gamma (IFNgamma) mRNA were determined. |
| 1223 | 20056331 | All cytokine mRNAs were found at detectable levels; however, the levels of IFNgamma, TNFalpha, IL-2 and IL-10 were significantly higher in the vaccinated group compared to the non-vaccinated group. |
| 1224 | 20056331 | All cytokine mRNAs were found at detectable levels; however, the levels of IFNgamma, TNFalpha, IL-2 and IL-10 were significantly higher in the vaccinated group compared to the non-vaccinated group. |
| 1225 | 20054688 | We reported that murine tumor lysate-pulsed dendritic cells (TP-DC) could elicit tumor-specific CD4(+) and CD8(+) T cells in vitro and in vivo. |
| 1226 | 20054688 | TP-DC remained viable after anti-MARCO antibody treatment; had little, if any, change in production of IL-10, IL-12p70 and TNF-alpha; but demonstrated enhanced migratory capacity in a microchemotaxis assay. |
| 1227 | 20054688 | The use of a selective inhibitor showed MARCO expression to be linked to the p38 mitogen-activated protein kinase (MAPK) pathway. |
| 1228 | 20031926 | The tumor necrosis factor-alpha response for most of the fractions did not significantly differ in the tested groups, and the interleukin-4 response was below the detectable range for all fractions and both study groups. |
| 1229 | 20022123 | This FcgammaR ligation induced a significantly enhanced expression of Major Histocompatibility complex (MHCII) class II and the costimulatory molecules CD80/86 and CD40 by MoDC compared with immature MoDC. |
| 1230 | 20022123 | The F4-IC induced DC maturation correlated with significant higher expression levels of several pro-inflammatory cytokines such as interleukine (IL) 1beta, IL-6 and Tumor necrosis factor alpha, the chemokine IL-8 and IL-12p40 in comparison with immature MoDC. |
| 1231 | 20017188 | Multiple CD4+ T-cell subsets, based on expression of IFN-gamma, TNF-alpha, IL-2, IL-17 and GM-CSF, were induced. |
| 1232 | 20017188 | Multiple CD4+ T-cell subsets, based on expression of IFN-gamma, TNF-alpha, IL-2, IL-17 and GM-CSF, were induced. |
| 1233 | 20017188 | Polyfunctional CD4+ T cells co-expressing IFN-gamma, TNF-alpha and IL-2 dominated the response in both age groups. |
| 1234 | 20017188 | Polyfunctional CD4+ T cells co-expressing IFN-gamma, TNF-alpha and IL-2 dominated the response in both age groups. |
| 1235 | 20017188 | A novel CD4+ cell subset co-expressing these three Th1 cytokines and IL-17 was induced in adolescents, while a novel CD4+ T-cell subset co-expressing Th1 cytokines and GM-CSF was induced in children. |
| 1236 | 20017188 | A novel CD4+ cell subset co-expressing these three Th1 cytokines and IL-17 was induced in adolescents, while a novel CD4+ T-cell subset co-expressing Th1 cytokines and GM-CSF was induced in children. |
| 1237 | 20007364 | Association of reduced tumor necrosis factor alpha, gamma interferon, and interleukin-1beta (IL-1beta) but increased IL-10 expression with improved chest radiography in patients with pulmonary tuberculosis. |
| 1238 | 20007364 | Association of reduced tumor necrosis factor alpha, gamma interferon, and interleukin-1beta (IL-1beta) but increased IL-10 expression with improved chest radiography in patients with pulmonary tuberculosis. |
| 1239 | 20007364 | The objective of the present study was to correlate the modulation of cytokine expression (interleukin-1 [IL-1], IL-6, IL-8, IL-10, IL-12, gamma interferon [IFN-gamma], interferon-inducible protein [IP-10], and monocyte chemotactic protein 1 [MCP-1]) with the clinical response to 2 months of intensive therapy. |
| 1240 | 20007364 | The objective of the present study was to correlate the modulation of cytokine expression (interleukin-1 [IL-1], IL-6, IL-8, IL-10, IL-12, gamma interferon [IFN-gamma], interferon-inducible protein [IP-10], and monocyte chemotactic protein 1 [MCP-1]) with the clinical response to 2 months of intensive therapy. |
| 1241 | 20007364 | The levels of expression of TNF-alpha, MCP-1, IFN-gamma, and IL-1beta were decreased; and the level of IL-10 increased in early responders. |
| 1242 | 20007364 | The levels of expression of TNF-alpha, MCP-1, IFN-gamma, and IL-1beta were decreased; and the level of IL-10 increased in early responders. |
| 1243 | 20007364 | After adjustment for age, gender, and the result of sputum culture for M. tuberculosis, significant differences in the levels of MCP-1 and IP-10 expression were observed between the early and the late responders after 2 months of intensive anti-M. tuberculosis therapy. |
| 1244 | 20007364 | After adjustment for age, gender, and the result of sputum culture for M. tuberculosis, significant differences in the levels of MCP-1 and IP-10 expression were observed between the early and the late responders after 2 months of intensive anti-M. tuberculosis therapy. |
| 1245 | 20006311 | ESAT-6 also inhibited T-cell production of IL-17 and TNF-a, but not IL-2. |
| 1246 | 20006311 | ESAT-6 reduced IFN-gamma mRNA levels by inhibiting the expression of the transcription factors, ATF-2, c-Jun and CREB, which upregulate IFN-gamma gene expression in T cells through binding to the IFN-gamma proximal promoter. |
| 1247 | 19967427 | The role of neutrophils and TNF-related apoptosis-inducing ligand (TRAIL) in bacillus Calmette-Guérin (BCG) immunotherapy for urothelial carcinoma of the bladder. |
| 1248 | 19967427 | The role of neutrophils and TNF-related apoptosis-inducing ligand (TRAIL) in bacillus Calmette-Guérin (BCG) immunotherapy for urothelial carcinoma of the bladder. |
| 1249 | 19967427 | Observations regarding the role of neutrophils in BCG immunotherapy have led to exciting discoveries regarding the potential role of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) in creating the therapeutic benefit of BCG immunotherapy. |
| 1250 | 19967427 | Observations regarding the role of neutrophils in BCG immunotherapy have led to exciting discoveries regarding the potential role of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) in creating the therapeutic benefit of BCG immunotherapy. |
| 1251 | 19959244 | Furthermore, the sera from GST-mSEC-immunized cows significantly inhibited interferon-gamma and tumor necrosis factor-alpha production from mouse spleen cells induced by wild-type SEC. |
| 1252 | 19940990 | Real-time PCR analysis revealed that combination therapy led to an increase in IFN-gamma and tumor necrosis factor-alpha mRNA expression; however, levels of Foxp3 and transforming growth factor-beta within the remote tumor tissues were decreased. |
| 1253 | 19933869 | This longitudinal analysis showed the following. 1) Memory CD8(+) T cells appear to pass through an effector phase and then gradually down-regulate expression of activation markers and effector molecules. 2) This effector phase was characterized by down-regulation of CD127, Bcl-2, CCR7, and CD45RA and was followed by a substantial contraction resulting in a pool of memory T cells that re-expressed CD127, Bcl-2, and CD45RA. 3) These memory cells were polyfunctional in terms of degranulation and production of the cytokines IFN-gamma, TNF-alpha, IL-2, and MIP-1beta. 4) The YF-17D-specific memory CD8(+) T cells had a phenotype (CCR7(-)CD45RA(+)) that is typically associated with terminally differentiated cells with limited proliferative capacity (T(EMRA)). |
| 1254 | 19923573 | In this study, WB and PBMC interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-alpha) release assays were used to estimate the endotoxic activities of purified LPS and native outer membrane vesicle (NOMV) vaccines derived from wild-type (hexa-acylated lipid A) and genetically detoxified (penta- and tetra-acylated lipid A) group B Neisseria meningitidis. |
| 1255 | 19923573 | In this study, WB and PBMC interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-alpha) release assays were used to estimate the endotoxic activities of purified LPS and native outer membrane vesicle (NOMV) vaccines derived from wild-type (hexa-acylated lipid A) and genetically detoxified (penta- and tetra-acylated lipid A) group B Neisseria meningitidis. |
| 1256 | 19923573 | The IL-6 and TNF-alpha assays with WB but not the assays with PBMCs distinguished between vaccines containing LPS from penta- and tetra-acylated strains. |
| 1257 | 19923573 | The IL-6 and TNF-alpha assays with WB but not the assays with PBMCs distinguished between vaccines containing LPS from penta- and tetra-acylated strains. |
| 1258 | 19921187 | No differences in the number of CD4(+)CD25(+) T-regulatory cells were measured in the lungs of DC-TNF-treated mice. |
| 1259 | 19921187 | On examination of the infiltrating lymphocytes, an enhanced secretion of IL-10 and a higher percentage of CD4(+)IL -10(+) T cells were measured in the lungs of DC-TNF-treated mice. |
| 1260 | 19921187 | However, treatment with DC-TNF did not enhance the number of melanoma lesions in the lungs of IL-10 knockout mice or in mice depleted of CD4(+) T cells. |
| 1261 | 19921187 | Together, these studies indicate that treatment of melanoma-bearing mice with DC treated with TNF-alpha can induce IL-10 production by resident cells at the tumor site, leading to immune tolerance and exacerbation of disease. |
| 1262 | 19906894 | The patient exhibited a decreased level of expression of Fc-gammaR in monocytes (CD16, CD32, and CD64), along with increased levels of NK T cells (an increased CD3(+) CD16(+/-) CD56(+/-)/CD3(+) ratio), activated T cells (CD4(+) and CD8(+) cells), and B lymphocytes. |
| 1263 | 19906894 | The patient exhibited a decreased level of expression of Fc-gammaR in monocytes (CD16, CD32, and CD64), along with increased levels of NK T cells (an increased CD3(+) CD16(+/-) CD56(+/-)/CD3(+) ratio), activated T cells (CD4(+) and CD8(+) cells), and B lymphocytes. |
| 1264 | 19906894 | Enhanced levels of plasmatic cytokines (interleukin-6 [IL-6], IL-17, IL-4, IL-5, and IL-10) as well as an exacerbated ex vivo intracytoplasmic cytokine pattern, mainly observed within NK cells (gamma interferon positive [IFN-gamma(+)], tumor necrosis factor alpha positive [TNF-alpha(+)], and IL-4 positive [IL-4(+)]), CD8(+) T cells (IL-4(+) and IL-5(+)), and B lymphocytes (TNF-alpha(+), IL-4(+), and IL-10(+)). |
| 1265 | 19906894 | Enhanced levels of plasmatic cytokines (interleukin-6 [IL-6], IL-17, IL-4, IL-5, and IL-10) as well as an exacerbated ex vivo intracytoplasmic cytokine pattern, mainly observed within NK cells (gamma interferon positive [IFN-gamma(+)], tumor necrosis factor alpha positive [TNF-alpha(+)], and IL-4 positive [IL-4(+)]), CD8(+) T cells (IL-4(+) and IL-5(+)), and B lymphocytes (TNF-alpha(+), IL-4(+), and IL-10(+)). |
| 1266 | 19906894 | The analysis of CD4(+) T cells revealed a complex profile that consisted of an increased frequency of IL-12(+) and IFN-gamma(+) cells and a decreased percentage of TNF-alpha(+), IL-4(+), and IL-5(+) cells. |
| 1267 | 19906894 | The analysis of CD4(+) T cells revealed a complex profile that consisted of an increased frequency of IL-12(+) and IFN-gamma(+) cells and a decreased percentage of TNF-alpha(+), IL-4(+), and IL-5(+) cells. |
| 1268 | 19902255 | Twenty-two significant associations (range of P values 0.002-0.048) were found between SNPs in the vitamin A receptor family (RARA, RARB, TOP2B and RARG), vitamin D receptor and downstream mediator of vitamin D signaling (RXRA) genes and rubella virus-specific (IFN-gamma, IL-2, IL-10, TNF-alpha, and GM-CSF) cytokine immune responses. |
| 1269 | 19902255 | Twenty-two significant associations (range of P values 0.002-0.048) were found between SNPs in the vitamin A receptor family (RARA, RARB, TOP2B and RARG), vitamin D receptor and downstream mediator of vitamin D signaling (RXRA) genes and rubella virus-specific (IFN-gamma, IL-2, IL-10, TNF-alpha, and GM-CSF) cytokine immune responses. |
| 1270 | 19902255 | Twenty-two significant associations (range of P values 0.002-0.048) were found between SNPs in the vitamin A receptor family (RARA, RARB, TOP2B and RARG), vitamin D receptor and downstream mediator of vitamin D signaling (RXRA) genes and rubella virus-specific (IFN-gamma, IL-2, IL-10, TNF-alpha, and GM-CSF) cytokine immune responses. |
| 1271 | 19902255 | A TLR3 gene promoter region SNP (rs5743305, -8441A > T) was associated with rubella-specific GM-CSF secretion. |
| 1272 | 19902255 | A TLR3 gene promoter region SNP (rs5743305, -8441A > T) was associated with rubella-specific GM-CSF secretion. |
| 1273 | 19902255 | A TLR3 gene promoter region SNP (rs5743305, -8441A > T) was associated with rubella-specific GM-CSF secretion. |
| 1274 | 19902255 | Importantly, SNPs in the TRIM5 gene coding regions, rs3740996 (His43Tyr) and rs10838525 (Gln136Arg), were associated with an allele dose-related secretion of rubella virus-specific TNF-alpha and IL-2/GM-CSF, respectively, and have been previously shown to have functional consequences regarding the antiviral activity and susceptibility to HIV-1 infection. |
| 1275 | 19902255 | Importantly, SNPs in the TRIM5 gene coding regions, rs3740996 (His43Tyr) and rs10838525 (Gln136Arg), were associated with an allele dose-related secretion of rubella virus-specific TNF-alpha and IL-2/GM-CSF, respectively, and have been previously shown to have functional consequences regarding the antiviral activity and susceptibility to HIV-1 infection. |
| 1276 | 19902255 | Importantly, SNPs in the TRIM5 gene coding regions, rs3740996 (His43Tyr) and rs10838525 (Gln136Arg), were associated with an allele dose-related secretion of rubella virus-specific TNF-alpha and IL-2/GM-CSF, respectively, and have been previously shown to have functional consequences regarding the antiviral activity and susceptibility to HIV-1 infection. |
| 1277 | 19902255 | We identified associations between individual SNPs and haplotypes in, or involving, the RIG-I (DDX58) gene and rubella-specific TNF-alpha secretion. |
| 1278 | 19902255 | We identified associations between individual SNPs and haplotypes in, or involving, the RIG-I (DDX58) gene and rubella-specific TNF-alpha secretion. |
| 1279 | 19902255 | We identified associations between individual SNPs and haplotypes in, or involving, the RIG-I (DDX58) gene and rubella-specific TNF-alpha secretion. |
| 1280 | 19901066 | Polyfunctional CD4 lymphocytes, defined as producing intracellular interleukin 2 (IL-2), gamma interferon (IFN-gamma), and tumor necrosis factor alpha simultaneously, had a frequency of 137 per 400,000 events among peripheral blood mononuclear cells (PBMC) of immune donors compared to 11 per 400,000 PBMC from nonimmune donors (P = 0.03). |
| 1281 | 19901066 | When monocyte-derived mature dendritic cells pulsed with T27K (mDC(T27K)) were used for antigen presentation, the frequency of polyfunctional CD4 T lymphocytes did not significantly increase for either group, although mDC(T27K) did significantly increase the concentrations of IL-2 and IFN-gamma released by PBMC from nonimmune donors (P = 0.02). |
| 1282 | 19901066 | After in vitro stimulation with T27K, polyfunctional CD4 and CD8 lymphocytes of PBMC from immune donors had a mixture of low- and high-expression CCR7 cells, suggesting both effector and central memory, compared with predominantly high-expression CCR7 cells when PBMC were incubated with the mitogen phytohemagglutinin (P = 0.03). |
| 1283 | 19884336 | The levels of specific proinflammatory cytokines (interleukin-1beta [IL-1beta], macrophage inflammatory protein 1alpha [MIP-1alpha], and tumor necrosis factor alpha [TNF-alpha]) were also significantly reduced after infection of mouse macrophages with either single or double msbB mutants. |
| 1284 | 19877124 | Therapy-induced antitumor vaccination in neuroblastomas by the combined targeting of IL-2 and TNFalpha. |
| 1285 | 19877124 | Therapy-induced antitumor vaccination in neuroblastomas by the combined targeting of IL-2 and TNFalpha. |
| 1286 | 19877124 | Therapy-induced antitumor vaccination in neuroblastomas by the combined targeting of IL-2 and TNFalpha. |
| 1287 | 19877124 | L19-IL2 and L19TNFalpha are fusion proteins composed of L19(scFv), specific for the angiogenesis-associated ED-B containing fibronectin isoform and IL-2 or TNFalpha. |
| 1288 | 19877124 | L19-IL2 and L19TNFalpha are fusion proteins composed of L19(scFv), specific for the angiogenesis-associated ED-B containing fibronectin isoform and IL-2 or TNFalpha. |
| 1289 | 19877124 | L19-IL2 and L19TNFalpha are fusion proteins composed of L19(scFv), specific for the angiogenesis-associated ED-B containing fibronectin isoform and IL-2 or TNFalpha. |
| 1290 | 19877124 | Because of the tumor targeting properties of L19, IL-2 and TNFalpha concentrate at therapeutic doses at the tumor vascular level. |
| 1291 | 19877124 | Because of the tumor targeting properties of L19, IL-2 and TNFalpha concentrate at therapeutic doses at the tumor vascular level. |
| 1292 | 19877124 | Because of the tumor targeting properties of L19, IL-2 and TNFalpha concentrate at therapeutic doses at the tumor vascular level. |
| 1293 | 19877124 | A highly efficient priming of CD4(+) T helper cells and CD8(+) CTL effectors was generated, paralleled by massive infiltration in the tumor tissue of CD4(+) and CD8(+) T cells at day 16 after tumor cell implantation, when, after therapy, tumor volume was drastically reduced and tumor necrosis reached about 80%. |
| 1294 | 19877124 | A highly efficient priming of CD4(+) T helper cells and CD8(+) CTL effectors was generated, paralleled by massive infiltration in the tumor tissue of CD4(+) and CD8(+) T cells at day 16 after tumor cell implantation, when, after therapy, tumor volume was drastically reduced and tumor necrosis reached about 80%. |
| 1295 | 19877124 | A highly efficient priming of CD4(+) T helper cells and CD8(+) CTL effectors was generated, paralleled by massive infiltration in the tumor tissue of CD4(+) and CD8(+) T cells at day 16 after tumor cell implantation, when, after therapy, tumor volume was drastically reduced and tumor necrosis reached about 80%. |
| 1296 | 19877124 | Concluding, L19-IL2 and L19mTNFalpha efficiently cooperate in determining a high percentage of NB cure that, in our experimental models, is strongly associated to the generation of adaptive immunity involving CD4(+) and CD8(+) T cells. |
| 1297 | 19877124 | Concluding, L19-IL2 and L19mTNFalpha efficiently cooperate in determining a high percentage of NB cure that, in our experimental models, is strongly associated to the generation of adaptive immunity involving CD4(+) and CD8(+) T cells. |
| 1298 | 19877124 | Concluding, L19-IL2 and L19mTNFalpha efficiently cooperate in determining a high percentage of NB cure that, in our experimental models, is strongly associated to the generation of adaptive immunity involving CD4(+) and CD8(+) T cells. |
| 1299 | 19863224 | GM-CSF, IL-2, IL-6, TNF-alpha, IFN-gamma, IL-4, IL-8, IL-1b, IL-5, IL-10, IL-12, MIP-1b, IP-10 and Eotaxin were analyzed in a multiplex assay with a Luminex 100 instrument. |
| 1300 | 19863224 | GM-CSF, IL-2, IL-6, TNF-alpha, IFN-gamma, IL-4, IL-8, IL-1b, IL-5, IL-10, IL-12, MIP-1b, IP-10 and Eotaxin were analyzed in a multiplex assay with a Luminex 100 instrument. |
| 1301 | 19863224 | CEA and TIMP-1 were analysed on ELISA platforms. |
| 1302 | 19863224 | CEA and TIMP-1 were analysed on ELISA platforms. |
| 1303 | 19863224 | Patients achieving stable disease showed increasing levels of plasma GM-CSF, TNF-alpha, IFN-gamma, IL-2, and IL-5. |
| 1304 | 19863224 | Patients achieving stable disease showed increasing levels of plasma GM-CSF, TNF-alpha, IFN-gamma, IL-2, and IL-5. |
| 1305 | 19863224 | Patients with progressive disease showed significant increase in CEA and TIMP-1 levels, while patients with stable disease showed relatively unaltered levels. |
| 1306 | 19863224 | Patients with progressive disease showed significant increase in CEA and TIMP-1 levels, while patients with stable disease showed relatively unaltered levels. |
| 1307 | 19858306 | Kinetic analysis showed that the MVA boost made the adenoviral-primed T cells markedly more polyfunctional, with the number of gamma interferon (INF-gamma), tumor necrosis factor alpha (TNF-alpha), and interleukin-2 (IL-2) triple-positive and INF-gamma and TNF-alpha double-positive cells increasing over time, while INF-gamma single-positive cells declined with time. |
| 1308 | 19853910 | The effect of R1, R2 and R3 on the expression of the pro- and anti-inflammatory cytokines (TNF-alpha, IL-6, and IL-12) and the co-stimulatory molecules (CD40, CD80, CD86, and MHC class II) in MDDCs was examined. |
| 1309 | 19853910 | The effect of R1, R2 and R3 on the expression of the pro- and anti-inflammatory cytokines (TNF-alpha, IL-6, and IL-12) and the co-stimulatory molecules (CD40, CD80, CD86, and MHC class II) in MDDCs was examined. |
| 1310 | 19853910 | The exposure of R1 caused a dose-dependent increase in the expression of TNF-alpha, IL-12, CD86 and CD40, while R2 and R3 did not up-regulate these cytokines and co-stimulatory molecules. |
| 1311 | 19853910 | The exposure of R1 caused a dose-dependent increase in the expression of TNF-alpha, IL-12, CD86 and CD40, while R2 and R3 did not up-regulate these cytokines and co-stimulatory molecules. |
| 1312 | 19853910 | Furthermore, we found that R1 significantly increased the NF-kappaB expression in the nucleus (in a dose-dependent manner) and promoted the degradation of total IkappaBalpha levels, indicating that the NF-kappaB signaling pathway might involve in an R1-induced DC activation. |
| 1313 | 19853910 | Furthermore, we found that R1 significantly increased the NF-kappaB expression in the nucleus (in a dose-dependent manner) and promoted the degradation of total IkappaBalpha levels, indicating that the NF-kappaB signaling pathway might involve in an R1-induced DC activation. |
| 1314 | 19828771 | V. parvula LPS stimulated tumor necrosis factor alpha (TNF-alpha) and interleukin-6 (IL-6) release in human peripheral blood mononuclear cells (PBMC) in a dose-dependent manner. |
| 1315 | 19828771 | V. parvula LPS stimulated tumor necrosis factor alpha (TNF-alpha) and interleukin-6 (IL-6) release in human peripheral blood mononuclear cells (PBMC) in a dose-dependent manner. |
| 1316 | 19828771 | V. parvula LPS stimulated tumor necrosis factor alpha (TNF-alpha) and interleukin-6 (IL-6) release in human peripheral blood mononuclear cells (PBMC) in a dose-dependent manner. |
| 1317 | 19828771 | V. parvula LPS stimulated tumor necrosis factor alpha (TNF-alpha) and interleukin-6 (IL-6) release in human peripheral blood mononuclear cells (PBMC) in a dose-dependent manner. |
| 1318 | 19828771 | Pretreatment of cells with a TLR4 antagonist significantly reduced TNF-alpha and IL-6 production in PBMC stimulated with either Veillonella or Escherichia coli LPS. |
| 1319 | 19828771 | Pretreatment of cells with a TLR4 antagonist significantly reduced TNF-alpha and IL-6 production in PBMC stimulated with either Veillonella or Escherichia coli LPS. |
| 1320 | 19828771 | Pretreatment of cells with a TLR4 antagonist significantly reduced TNF-alpha and IL-6 production in PBMC stimulated with either Veillonella or Escherichia coli LPS. |
| 1321 | 19828771 | Pretreatment of cells with a TLR4 antagonist significantly reduced TNF-alpha and IL-6 production in PBMC stimulated with either Veillonella or Escherichia coli LPS. |
| 1322 | 19828771 | TNF-alpha, IL-1beta, IL-6, and IL-10 were released in wild-type and TLR2(-/-), but not TLR4(-/-), mouse macrophage cultures. |
| 1323 | 19828771 | TNF-alpha, IL-1beta, IL-6, and IL-10 were released in wild-type and TLR2(-/-), but not TLR4(-/-), mouse macrophage cultures. |
| 1324 | 19828771 | TNF-alpha, IL-1beta, IL-6, and IL-10 were released in wild-type and TLR2(-/-), but not TLR4(-/-), mouse macrophage cultures. |
| 1325 | 19828771 | TNF-alpha, IL-1beta, IL-6, and IL-10 were released in wild-type and TLR2(-/-), but not TLR4(-/-), mouse macrophage cultures. |
| 1326 | 19828771 | V. parvula LPS was able to activate the human PBMC p38 mitogen-activated protein kinase (MAPK). |
| 1327 | 19828771 | V. parvula LPS was able to activate the human PBMC p38 mitogen-activated protein kinase (MAPK). |
| 1328 | 19828771 | V. parvula LPS was able to activate the human PBMC p38 mitogen-activated protein kinase (MAPK). |
| 1329 | 19828771 | V. parvula LPS was able to activate the human PBMC p38 mitogen-activated protein kinase (MAPK). |
| 1330 | 19828771 | A specific p38 MAPK inhibitor strongly inhibited V. parvula LPS-induced TNF-alpha, IL-1beta, IL-6, and IL-10. |
| 1331 | 19828771 | A specific p38 MAPK inhibitor strongly inhibited V. parvula LPS-induced TNF-alpha, IL-1beta, IL-6, and IL-10. |
| 1332 | 19828771 | A specific p38 MAPK inhibitor strongly inhibited V. parvula LPS-induced TNF-alpha, IL-1beta, IL-6, and IL-10. |
| 1333 | 19828771 | A specific p38 MAPK inhibitor strongly inhibited V. parvula LPS-induced TNF-alpha, IL-1beta, IL-6, and IL-10. |
| 1334 | 19828771 | V. parvula LPS-stimulated cytokine induction, as well as p38 MAPK activation, are TLR4-dependent features. |
| 1335 | 19828771 | V. parvula LPS-stimulated cytokine induction, as well as p38 MAPK activation, are TLR4-dependent features. |
| 1336 | 19828771 | V. parvula LPS-stimulated cytokine induction, as well as p38 MAPK activation, are TLR4-dependent features. |
| 1337 | 19828771 | V. parvula LPS-stimulated cytokine induction, as well as p38 MAPK activation, are TLR4-dependent features. |
| 1338 | 19822650 | Mast cell-deficient Kitl(Sl)/Kitl(Sl-d) and control mice were immunized with H. pylori sonicate plus cholera toxin and challenged with H. pylori, and the bacterial loads, inflammatory infiltrates, and cytokine responses were evaluated and compared at 1, 2, and 4 weeks postchallenge. |
| 1339 | 19822650 | Neutrophil numbers in the gastric mucosa of immune Kitl(Sl)/Kitl(Sl-d) mice were lower than those for immune wild-type mice (P < 0.05). |
| 1340 | 19822650 | Levels of gastric interleukin-17 (IL-17) and tumor necrosis factor alpha (TNF-alpha) were also significantly lower in immune Kitl(Sl)/Kitl(Sl-d) mice than in wild-type mice (P < 0.001). |
| 1341 | 19822650 | Immunized mast cell-deficient and wild-type mouse spleen cells produced IFN-gamma and IL-17 in response to H. pylori antigen stimulation. |
| 1342 | 19819209 | Significant associations were observed between SNPs in the TNFalpha, IL-12B, IL-4Ralpha, and IL-10 genes and vaccine-specific immune responses (p<0.05). |
| 1343 | 19819209 | Significant associations were observed between SNPs in the TNFalpha, IL-12B, IL-4Ralpha, and IL-10 genes and vaccine-specific immune responses (p<0.05). |
| 1344 | 19819209 | In addition, SNPs in the IL-1beta, TNFalpha, IL-2, IL-4, IL-10, IL-4Ralpha, and IL-12B genes were associated with variations in serum levels of immunoglobulins (IgG, IgA, IgM) and IgG isotypes (IgG1-IgG3) (p<0.05). |
| 1345 | 19819209 | In addition, SNPs in the IL-1beta, TNFalpha, IL-2, IL-4, IL-10, IL-4Ralpha, and IL-12B genes were associated with variations in serum levels of immunoglobulins (IgG, IgA, IgM) and IgG isotypes (IgG1-IgG3) (p<0.05). |
| 1346 | 19812194 | The production of IFN-gamma by CD8(+) T cells is an important hallmark of protective immunity induced by irradiation-attenuated sporozoites against malaria. |
| 1347 | 19812194 | Here, we demonstrate that protracted sterile protection conferred by a Plasmodium yoelii genetically attenuated parasite (PyGAP) vaccine was completely dependent on CD8(+) T lymphocytes but only partially dependent on IFN-gamma. |
| 1348 | 19812194 | This was further supported by our observation that both liver and spleen CD8(+) T cells from PyGAP-immunized mice induced massive apoptosis of liver stage-infected hepatocytes in vitro without the release of detectable IFN-gamma and TNF-alpha. |
| 1349 | 19800561 | In clinical trials, Th1 and CD8 responses were induced with an IFN-gamma/TNF-alpha ratio favouring IFN-gamma in both cases, regardless of whether the vaccine recipients were flavivirus naive or not. |
| 1350 | 19793902 | Mycoplasma genitalium-derived lipid-associated membrane proteins activate NF-kappaB through toll-like receptors 1, 2, and 6 and CD14 in a MyD88-dependent pathway. |
| 1351 | 19793902 | Mycoplasma genitalium-derived lipid-associated membrane proteins activate NF-kappaB through toll-like receptors 1, 2, and 6 and CD14 in a MyD88-dependent pathway. |
| 1352 | 19793902 | However, the interaction of M. genitalium-derived LAMPs as pathogenic agents with Toll-like receptors (TLRs) and the signaling pathways responsible for active inflammation and NF-kappaB activation have not been fully elucidated. |
| 1353 | 19793902 | However, the interaction of M. genitalium-derived LAMPs as pathogenic agents with Toll-like receptors (TLRs) and the signaling pathways responsible for active inflammation and NF-kappaB activation have not been fully elucidated. |
| 1354 | 19793902 | In this study, LAMPs induced the production of tumor necrosis factor alpha (TNF-alpha) and interleukin-6 (IL-6) in a dose-dependent manner. |
| 1355 | 19793902 | In this study, LAMPs induced the production of tumor necrosis factor alpha (TNF-alpha) and interleukin-6 (IL-6) in a dose-dependent manner. |
| 1356 | 19793902 | Blocking assays showed that TLR2- and CD14-neutralizing antibodies reduced the expression of TNF-alpha and IL-6 in THP-1 cells. |
| 1357 | 19793902 | Blocking assays showed that TLR2- and CD14-neutralizing antibodies reduced the expression of TNF-alpha and IL-6 in THP-1 cells. |
| 1358 | 19793902 | Furthermore, LAMP-induced NF-kappaB activation was increased in 293T cells transfected with TLR2 plasmid. |
| 1359 | 19793902 | Furthermore, LAMP-induced NF-kappaB activation was increased in 293T cells transfected with TLR2 plasmid. |
| 1360 | 19793902 | The activity of NF-kappaB was synergically augmented by cotransfected TLR1, TLR6, and CD14. |
| 1361 | 19793902 | The activity of NF-kappaB was synergically augmented by cotransfected TLR1, TLR6, and CD14. |
| 1362 | 19793902 | Additionally, LAMPs were shown to inhibit NF-kappaB expression by cotransfection with dominant-negative MyD88 and TLR2 plasmids. |
| 1363 | 19793902 | Additionally, LAMPs were shown to inhibit NF-kappaB expression by cotransfection with dominant-negative MyD88 and TLR2 plasmids. |
| 1364 | 19793902 | These results suggest that M. genitalium-derived LAMPs activate NF-kappaB via TLR1, TLR2, TLR6, and CD14 in a MyD88-dependent pathway. |
| 1365 | 19793902 | These results suggest that M. genitalium-derived LAMPs activate NF-kappaB via TLR1, TLR2, TLR6, and CD14 in a MyD88-dependent pathway. |
| 1366 | 19776194 | Upregulation of a tumor necrosis factor alpha-inducing factor homolog in challenged chickens compared to naïve chickens was observed, regardless of the incidence of necrotic enteritis. |
| 1367 | 19776194 | In addition, the members of the TLR2 subfamily were found to be most strongly involved in the host response to C. perfringens challenge, although the expression of TLR4 and TLR7 was also upregulated in spleen tissues. |
| 1368 | 19776194 | While the combination of TLR1.2, TLR2.1, and TLR15 appeared to play a major role in the splenic response, the expression of TLR2.2 and TLR1.1 was positively correlated to the expression of adaptor molecules MyD88, TRAF6, TRIF, and receptor interacting protein 1 in the ileal tissues, demonstrating a dynamic spatial and temporal innate host response to C. perfringens. |
| 1369 | 19772942 | In vitro, CoVaccineHT upregulated the expression of co-stimulatory molecules both on mouse and human dendritic cells and induced the secretion of pro-inflammatory cytokines TNF-alpha, IL-6, IL-1beta and IL-12p70 in mouse- and IL-6 in human dendritic cells. |
| 1370 | 19769731 | The human cancer antigen mesothelin is more efficiently presented to the mouse immune system when targeted to the DEC-205/CD205 receptor on dendritic cells. |
| 1371 | 19769731 | To develop a tumor vaccine directly targeting tumor antigen to dendritic cells in situ, we engineered human mesothelin (MSLN) into an antibody specific for mouse DEC-205, a receptor for antigen presentation. |
| 1372 | 19769731 | We then characterized both T cell and humoral responses to human MSLN and compared immunizing efficacy of DEC-205-targeted MSLN to nontargeted protein after a single-dose immunization. |
| 1373 | 19769731 | Targeting human MSLN to DEC-205 receptor induced stronger CD4(+) T-cell responses compared to high doses of mesothelin protein. |
| 1374 | 19769731 | Approximately 0.5% CD4(+) T cells were primed to produce IFN-gamma, tumor necrosis factor-alpha, and IL-2 via intracellular cytokine staining, and the T cells also could proliferate rapidly. |
| 1375 | 19769731 | Targeting MSLN protein to DEC-205 receptor also resulted in cross-presentation to CD8(+) T cells. |
| 1376 | 19769731 | In summary, targeting of MSLN to DEC-205 improves the induction of CD4(+) and CD8(+) T-cell immunity accompanied by an antibody response. |
| 1377 | 19769731 | DEC-205-targeting could be valuable for enhancing immunity to MSLN in cancers where this nonmutated protein is expressed. |
| 1378 | 19741603 | We compared the efficacy of an intranasal or intramuscular Simian immunodeficiency virus (SIV)+ interleukin (IL)-2+IL-15 DNA/SIV-MVA (modified vaccinia virus Ankara) vaccination in preventing disease progression in SIVmac251 intrarectally challenged rhesus macaques. |
| 1379 | 19741603 | Regardless of vaccination status, long-term viremia control and preservation of CD4(+) C(M) T cells was detected in animals with significantly higher systemic CD8(+)/tumor necrosis factor (TNF)-alpha(+) and CD8(+)/interferon (IFN)-gamma(+) T-cell responses and higher SIV-specific CD4(+)/IL-2(+) responses in colorectal T cells. |
| 1380 | 19733586 | In the immediate response and tuberculin response, BCG-vaccinated fish showed higher gene expression levels of inflammatory cytokines such as IL-1beta, IL-6, IFN-gamma and TNFalpha. |
| 1381 | 19727134 | Dendritic cells (DC) engineered in vitro by DNA encoding OVAhsp70 and IL-15 up-regulated their expressions of CD80, CD86, CCR7 and IL-15Ralpha and promoted their productions of IL-6, IL-12 and TNF-alpha. |
| 1382 | 19710295 | The cytokines IFN-gamma and tumor necrosis factor alpha can cooperate with anti-LcrV to promote protection against lethal Y. pestis infection in mice. |
| 1383 | 19706905 | Antigen-specific antibodies and Th1 cytokines, interleukin-2, interferon-gamma, and tumor necrosis factor-alpha were induced in rVCG-TBCA2-immunized mice and in vitro on antigen stimulation of splenic immune T cells, but the corresponding Th2-type response was unremarkable. |
| 1384 | 19696891 | Vibrio cholerae proteome-wide screen for immunostimulatory proteins identifies phosphatidylserine decarboxylase as a novel Toll-like receptor 4 agonist. |
| 1385 | 19696891 | PSD in concentrations as low as 100 ng/ml stimulated RAW264.7 murine macrophage cells and primary peritoneal macrophage cells to secrete TNFalpha and IL-6, respectively. |
| 1386 | 19696891 | Moreover, no detectable IL-6 was produced in TLR4-deficient mouse macrophages by PSD. |
| 1387 | 19696891 | Anti-BSA response was decreased in TLR4-deficient mice immunized with BSA in combination with PSD, further proving the role of TLR4 in PSD signaling in vivo. |
| 1388 | 19669608 | These cells were cultured with cytokines GM-CSF, IL-4, and TNFalpha to induce their maturation. |
| 1389 | 19669608 | Phenotypically, FACS analysis showed that they expressed high levels of MHC II, CD11b, CD80, and CD86 antigen, and were negative for CD8alpha. |
| 1390 | 19668260 | Addition of ADA to the co-cultures resulted in enhanced CD4(+) and CD8(+) T-cell proliferation and robust ADA-induced increase in cytokine production (IFN-gamma, TNF-alpha and IL-6). |
| 1391 | 19668260 | Addition of ADA to the co-cultures resulted in enhanced CD4(+) and CD8(+) T-cell proliferation and robust ADA-induced increase in cytokine production (IFN-gamma, TNF-alpha and IL-6). |
| 1392 | 19668260 | As IFN-gamma, TNF-alpha and IL-6 promote the Th1 versus Th2 phenotype and improve T helper proliferation responses and antigen-specific CTL responses ADA may be considered a promising candidate for therapeutic vaccine adjuvant. |
| 1393 | 19668260 | As IFN-gamma, TNF-alpha and IL-6 promote the Th1 versus Th2 phenotype and improve T helper proliferation responses and antigen-specific CTL responses ADA may be considered a promising candidate for therapeutic vaccine adjuvant. |
| 1394 | 19665607 | The neutralization antibody, interferon gamma (IFN-gamma), tumor necrosis factors alpha (TNF-alpha) or interleukin-6 (IL-6), and virus-specific CD8+ cytotoxic T-lymphocyte (CTL) levels, as well as survival rates, were analyzed and compared with inactivated vaccine and DCs control groups. |
| 1395 | 19665607 | The neutralization antibody, interferon gamma (IFN-gamma), tumor necrosis factors alpha (TNF-alpha) or interleukin-6 (IL-6), and virus-specific CD8+ cytotoxic T-lymphocyte (CTL) levels, as well as survival rates, were analyzed and compared with inactivated vaccine and DCs control groups. |
| 1396 | 19665607 | The results demonstrated that intravenous (i.v.) injection of 2 x 10(5) JEV-pulsed bmDCs into each mouse produced notable levels of JEV-specific neutralizing antibodies and higher levels of CD8+ CTL, IFN-gamma and TNF-alpha compared with JEV-inactivated vaccine. |
| 1397 | 19665607 | The results demonstrated that intravenous (i.v.) injection of 2 x 10(5) JEV-pulsed bmDCs into each mouse produced notable levels of JEV-specific neutralizing antibodies and higher levels of CD8+ CTL, IFN-gamma and TNF-alpha compared with JEV-inactivated vaccine. |
| 1398 | 19652662 | WAg 206, unlike WAg 207, did not elicit inflammatory cytokine production (TNFalpha, IL-1beta, IL-12) or costimulatory molecule expression (HLA-DR, CD83, CD80, CD86) by human MDDCs in vitro. |
| 1399 | 19651871 | Perforin and gamma interferon expression are required for CD4+ and CD8+ T-cell-dependent protective immunity against a human parasite, Trypanosoma cruzi, elicited by heterologous plasmid DNA prime-recombinant adenovirus 5 boost vaccination. |
| 1400 | 19651871 | A heterologous prime-boost strategy using plasmid DNA, followed by replication-defective recombinant adenovirus 5, is being proposed as a powerful way to elicit CD4(+) and CD8(+) T-cell-mediated protective immunity against intracellular pathogens. |
| 1401 | 19651871 | We confirmed this concept and furthered existing research by providing evidence that the heterologous prime-boost regimen using the gene encoding amastigote surface protein 2 elicited CD4(+) and CD8(+) T-cell-mediated protective immunity (reduction of acute parasitemia and prolonged survival) against experimental infection with Trypanosoma cruzi. |
| 1402 | 19651871 | In spite of a normal numeric expansion, specific CD8(+) T cells presented several functional defects detected in vivo (cytotoxicity) and in vitro (simultaneous expression of CD107a/IFN-gamma or IFN-gamma/tumor necrosis factor alpha) paralleled by a decreased expression of CD44 and KLRG-1. |
| 1403 | 19651643 | PD1 blockade reverses the suppression of melanoma antigen-specific CTL by CD4+ CD25(Hi) regulatory T cells. |
| 1404 | 19651643 | Regulatory CD4(+)CD25(Hi) T cells (Treg) and programmed death-1 (PD-1) molecule have emerged as pivotal players in immune regulation. |
| 1405 | 19651643 | We identified Treg in the circulation of vaccinated melanoma patients and detected PD-1 expression on vaccine-induced melanoma antigen-specific CTLs, as well as on and within Treg from patients' peripheral blood. |
| 1406 | 19651643 | PD-1 blockade promoted the generation of melanoma antigen-specific CTLs and masked their inhibition by Treg. |
| 1407 | 19651643 | The mechanisms by which PD-1 blockade mediated immune enhancement included direct augmentation of melanoma antigen-specific CTL proliferation, heightening their resistance to inhibition by Treg and direct limitation of the inhibitory ability of Treg. |
| 1408 | 19651643 | PD-1 blockade reversed the increased expression of PD-1 and PD-L1 on melanoma antigen-specific CTL by Treg, rescued INF-gamma and IL-2 or INF-gamma and tumor necrosis factor-alpha co-expression and expression of IL-7 receptor by melanoma antigen-specific CTL which were diminished by Treg. |
| 1409 | 19620345 | The protection was correlated mainly with a low level of interleukin-1 beta (IL-1 beta) and with high levels of PA-specific immunoglobulin G1, IL-6, and tumor necrosis factor alpha. |
| 1410 | 19620344 | T cells provide a substantial degree of this protection, as vaccine efficacy is maintained in B-cell-deficient muMT mice unless those animals are depleted of CD4 and CD8 T cells at the time of challenge. |
| 1411 | 19620344 | Upon challenge with Y. pestis, pulmonary T-cell numbers decline in naive mice, whereas immunized mice show increased numbers of CD44(high) CD43(high) effector T cells and T cells primed to produce tumor necrosis factor alpha and gamma interferon; neutralizing these cytokines at the time of challenge abrogates protection. |
| 1412 | 19620314 | The vaccine-promoted response consists mainly of double- (TNF-alpha and IL-2) or triple-positive (IFN-gamma, TNF-alpha, and IL-2) polyfunctional T cells. |
| 1413 | 19620310 | Importantly, a simple synthetic analog of MMG, based on a 32 carbon mycolic acid, was found to give rise to comparable high Th1-biased responses with a major representation of polyfunctional CD4 T cells coexpressing IFN-gamma, TNF-alpha, and IL-2. |
| 1414 | 19609238 | Maturation pathways of dendritic cells determine TAP1 and TAP2 levels and cross-presenting function. |
| 1415 | 19609238 | Here, we compare DC matured with 3 clinically relevant cytokine combinations including interleukin (IL)-1 beta, tumor necrosis factor-alpha, IL-6 (termed DC-0), DC-0 cells incubated with prostaglandin-2 (termed DC-0+prostaglandin-2), or DC treated with interferon-gamma, interferon-alpha, tumor necrosis factor-alpha, Poly I:C, and IL1-beta (termed DC-1). |
| 1416 | 19609238 | TA cross presentation and CTL priming were strongly correlated with level of expression of the antigen processing machinery components, TAP1 and TAP2, indicating that these components could be used as biomarkers to standardize DC preparations for optimal function. |
| 1417 | 19609238 | However, the up-regulation of TAP1/TAP2 was not sufficient to explain the enhanced cross-presentation ability of DC-1 cells, as the use of IFN-gamma alone to up-regulate TAP1/TAP2 did not generate DC as effective at cross-presentation as the full DC-1 maturation cytokine combination. |
| 1418 | 19592661 | Upon virulent challenge, the immunized mice displayed in the CD4(+) T cell population a significant increase of single and multiple cytokine (IFN-gamma, IL-2, and TNF) producing cells and IFN-gamma/IL10 ratio. |
| 1419 | 19564375 | The cell-mediated immune (CMI) response was characterized by significant gamma interferon (IFN-gamma), interleukin 12 (IL-12), IL-2, IL-10, and IL-17 production. |
| 1420 | 19564375 | Several antibody and CMI cytokine responses were examined for correlates of protection, and prechallenge IFN-gamma(+) or IFN-gamma-, IL-2-, and tumor necrosis factor alpha-triple-positive CD4 cells in blood were statistically associated with protection. |
| 1421 | 19553557 | Lipoprotein lipase and hydrofluoric acid deactivate both bacterial lipoproteins and lipoteichoic acids, but platelet-activating factor-acetylhydrolase degrades only lipoteichoic acids. |
| 1422 | 19553557 | To identify the Toll-like receptor 2 ligand critically involved in infections with gram-positive bacteria, lipoprotein lipase (LPL) or hydrogen peroxide (H(2)O(2)) is often used to selectively inactivate lipoproteins, and hydrofluoric acid (HF) or platelet-activating factor-acetylhydrolase (PAF-AH) is used to selectively inactivate lipoteichoic acid (LTA). |
| 1423 | 19553557 | We investigated the reaction specificities by using two synthetic lipoproteins (Pam(3)CSK(4) and FSL-1) and LTAs from pneumococci and staphylococci. |
| 1424 | 19553557 | Changes in the structures of the two synthetic proteins and the LTAs were monitored by mass spectrometry, and biological activity changes were evaluated by measuring tumor necrosis factor alpha production by mouse macrophage cells (RAW 264.7) following stimulation. |
| 1425 | 19553557 | PAF-AH inactivated LTA without reducing the biological activities of Pam(3)CSK(4) and FSL-1. |
| 1426 | 19553557 | Our results indicate that treatment with 1% H(2)O(2) for 6 h at 37 degrees C inactivates Pam(3)CSK(4), FSL-1, and LTA by more than 80%. |
| 1427 | 19553557 | Although HF, LPL, and H(2)O(2) treatments degrade and inactivate both lipopeptides and LTA, PAF-AH selectively inactivated LTA with no effect on the biological and structural properties of the two lipopeptides. |
| 1428 | 19553556 | Intracellular infections enhance interleukin-6 and plasminogen activator inhibitor 1 production by cocultivated human adipocytes and THP-1 monocytes. |
| 1429 | 19553556 | After 48 h, transinfection was evaluated and interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-alpha), adiponectin, and plasminogen activator inhibitor 1 (PAI-1) were measured. |
| 1430 | 19553556 | Infection of cocultivated human adipocytes and THP-1 monocytes with CMV or influenza A virus led to increased production of IL-6 and PAI-1. |
| 1431 | 19553556 | Thus, infection of adipose tissue evokes an inflammatory response, leading to adipose tissue dysfunction and subsequent overproduction of IL-6 and PAI-1. |
| 1432 | 19551822 | Affymetrix GeneChip analysis of human primary monocytes, B cells and dendritic cells infected with DENV in vitro showed strong induction of monocyte chemotactic protein 2 (MCP-2/CCL8), interferon gamma-induced protein 10 (IP-10/CXCL10) and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL/TNFSF10). |
| 1433 | 19551822 | Results showed significant increase of MCP-2, IP-10, and TRAIL levels in patients infected with DENV during the febrile period, when compared to healthy donors and patients with other febrile illnesses. |
| 1434 | 19551822 | MCP-2 and IP-10 levels were still elevated during the post-febrile period while TRAIL levels dropped close to normal after defervescense. |
| 1435 | 19551822 | Increased levels of IP-10, TRAIL and MCP-2 in acute DENV infections suggest a role for these mediators in the immune response to the infection. |
| 1436 | 19551822 | MCP-2 was identified in this work as a new unreported and important dengue-related protein and IP-10 was confirmed as a novel and strong pro-inflammatory marker in acute disease. |
| 1437 | 19549606 | Compared to the vaccination with rHBsAg alone, LMS could up-regulate the expressions of TLR7&8, MyD88, IRF7 and their downstream pro-inflammatory cytokines including IFN-alpha and TNF-alpha, which promote DCs activation. |
| 1438 | 19549606 | Strikingly, we find that the combination of LMS and alum adjuvant synergistically enhances immunogenicity of rHBsAg and leads to a robust cell-mediated response demonstrated by the higher level of IgG2a/IgG1, T cell proliferation, and importantly, a high level of antigen-specific CTL and IFN-gamma production within these activated CD8(+) T cells. |
| 1439 | 19542458 | The efficacy was supported by a surge in inducible NO synthase, IFN-gamma, TNF-alpha, and IL-12 mRNA levels along with extreme down-regulation of TGF-beta, IL-4, and IL-10. |
| 1440 | 19540885 | The Th1 (TNF-alpha, IL-12p70, IFN-gamma, IL-2) and Th2 (IL-10, IL-6) cytokine profiles were analyzed after stimulation of spleen cells from mice immunized with purified RF-412 protein. |
| 1441 | 19540594 | Requirement of TLR4 and CD14 in dendritic cell activation by Hemagglutinin B from Porphyromonas gingivalis. |
| 1442 | 19540594 | Requirement of TLR4 and CD14 in dendritic cell activation by Hemagglutinin B from Porphyromonas gingivalis. |
| 1443 | 19540594 | Using an endotoxin free rHagB preparation, our results show that stimulation of murine bone marrow-derived DC with rHagB leads to upregulation of the costimulatory molecules CD86 and CD40, activation of p38 and ERK MAP kinases, transcription factors NF-kappaB, CREB and IRF-3 and the production of IL-6, TNF-alpha, IL-12p40 and to a lesser extent IL-10 and IFN-beta. |
| 1444 | 19540594 | Using an endotoxin free rHagB preparation, our results show that stimulation of murine bone marrow-derived DC with rHagB leads to upregulation of the costimulatory molecules CD86 and CD40, activation of p38 and ERK MAP kinases, transcription factors NF-kappaB, CREB and IRF-3 and the production of IL-6, TNF-alpha, IL-12p40 and to a lesser extent IL-10 and IFN-beta. |
| 1445 | 19540594 | This activation process was absolutely dependent on TLR4 and CD14. |
| 1446 | 19540594 | This activation process was absolutely dependent on TLR4 and CD14. |
| 1447 | 19540594 | While upregulation of CD86 was independent of the adaptor molecule MyD88, CD40 upregulation and optimal cytokine (IL-6, TNF-alpha, IL-12p40, IL-10 and IFN-beta) production required both MyD88 and TRIF molecules. |
| 1448 | 19540594 | While upregulation of CD86 was independent of the adaptor molecule MyD88, CD40 upregulation and optimal cytokine (IL-6, TNF-alpha, IL-12p40, IL-10 and IFN-beta) production required both MyD88 and TRIF molecules. |
| 1449 | 19539586 | Both vaccines elicited CD4(+) T-cell responses, but with significant differences in the phenotype of the Gag-specific cells: the native Gag induced CD4(+) responses with a phenotype of central memory-like T cells (CD28(+) CD45RA(-)), whereas the LAMP/Gag chimera induced CD4(+) responses with effector memory phenotype (CD28(-) CD45RA(-)). |
| 1450 | 19539586 | Antigen-specific T cells producing both IFN-gamma and TNFalpha were found in the animals receiving the native Gag, whereas the LAMP/Gag chimera induced humoral responses faster. |
| 1451 | 19526193 | Cytometry analysis indicated that the majority of memory CD8(+) T cells produced IFN-gamma, whereas memory CD4(+) T cells produced IFN-gamma, IL-2 or TNF-alpha. |
| 1452 | 19523909 | The IN defective vector was able to efficiently elicit specific and long-lasting polyfunctional immune responses as evaluated by enzyme-linked immunospot (ELISPOT) assays for interferon-gamma (IFN-gamma) in spleens, bone marrow (BM) and draining lymph nodes, and by intracellular staining (ICS) for IFN-gamma, Interleukin-2 (IL-2) and tumor necrosis factor (TNF-alpha) in both splenocytes and BM cells without integration of the vector into the host genome. |
| 1453 | 19494812 | Here we show that tumour necrosis factor (TNF) receptor-associated factor 6 (TRAF6), an adaptor protein in the TNF-receptor and interleukin-1R/Toll-like receptor superfamily, regulates CD8 T(M)-cell development after infection by modulating fatty acid metabolism. |
| 1454 | 19494812 | We show that mice with a T-cell-specific deletion of TRAF6 mount robust CD8 T(E)-cell responses, but have a profound defect in their ability to generate T(M) cells that is characterized by the disappearance of antigen-specific cells in the weeks after primary immunization. |
| 1455 | 19494812 | Microarray analyses revealed that TRAF6-deficient CD8 T cells exhibit altered expression of genes that regulate fatty acid metabolism. |
| 1456 | 19494812 | Consistent with this, activated CD8 T cells lacking TRAF6 display defective AMP-activated kinase activation and mitochondrial fatty acid oxidation (FAO) in response to growth factor withdrawal. |
| 1457 | 19494812 | Administration of the anti-diabetic drug metformin restored FAO and CD8 T(M)-cell generation in the absence of TRAF6. |
| 1458 | 19494330 | Characterization of the CD4 memory T cells by multicolor flow cytometry demonstrated that the long-lived memory population consisted almost exclusively of TNF-alpha(+)IL-2(+) and IFN-gamma(+)TNF-alpha(+)IL-2(+) multifunctional T cells. |
| 1459 | 19494330 | Characterization of the CD4 memory T cells by multicolor flow cytometry demonstrated that the long-lived memory population consisted almost exclusively of TNF-alpha(+)IL-2(+) and IFN-gamma(+)TNF-alpha(+)IL-2(+) multifunctional T cells. |
| 1460 | 19494330 | Long-term memory induced by the BCG vaccine contained fewer multifunctional T cells and was biased toward effector cells mainly of the TNF-alpha(+)IFN-gamma(+)-coexpressing subset. |
| 1461 | 19494330 | Long-term memory induced by the BCG vaccine contained fewer multifunctional T cells and was biased toward effector cells mainly of the TNF-alpha(+)IFN-gamma(+)-coexpressing subset. |
| 1462 | 19494321 | Bone marrow-derived mesenchymal stromal cells (MSC) possess an immune plasticity manifested by either an immunosuppressive or, when activated with IFN-gamma, an APC phenotype. |
| 1463 | 19494321 | We observed that human MSC and macrophages expressed TLR3 and TLR4 at comparable levels and TLR-mediated activation of MSC resulted in the production of inflammatory mediators such as IL-1beta, IL-6, IL-8/CXCL8, and CCL5. |
| 1464 | 19494321 | IFN-alpha or IFN-gamma priming up-regulated production of these inflammatory mediators and expression of IFNB, inducible NO synthase (iNOS), and TRAIL upon TLR activation in MSC and macrophages, but failed to induce IL-12 and TNF-alpha production in MSC. |
| 1465 | 19494321 | In addition, IFN priming combined with TLR activation may increase immune responses induced by Ag-presenting MSC through presentation of Ag in an inflammatory context, a mechanism that could be applied in a cell-based vaccine. |
| 1466 | 19494083 | Adherent peritoneal cells from rats treated with HKC-CFA showed upregulated ED2, CD80, and CD86 expression; an increase in the level of production of anticryptococcal metabolites; and the enhanced production of interleukin-12 (IL-12) in comparison with the findings for cells from rats treated with CFA-phosphate-buffered saline (PBS). |
| 1467 | 19494083 | Adherent peritoneal cells from rats treated with PSC-CFA, however, also presented upregulated ED2, CD80, and CD86 expression compared to the level of expression for peritoneal cells from controls, but these cells showed an increase in arginase activity and decreased levels of production of IL-12 and tumor necrosis factor (TNF) compared with the activity and levels of production by peritoneal cells from CFA-PBS-treated rats. |
| 1468 | 19467253 | The significantly high serum level of IL8, TNFalpha (P<0.001) and nitric oxide (P<0.0001) observed in the present study supports the evidence for the role of these potent vasodilators in the terminal hypotension that is usually observed in humans and animals after envenomation. |
| 1469 | 19464559 | Vaccination with vif-deleted feline immunodeficiency virus provirus, GM-CSF, and TNF-alpha plasmids preserves global CD4 T lymphocyte function after challenge with FIV. |
| 1470 | 19464559 | Vaccination with vif-deleted feline immunodeficiency virus provirus, GM-CSF, and TNF-alpha plasmids preserves global CD4 T lymphocyte function after challenge with FIV. |
| 1471 | 19464559 | Vaccination with vif-deleted feline immunodeficiency virus provirus, GM-CSF, and TNF-alpha plasmids preserves global CD4 T lymphocyte function after challenge with FIV. |
| 1472 | 19464559 | Vaccination with vif-deleted feline immunodeficiency virus provirus, GM-CSF, and TNF-alpha plasmids preserves global CD4 T lymphocyte function after challenge with FIV. |
| 1473 | 19464559 | Vaccine protocols included FIV-pPPRDeltavif plasmid alone; a combination of FIV-pPPRDeltavif DNA and feline granulocyte macrophage-colony stimulating factor (GM-CSF) and tumor necrosis factor (TNF)-alpha expression plasmids; or a combination of FIV-pPPRDeltavif and feline interleukin (IL)-15 plasmids. |
| 1474 | 19464559 | Vaccine protocols included FIV-pPPRDeltavif plasmid alone; a combination of FIV-pPPRDeltavif DNA and feline granulocyte macrophage-colony stimulating factor (GM-CSF) and tumor necrosis factor (TNF)-alpha expression plasmids; or a combination of FIV-pPPRDeltavif and feline interleukin (IL)-15 plasmids. |
| 1475 | 19464559 | Vaccine protocols included FIV-pPPRDeltavif plasmid alone; a combination of FIV-pPPRDeltavif DNA and feline granulocyte macrophage-colony stimulating factor (GM-CSF) and tumor necrosis factor (TNF)-alpha expression plasmids; or a combination of FIV-pPPRDeltavif and feline interleukin (IL)-15 plasmids. |
| 1476 | 19464559 | Vaccine protocols included FIV-pPPRDeltavif plasmid alone; a combination of FIV-pPPRDeltavif DNA and feline granulocyte macrophage-colony stimulating factor (GM-CSF) and tumor necrosis factor (TNF)-alpha expression plasmids; or a combination of FIV-pPPRDeltavif and feline interleukin (IL)-15 plasmids. |
| 1477 | 19464559 | Cats immunized with FIV-pPPRDeltavif, GM-CSF and TNF-alpha plasmids demonstrated an increased frequency of FIV-specific T cell proliferation responses compared to other vaccine groups. |
| 1478 | 19464559 | Cats immunized with FIV-pPPRDeltavif, GM-CSF and TNF-alpha plasmids demonstrated an increased frequency of FIV-specific T cell proliferation responses compared to other vaccine groups. |
| 1479 | 19464559 | Cats immunized with FIV-pPPRDeltavif, GM-CSF and TNF-alpha plasmids demonstrated an increased frequency of FIV-specific T cell proliferation responses compared to other vaccine groups. |
| 1480 | 19464559 | Cats immunized with FIV-pPPRDeltavif, GM-CSF and TNF-alpha plasmids demonstrated an increased frequency of FIV-specific T cell proliferation responses compared to other vaccine groups. |
| 1481 | 19464559 | However, prior immunization with FIV-pPPRDeltavif, GM-CSF, and TNF-alpha plasmids resulted in preservation of CD4 T cell functions, including mitogen-induced cytokine expression and antigen-specific proliferation upon infection with FIV. |
| 1482 | 19464559 | However, prior immunization with FIV-pPPRDeltavif, GM-CSF, and TNF-alpha plasmids resulted in preservation of CD4 T cell functions, including mitogen-induced cytokine expression and antigen-specific proliferation upon infection with FIV. |
| 1483 | 19464559 | However, prior immunization with FIV-pPPRDeltavif, GM-CSF, and TNF-alpha plasmids resulted in preservation of CD4 T cell functions, including mitogen-induced cytokine expression and antigen-specific proliferation upon infection with FIV. |
| 1484 | 19464559 | However, prior immunization with FIV-pPPRDeltavif, GM-CSF, and TNF-alpha plasmids resulted in preservation of CD4 T cell functions, including mitogen-induced cytokine expression and antigen-specific proliferation upon infection with FIV. |
| 1485 | 19458207 | Among the consistently upregulated cytokines detected in the immune cocultures are gamma interferon, growth differentiation factor 15, interleukin-21 (IL-21), IL-27, and tumor necrosis factor alpha. |
| 1486 | 19428898 | In BALB/c mice the vaccine preparation induced antigen-specific multi-functional CD4(+) T cells capable of producing IFN-gamma, IL-2, and/or TNF-alpha upon antigen re-exposure, and MPL-SE was indispensable to direct immune responses to SMT towards Th1. |
| 1487 | 19428835 | In order to obtain full functional capacity, these DCs need to be maturated, and the current "gold standard" for this process is maturation with TNF-alpha, IL-1beta, IL-6 and PGE(2) used for generating standard DCs (sDC). |
| 1488 | 19428835 | We observed that maturation by IFN-alpha differs from sDC maturation: The major phenotypic change after IFN-alpha maturation was dose-dependent up-regulation of CD38 but not CD83, while sDCs expressed the opposite profile with low CD38 and high CD83 expression. |
| 1489 | 19428835 | Similarly, maturation by Poly I:C leads to CD38high, CD83low DCs indicating a functional relationship between CD38, IFN-alpha and TLR3. |
| 1490 | 19428835 | Thus, CD38 appear to be a relevant marker for activation by TLR3 or IFN-alpha. |
| 1491 | 19428835 | Addition of IFN-alpha to the sDC cocktail results in up-regulation of both CD38 and CD83 and improved capacity for induction of autologous T-cell responses despite few other changes in DC phenotype and cytokine secretion. |
| 1492 | 19428835 | Our observations suggest that IFN-alpha could be included in maturation protocols for clinical grade DCs used for immunotherapy against cancer and should be included if DCs are used for CD8+ T-cell stimulation in vitro. |
| 1493 | 19428830 | In vitro, the adjuvant combination of CpG ODN, indolicidin and polyphosphazene (CpG/indol/PP) enhanced the secretion of TNF-alpha, IL-12p40, and IL-6 by bone marrow-derived DCs (BMDCs) when compared to the individual components. |
| 1494 | 19428829 | Furthermore, the addition of polyphosphazene to CpG ODN and indolicidin dose-dependently enhanced the secretion of the cytokines IFN-alpha, TNF-alpha and IFN-gammain vitro, indicating that polyphosphazene can also synergize with CpG ODN and indolicidin to stimulate innate immune responses. |
| 1495 | 19424635 | BM-DCs were loaded with MC38 colon carcinoma cell lysate (TAg) alone, to become partially differentiated, or were additionally stimulated with inflammatory cytokines such as TNF-alpha, IFN-gamma, or IL-12 to reach complete maturity. |
| 1496 | 19424635 | BM-DCs simultaneously stimulated with TAg and cytokines (especially IL-12 or IFN-gamma+IL-12) were in vitro more effective immune response activators than BM-DC/TAg cells. |
| 1497 | 19406180 | However, intradermally inoculated hamsters presented a robust Th1-like immune response, characterized by high levels of INF-gamma and TNF-alpha cytokines, detected in the liver of animals challenged with virulent trophozoites. |
| 1498 | 19406102 | TNF superfamily member, TL1A, is a potential mucosal vaccine adjuvant. |
| 1499 | 19406102 | TNF superfamily member, TL1A, is a potential mucosal vaccine adjuvant. |
| 1500 | 19406102 | Among the TNFS cytokines, intranasal immunization with OVA plus APRIL, TL1A, and TNF-alpha exhibited stronger immune response than those immunized with OVA alone. |
| 1501 | 19406102 | Among the TNFS cytokines, intranasal immunization with OVA plus APRIL, TL1A, and TNF-alpha exhibited stronger immune response than those immunized with OVA alone. |
| 1502 | 19406102 | The OVA-specific immune response of TL1A was characterized by high levels of serum IgG1 and increased production of IL-4 and IL-5 from splenocytes of immunized mice, suggesting that TL1A might induce Th2-type responses. |
| 1503 | 19406102 | The OVA-specific immune response of TL1A was characterized by high levels of serum IgG1 and increased production of IL-4 and IL-5 from splenocytes of immunized mice, suggesting that TL1A might induce Th2-type responses. |
| 1504 | 19384924 | The well characterized human-mouse chimeric G250 (cG250) antibody has been shown in human studies to specifically enrich in CA-IX positive tumors and was chosen as a carrier for site specific delivery of TNF in form of our IgG-TNF-fusion protein (cG250-TNF) to RCC xenografts. |
| 1505 | 19380779 | LPS is a natural adjuvant that potentiates Ag-specific T cell survival and Th1 differentiation by stimulating MyD88 and Toll/IL-1R domain-containing adaptor-inducing IFN-beta (TRIF) signaling pathways. |
| 1506 | 19380779 | Most of the T cells primed in TRIF-deficient mice failed to up-regulate CXCR3 and had an overall reduced capacity to produce IFN-gamma, demonstrating effector T cell differentiation was linked to their migration. |
| 1507 | 19380779 | Although TNF neutralization reduced T cell numbers, its coneutralization with IL-10 unexpectedly restored the T cells, suggesting the balance between pro- and anti-inflammatory cytokines influences T cell survival rather than their magnitude. |
| 1508 | 19380779 | Boosting with a CD40 agonist in addition to LPS restored the effector CD8 T cell response in livers of TRIF-deficient mice while only partially restoring CD4 T cells, suggesting that LPS primes CD8 and CD4 T cell immunity through different mechanisms. |
| 1509 | 19364838 | B-cell activating factor (BAFF), a member of the TNF family, is a potent cytokine with stimulatory effects on B and T cells. |
| 1510 | 19357176 | Here we show that a primary CD8(+) T-cell response can be induced by HIV-1 peptide-loaded DC derived from blood monocytes of HIV-1-negative adults and neonates (moDC) and by Langerhans cells (LC) and interstitial, dermal-intestinal DC (idDC) derived from CD34(+) stem cells of neonatal cord blood. |
| 1511 | 19357176 | Optimal priming of single-cell gamma interferon (IFN-gamma) production by CD8(+) T cells required CD4(+) T cells and was broadly directed to multiple regions of Gag, Env, and Nef that corresponded to known and predicted major histocompatibility complex class I epitopes. |
| 1512 | 19357176 | Polyfunctional CD8(+) T-cell responses, defined as single-cell production of more than one cytokine (IFN-gamma, interleukin 2, or tumor necrosis factor alpha), chemokine (macrophage inhibitory factor 1beta), or cytotoxic degranulation marker CD107a, were primed by moDC, LC, and idDC to HIV-1 Gag and reverse transcriptase epitopes, as well as to Epstein-Barr virus and influenza A virus epitopes. |
| 1513 | 19342965 | Immature dendritic cells (iDCs) are often produced by the stimulation of peripheral blood monocytes with interleukin (IL)-4 and granulocyte macrophage-colony stimulating factor. |
| 1514 | 19342965 | Immature dendritic cells (iDCs) are often produced by the stimulation of peripheral blood monocytes with interleukin (IL)-4 and granulocyte macrophage-colony stimulating factor. |
| 1515 | 19342965 | Immature dendritic cells (iDCs) are often produced by the stimulation of peripheral blood monocytes with interleukin (IL)-4 and granulocyte macrophage-colony stimulating factor. |
| 1516 | 19342965 | The purpose of this study was to determine if the DC maturation cocktail LPS plus IFN-gamma could be improved by the addition of 2 other DC maturation agents IL-1beta and tumor necrosis factor (TNF)-alpha. |
| 1517 | 19342965 | The purpose of this study was to determine if the DC maturation cocktail LPS plus IFN-gamma could be improved by the addition of 2 other DC maturation agents IL-1beta and tumor necrosis factor (TNF)-alpha. |
| 1518 | 19342965 | The purpose of this study was to determine if the DC maturation cocktail LPS plus IFN-gamma could be improved by the addition of 2 other DC maturation agents IL-1beta and tumor necrosis factor (TNF)-alpha. |
| 1519 | 19342965 | Monocytes were isolated from the peripheral blood mononuclear cell concentrates by elutriation and were incubated for 3 days with granulocyte macrophage-colony stimulating factor and IL-4 to produce iDCs. iDCs from each subject were divided into 3 and were incubated for 24 hours with LPS plus IFN-gamma; LPS, IFN-gamma, plus IL-1beta; or LPS, IFN-gamma, IL-1beta, plus TNF-alpha to produce mDCs. |
| 1520 | 19342965 | Monocytes were isolated from the peripheral blood mononuclear cell concentrates by elutriation and were incubated for 3 days with granulocyte macrophage-colony stimulating factor and IL-4 to produce iDCs. iDCs from each subject were divided into 3 and were incubated for 24 hours with LPS plus IFN-gamma; LPS, IFN-gamma, plus IL-1beta; or LPS, IFN-gamma, IL-1beta, plus TNF-alpha to produce mDCs. |
| 1521 | 19342965 | Monocytes were isolated from the peripheral blood mononuclear cell concentrates by elutriation and were incubated for 3 days with granulocyte macrophage-colony stimulating factor and IL-4 to produce iDCs. iDCs from each subject were divided into 3 and were incubated for 24 hours with LPS plus IFN-gamma; LPS, IFN-gamma, plus IL-1beta; or LPS, IFN-gamma, IL-1beta, plus TNF-alpha to produce mDCs. |
| 1522 | 19342965 | The DCs were compared by measuring the expression of costimulator and antigen presenting molecules (CD80, CD83, CD86, and human leukocyte antigen-DR) by flow cytometry, cytokine production (IL-12p70 and IL-10) by enzyme-linked immunosorbent assay and global gene expression using an oligonucleotide microarray. |
| 1523 | 19342965 | The DCs were compared by measuring the expression of costimulator and antigen presenting molecules (CD80, CD83, CD86, and human leukocyte antigen-DR) by flow cytometry, cytokine production (IL-12p70 and IL-10) by enzyme-linked immunosorbent assay and global gene expression using an oligonucleotide microarray. |
| 1524 | 19342965 | The DCs were compared by measuring the expression of costimulator and antigen presenting molecules (CD80, CD83, CD86, and human leukocyte antigen-DR) by flow cytometry, cytokine production (IL-12p70 and IL-10) by enzyme-linked immunosorbent assay and global gene expression using an oligonucleotide microarray. |
| 1525 | 19342965 | There was no benefit of adding IL-1beta and TNF-alpha to LPS and IFN-gamma to produce mDCs. |
| 1526 | 19342965 | There was no benefit of adding IL-1beta and TNF-alpha to LPS and IFN-gamma to produce mDCs. |
| 1527 | 19342965 | There was no benefit of adding IL-1beta and TNF-alpha to LPS and IFN-gamma to produce mDCs. |
| 1528 | 19342665 | S221 did not replicate well in wild-type mice, but did induce a CD8(+) T cell response, whereas viral replication and a robust CD8(+) T cell response were observed after infection of IFN-alpha/betaR(-/-) mice. |
| 1529 | 19342665 | Depletion of CD8(+) T cells from IFN-alpha/betaR(-/-) mice before infection resulted in significantly higher viral loads compared with undepleted mice. |
| 1530 | 19342665 | Mapping the specificity of the CD8(+) T cell response led to the identification of 12 epitopes derived from 6 of the 10 DENV proteins, with a similar immunodominance hierarchy observed in wild-type and IFN-alpha/betaR(-/-) mice. |
| 1531 | 19342665 | DENV-specific CD8(+) T cells produced IFN-gamma, TNF-alpha, expressed cell surface CD107a, and exhibited cytotoxic activity in vivo. |
| 1532 | 19330258 | Genetic polymorphisms in vitamin D receptor, vitamin D-binding protein, Toll-like receptor 2, nitric oxide synthase 2, and interferon-gamma genes and its association with susceptibility to tuberculosis. |
| 1533 | 19330258 | Many studies have focused on the candidate genes for tuberculosis susceptibility ranging from those expressed in several cells from the innate or adaptive immune system such as Toll-like receptors, cytokines (TNF-alpha, TGF-beta, IFN-gamma, IL-1b, IL-1RA, IL-12, IL-10), nitric oxide synthase and vitamin D, both nuclear receptors and their carrier, the vitamin D-binding protein (VDBP). |
| 1534 | 19330258 | Thus, in this mini-review, we summarize the current state of investigation on some of the genetic determinants, such as the candidate polymorphisms of vitamin D, VDBP, Toll-like receptor, nitric oxide synthase 2 and interferon-gamma genes, to generate resistance or susceptibility to M. tuberculosis infection. |
| 1535 | 19328554 | An in vivo administration of rLyccys could significantly up-regulate the expression levels of large yellow croaker tumor necrosis factor-alpha2 (TNF-alpha2) and interleukin-10 in spleen and kidney, but to a lesser extent increase TNF-alpha1 expression. |
| 1536 | 19321612 | Persistent cytokine responses of antigen-specific CD4(+) and CD8(+) T cells of the central memory as well as the effector memory phenotype, capable of simultaneously eliciting multiple cytokines (IFN-gamma, interleukin 2, and tumor necrosis factor alpha), were induced. |
| 1537 | 19309560 | F1, V, and F1-V proteins engaged TLR2 signalling and activated IL-6 and CXCL-8 production by monocytes, without affecting the expression of TNF-alpha, IL-12, IL-10, IL-1beta, and CXCL10. |
| 1538 | 19307995 | In vitro analysis confirmed that OK-DC were mature, secreted tumor necrosis factor-alpha, interleukin-6, and interleukin-12, and stimulated both T cell and natural killer cell function. |
| 1539 | 19303121 | Using real-time PCR quantification assay, expression of Th1 (IL-2, IL-12p40, IFNgamma); Th2 (IL-4, IL-10) and inflammatory (IL-6, TNFalpha) cytokines were quantified weekly for the entire three-week duration of the experiment. |
| 1540 | 19303121 | Using real-time PCR quantification assay, expression of Th1 (IL-2, IL-12p40, IFNgamma); Th2 (IL-4, IL-10) and inflammatory (IL-6, TNFalpha) cytokines were quantified weekly for the entire three-week duration of the experiment. |
| 1541 | 19303121 | Using real-time PCR quantification assay, expression of Th1 (IL-2, IL-12p40, IFNgamma); Th2 (IL-4, IL-10) and inflammatory (IL-6, TNFalpha) cytokines were quantified weekly for the entire three-week duration of the experiment. |
| 1542 | 19303121 | It was noted that IFNgamma, IL-10 and TNFalpha had peaked on week three post-vaccination while the remaining cytokines peaked on the second week and decreased by the third week. |
| 1543 | 19303121 | It was noted that IFNgamma, IL-10 and TNFalpha had peaked on week three post-vaccination while the remaining cytokines peaked on the second week and decreased by the third week. |
| 1544 | 19303121 | It was noted that IFNgamma, IL-10 and TNFalpha had peaked on week three post-vaccination while the remaining cytokines peaked on the second week and decreased by the third week. |
| 1545 | 19303121 | The counteraction between IFNgamma and IL-4 was noted as well as the possible suppressive action of IL-10 to that of IL-2 and IL-12, which is a common phenomenon between Th1 and Th2 cytokines. |
| 1546 | 19303121 | The counteraction between IFNgamma and IL-4 was noted as well as the possible suppressive action of IL-10 to that of IL-2 and IL-12, which is a common phenomenon between Th1 and Th2 cytokines. |
| 1547 | 19303121 | The counteraction between IFNgamma and IL-4 was noted as well as the possible suppressive action of IL-10 to that of IL-2 and IL-12, which is a common phenomenon between Th1 and Th2 cytokines. |
| 1548 | 19303121 | Synergy between TNFa and IL-6 was also observed. |
| 1549 | 19303121 | Synergy between TNFa and IL-6 was also observed. |
| 1550 | 19303121 | Synergy between TNFa and IL-6 was also observed. |
| 1551 | 19291915 | Blast cells of two relapsed AML patients were harvested for DC generation in serum-free culture medium containing clinical-grade cytokines GM-CSF, IL-4 and TNF-alpha. |
| 1552 | 19291915 | These DC vaccines exhibited mature DC surface phenotypic markers of CD83, CD86 and HLA-DR, and negative for haemopoietic markers. |
| 1553 | 19291774 | Indirect action of tumor necrosis factor-alpha in liver injury during the CD8+ T cell response to an adeno-associated virus vector in mice. |
| 1554 | 19279169 | Characterization of protective mucosal and systemic immune responses elicited by pneumococcal surface protein PspA and PspC nasal vaccines against a respiratory pneumococcal challenge in mice. |
| 1555 | 19279169 | Pneumococcal surface protein A (PspA) and PspC are virulence factors that are involved in the adhesion of Streptococcus pneumoniae to epithelial cells and/or evasion from the immune system. |
| 1556 | 19279169 | Intranasal immunization with PspA5 elicited the highest level of protection, characterized by increased levels of secretion of interleukin-17 and gamma interferon by lung and spleen cells, respectively, and low levels of tumor necrosis factor alpha in the respiratory tract. |
| 1557 | 19278729 | Peptidoglycan (PGN), lipoteichoic acid (LTA), lipoprotein (LP), and DNA were also isolated from the bacteria, and used to stimulate BM-DCs. |
| 1558 | 19278729 | Peptidoglycan (PGN), lipoteichoic acid (LTA), lipoprotein (LP), and DNA were also isolated from the bacteria, and used to stimulate BM-DCs. |
| 1559 | 19278729 | Peptidoglycan (PGN), lipoteichoic acid (LTA), lipoprotein (LP), and DNA were also isolated from the bacteria, and used to stimulate BM-DCs. |
| 1560 | 19278729 | Peptidoglycan (PGN), lipoteichoic acid (LTA), lipoprotein (LP), and DNA were also isolated from the bacteria, and used to stimulate BM-DCs. |
| 1561 | 19278729 | Stimulation with TNF, S. gordonii, PGN, LTA, or LP all resulted in increased surface expression of MHCII, CD80, and CD86, compared to unstimulated BM-DCs. |
| 1562 | 19278729 | Stimulation with TNF, S. gordonii, PGN, LTA, or LP all resulted in increased surface expression of MHCII, CD80, and CD86, compared to unstimulated BM-DCs. |
| 1563 | 19278729 | Stimulation with TNF, S. gordonii, PGN, LTA, or LP all resulted in increased surface expression of MHCII, CD80, and CD86, compared to unstimulated BM-DCs. |
| 1564 | 19278729 | Stimulation with TNF, S. gordonii, PGN, LTA, or LP all resulted in increased surface expression of MHCII, CD80, and CD86, compared to unstimulated BM-DCs. |
| 1565 | 19278729 | Stimulation with S. gordonii elicited IL-6, IL-10, and IL-12p70 production from the BM-DCs, while stimulation with the bacterial components induced some or all of the three cytokines. |
| 1566 | 19278729 | Stimulation with S. gordonii elicited IL-6, IL-10, and IL-12p70 production from the BM-DCs, while stimulation with the bacterial components induced some or all of the three cytokines. |
| 1567 | 19278729 | Stimulation with S. gordonii elicited IL-6, IL-10, and IL-12p70 production from the BM-DCs, while stimulation with the bacterial components induced some or all of the three cytokines. |
| 1568 | 19278729 | Stimulation with S. gordonii elicited IL-6, IL-10, and IL-12p70 production from the BM-DCs, while stimulation with the bacterial components induced some or all of the three cytokines. |
| 1569 | 19278729 | When BM-DCs were simultaneously stimulated with S. gordonii and TNF, a marginal increase in surface marker upregulation was observed, and the two stimuli synergized to elicit substantially greater quantities of IL-6, IL-10, and IL-12p70. |
| 1570 | 19278729 | When BM-DCs were simultaneously stimulated with S. gordonii and TNF, a marginal increase in surface marker upregulation was observed, and the two stimuli synergized to elicit substantially greater quantities of IL-6, IL-10, and IL-12p70. |
| 1571 | 19278729 | When BM-DCs were simultaneously stimulated with S. gordonii and TNF, a marginal increase in surface marker upregulation was observed, and the two stimuli synergized to elicit substantially greater quantities of IL-6, IL-10, and IL-12p70. |
| 1572 | 19278729 | When BM-DCs were simultaneously stimulated with S. gordonii and TNF, a marginal increase in surface marker upregulation was observed, and the two stimuli synergized to elicit substantially greater quantities of IL-6, IL-10, and IL-12p70. |
| 1573 | 19278729 | The effect of TNF was abolished when BM-DCs were obtained from mice deficient for either TNFR1 or TNFR2, and cytokine induction by S. gordonii was entirely dependent on functional MyD88. |
| 1574 | 19278729 | The effect of TNF was abolished when BM-DCs were obtained from mice deficient for either TNFR1 or TNFR2, and cytokine induction by S. gordonii was entirely dependent on functional MyD88. |
| 1575 | 19278729 | The effect of TNF was abolished when BM-DCs were obtained from mice deficient for either TNFR1 or TNFR2, and cytokine induction by S. gordonii was entirely dependent on functional MyD88. |
| 1576 | 19278729 | The effect of TNF was abolished when BM-DCs were obtained from mice deficient for either TNFR1 or TNFR2, and cytokine induction by S. gordonii was entirely dependent on functional MyD88. |
| 1577 | 19278729 | Synergistic IL-10 induction by S. gordonii and TNF was not observed in TLR-2(-/-) BM-DCs, and TNF was found to cause TLR-2 upregulation, providing at least a partial mechanism for the observed synergy. |
| 1578 | 19278729 | Synergistic IL-10 induction by S. gordonii and TNF was not observed in TLR-2(-/-) BM-DCs, and TNF was found to cause TLR-2 upregulation, providing at least a partial mechanism for the observed synergy. |
| 1579 | 19278729 | Synergistic IL-10 induction by S. gordonii and TNF was not observed in TLR-2(-/-) BM-DCs, and TNF was found to cause TLR-2 upregulation, providing at least a partial mechanism for the observed synergy. |
| 1580 | 19278729 | Synergistic IL-10 induction by S. gordonii and TNF was not observed in TLR-2(-/-) BM-DCs, and TNF was found to cause TLR-2 upregulation, providing at least a partial mechanism for the observed synergy. |
| 1581 | 19277872 | THP-1 cells were exposed to these MPs for 24 h and characteristics of cell morphology, tumor necrosis factor-alpha (TNF-alpha) release, lactate dehydrogenase (LDH), N-acetyl-beta-D: -glucosaminidase (NAG) and alkaline phosphatase (ALP) activity in AMPhi culture supernatants were measured. |
| 1582 | 19273561 | These two beta-glucans failed to stimulate TNF-alpha in Dectin-1 (beta-glucan receptor) knockout BMDCs. |
| 1583 | 19273561 | These two beta-glucans failed to stimulate TNF-alpha in Dectin-1 (beta-glucan receptor) knockout BMDCs. |
| 1584 | 19273561 | The upregulation of TNF-alpha and downregulation of IL-12p70 required Dectin-1, but not IL-10. |
| 1585 | 19273561 | The upregulation of TNF-alpha and downregulation of IL-12p70 required Dectin-1, but not IL-10. |
| 1586 | 19273561 | Finally, costimulation of BMDCs with YGPs and either the TLR9 ligand, CpG, or the TLR2/1 ligand, Pam(3)CSK(4), resulted in upregulated secretion of IL-1alpha and IL-10 and downregulated secretion of IL-1beta, IL-6, and IFN-gamma-inducible protein 10 but had no significant effects on IL-12p40, keratinocyte-derived chemokine, monocyte chemotactic protein 1, or macrophage inflammatory protein alpha, compared with the TLR ligand alone. |
| 1587 | 19273561 | Finally, costimulation of BMDCs with YGPs and either the TLR9 ligand, CpG, or the TLR2/1 ligand, Pam(3)CSK(4), resulted in upregulated secretion of IL-1alpha and IL-10 and downregulated secretion of IL-1beta, IL-6, and IFN-gamma-inducible protein 10 but had no significant effects on IL-12p40, keratinocyte-derived chemokine, monocyte chemotactic protein 1, or macrophage inflammatory protein alpha, compared with the TLR ligand alone. |
| 1588 | 19272649 | Transcription of tumour necrosis factor-alpha (tnf alpha) and interleukin-6 (il6) genes, two cytokines directly related to TLR9 induction with unmethylated CpG oligodeoxynucleotides (CpG ODNs), was solely observed in head kidney and spleen of the fish immunised with pAE6-G. |
| 1589 | 19272649 | Transcription of tumour necrosis factor-alpha (tnf alpha) and interleukin-6 (il6) genes, two cytokines directly related to TLR9 induction with unmethylated CpG oligodeoxynucleotides (CpG ODNs), was solely observed in head kidney and spleen of the fish immunised with pAE6-G. |
| 1590 | 19272649 | Thus, the glycoprotein G of VHSV could be more implicated in triggering the pathways for TNF-alpha and IL6 production than the recognition of the unmethylated CpG motifs of the plasmid backbone by OmTLR9. |
| 1591 | 19272649 | Thus, the glycoprotein G of VHSV could be more implicated in triggering the pathways for TNF-alpha and IL6 production than the recognition of the unmethylated CpG motifs of the plasmid backbone by OmTLR9. |
| 1592 | 19268606 | The activation and expansion of naïve T cells require costimulatory signals provided by CD28 and TNF family members. |
| 1593 | 19268606 | Recent in vivo evidence, however, has challenged this and shown that both CD4+ and CD8+ memory T cells require CD28 costimulation for maximal expansion and pathogen clearance. |
| 1594 | 19261771 | CD3(+), CD4(+), CD8(+), and T-cell receptor gammadelta-positive (gammadelta(+)) cells were identified in the gate of blast lymphocytes. |
| 1595 | 19261771 | Gamma interferon, tumor necrosis factor alpha, interleukin-4 (IL-4), and IL-10 levels in supernatants and serum anti-PT IgG levels were determined using enzyme-linked immunosorbent assay (ELISA). |
| 1596 | 19261771 | The frequencies of proliferating CD4(+), CD8(+), and gammadelta(+) cells, cytokine concentrations in supernatants, and the geometric mean titers of anti-PT IgG were similar for the two vaccination groups. |
| 1597 | 19237526 | Only low doses were sublethal, and resolution of sublethal cloud aerosol infection was dependent on gamma interferon (IFN-gamma), tumor necrosis factor alpha, and inducible nitric oxide synthase. |
| 1598 | 19237318 | Low doses of alpha-defensins1-3 up-regulated CD83, CD86 and HLA-DR expression, increased TNF-alpha, IL-1beta, IL-12p40, IL-10 and IL-8 secretion, and slightly augmented allostimulatory capacity. |
| 1599 | 19237318 | Low doses of alpha-defensins1-3 up-regulated CD83, CD86 and HLA-DR expression, increased TNF-alpha, IL-1beta, IL-12p40, IL-10 and IL-8 secretion, and slightly augmented allostimulatory capacity. |
| 1600 | 19237318 | By contrast, high doses down-regulated CD86 and HLA-DR expression, TNF-alpha, IL-1beta, IL-12p40 and IL-10 secretion and allostimulatory capacity, whereas strongly up-regulated IL-8. |
| 1601 | 19237318 | By contrast, high doses down-regulated CD86 and HLA-DR expression, TNF-alpha, IL-1beta, IL-12p40 and IL-10 secretion and allostimulatory capacity, whereas strongly up-regulated IL-8. |
| 1602 | 19237318 | Furthermore, during the MDDC differentiation process, high doses of alpha-defensins1-3 affected CD14, CD11c and CD86 expression and strongly up-regulated IL-8. |
| 1603 | 19237318 | Furthermore, during the MDDC differentiation process, high doses of alpha-defensins1-3 affected CD14, CD11c and CD86 expression and strongly up-regulated IL-8. |
| 1604 | 19234218 | BCG induced TNF-alpha, IFN-gamma, and IDO mRNA steady-state transcripts in the brain as well as the enzyme 3-hydroxyanthranilic acid oxygenase (3-HAO) that lies downstream of IDO and generates the neuroactive metabolite, quinolinic acid. |
| 1605 | 19227283 | Experimental granulomatosis inflammation induced by BCG-M shown in mice with different type of an immune response has established that with the Tx1 immune type, the granulomatous inflammatory process is more pronounced and disseminated with the high production of tumor necrosis factor-a and interferon-gamma being found. |
| 1606 | 19224636 | TB cases had significantly higher levels of IFN-gamma(+)TNF-alpha(+)IL-2(+)CD4(+)T cells compared with contacts. |
| 1607 | 19224636 | TB cases had significantly higher levels of IFN-gamma(+)TNF-alpha(+)IL-2(+)CD4(+)T cells compared with contacts. |
| 1608 | 19224636 | TB cases also had a significantly higher proportion of cells single-positive for TNF-alpha, but lower proportion of cells producing IL-2 alone and these differences were seen for both CD4(+)and CD8(+) T cells. |
| 1609 | 19224636 | TB cases also had a significantly higher proportion of cells single-positive for TNF-alpha, but lower proportion of cells producing IL-2 alone and these differences were seen for both CD4(+)and CD8(+) T cells. |
| 1610 | 19224636 | Cytokine profiles from culture supernatants were significantly biased toward a Th1 phenotype (IFN-gamma and IL-12(p40)) together with a complete abrogation of IL-17 secretion in TB cases. |
| 1611 | 19224636 | Cytokine profiles from culture supernatants were significantly biased toward a Th1 phenotype (IFN-gamma and IL-12(p40)) together with a complete abrogation of IL-17 secretion in TB cases. |
| 1612 | 19219024 | RhCMV vectors expressing SIV Gag, Rev-Tat-Nef and Env persistently infected rhesus macaques, regardless of preexisting RhCMV immunity, and primed and maintained robust, SIV-specific CD4+ and CD8+ TEM cell responses (characterized by coordinate tumor necrosis factor, interferon-gamma and macrophage inflammatory protein-1beta expression, cytotoxic degranulation and accumulation at extralymphoid sites) in the absence of neutralizing antibodies. |
| 1613 | 19209886 | Of these, eight immunoreactive proteins represented homologues of the known mycobacterial antigens, namely heat shock protein GroEL, antigen 85A, elongation factor Tu (EF-Tu), L-asparaginase, polyketide synthase, PE-PGRS, PPE, and superoxide dismutase (SOD). |
| 1614 | 19209886 | The secretome eluate caused up-regulation of the proinflammatory cytokines TNF-alpha, IL-1beta, IL-6, and IL-18 and down-regulation of the anti-inflammatory cytokine IL-10, implying a potential of the secreted antigens to cause host immune response underlying the M. immunogenum-induced lung disease HP. |
| 1615 | 19201885 | In addition, mRNA expression levels of a B cell-activating factor of the TNF family were significantly increased in the spleens of MyD88(-/-) mice after oral administration, implying that T cell-independent B cell switching might be also enhanced in the MyD88 signal-deficient condition. |
| 1616 | 19188599 | Antigen-specific responses from protected monkeys receiving BCG and Mtb72F/AS02A had a distinctive cytokine profile characterized by an increased ratio between 3 Th1 cytokines, IFN-gamma, TNF, and IL-2 and an innate cytokine, IL-6. |
| 1617 | 19181353 | However, IL-4, IL-10, TNF-alpha and IFN-gamma were expressed in significantly higher levels by survivors (for all the four cytokines in lymph nodes; for IL-4, IL-10 and TNF-alpha in spleen; for IL-4, TNF-alpha and IFN-gamma in lung, and only for TNF-alpha in brain), thus suggesting a role of these four cytokines in the adaptive response, which might contribute to protection against H. parasuis infection. |
| 1618 | 19168741 | Macrophages from neonatal and infant mice stimulated with killed pneumococci in vitro showed significantly reduced cytokine production, including that of KC, granulocyte colony-stimulating factor, granulocyte-macrophage colony-stimulating factor, macrophage chemoattractant protein 1, interleukin-6 (IL-6), IL-1alpha, tumor necrosis factor alpha, and gamma interferon, whereas IL-10 expression was significantly increased compared to that in macrophages from adult mice. |
| 1619 | 19168741 | IL-17A production from adult immune CD4(+) T cells was significantly delayed when neonatal macrophages instead of adult macrophages were used as antigen-presenting cells. |
| 1620 | 19141400 | After 7 days of culture, DCs were harvested and the expression of CD1a, CD83, CD80, CD86 and HLA-DR antigens were analyzed by flow cytometry. |
| 1621 | 19141400 | The expression of co-stimulatory and maturation markers (CD86, CD83 and HLA-DR) was higher on DCs from the culture with tumor cell lysate compared with TNF-alpha culture as a control. |
| 1622 | 19140872 | Our results demonstrates that Mycobacterium bovis BCG (M. bovis BCG) downregulates tumour necrosis factor-alpha (TNF-alpha)-induced COX-2 gene expression in alveolar epithelial cells by inhibiting the phosphorylations of Raf-1 and p38 kinases. |
| 1623 | 19140872 | Our results demonstrates that Mycobacterium bovis BCG (M. bovis BCG) downregulates tumour necrosis factor-alpha (TNF-alpha)-induced COX-2 gene expression in alveolar epithelial cells by inhibiting the phosphorylations of Raf-1 and p38 kinases. |
| 1624 | 19140872 | Further, M. bovis BCG-mediated inhibition of COX-2 or p38 mitogen-activated protein kinase could be reversed by Calyculin A, a selective inhibitor of Ser/Thr phosphatases. |
| 1625 | 19140872 | Further, M. bovis BCG-mediated inhibition of COX-2 or p38 mitogen-activated protein kinase could be reversed by Calyculin A, a selective inhibitor of Ser/Thr phosphatases. |
| 1626 | 19140872 | Moreover, M. bovis BCG inhibited the TNF-alpha-triggered NF-kappaB activation following IkappaB degradation. |
| 1627 | 19140872 | Moreover, M. bovis BCG inhibited the TNF-alpha-triggered NF-kappaB activation following IkappaB degradation. |
| 1628 | 19129472 | To focus on the latter, we studied the uptake of fixed and fluorescently labeled bacterial particles in intestinal and bronchoepithelial cell cultures and found it to be enhanced in Caco-2BBe and NCI-H292 cells after treatment with tumor necrosis factor alpha and an agonist antibody against the lymphotoxin beta receptor. |
| 1629 | 19124765 | Typhi(F1) enhanced the activation and maturation of neonatal CD11c+ dendritic cells, shown by increased expression of CD80, CD86, CD40, and MHC-II cell surface markers and production of proinflammatory cytokines IL-12, TNF-alpha, IL-6, and MCP-1. |
| 1630 | 19124765 | Typhi(F1)-stimulated neonatal DC had improved capacity for Ag presentation and T cell stimulation in vitro and induced F1-specific CD4+ and CD8+ T cell responses when adoptively transferred to newborn mice. |
| 1631 | 19124761 | Harvested early, these cells produced IFN-gamma, TNF, and RANTES after ex vivo stimulation. |
| 1632 | 19124761 | By contrast, those recruited 5 days after challenge made IL-4, IL-5, and IL-10. |
| 1633 | 19110021 | We demonstrate for the first time that treatment with yeast-CEA can activate human DCs, resulting in increases in surface expression of CD80, CD83, CD54, CD58, and MHC class II, and increased production by DCs of IL-12p70, TNF-alpha, IFN-gamma, IL-8, IL-2, IL-13, IL-10, and IL-1beta. |
| 1634 | 19109135 | Activated human neonatal CD8+ T cells are subject to immunomodulation by direct TLR2 or TLR5 stimulation. |
| 1635 | 19109135 | In concert with TCR stimulation, only Pam(3)Cys (palmitoyl-3-Cys-Ser-(Lys)(4)) and flagellin monomers significantly enhanced proliferation, CD25(+) expression, IL-2, IFN-gamma, TNF-alpha, and intracellular granzyme B expression. |
| 1636 | 19109135 | TLR2 and TLR5 mRNA was detected in the CD8(+) T cells. |
| 1637 | 19109135 | Blocking studies confirmed that the increase in IFN-gamma production was by the direct triggering of surface TLR2 or TLR5. |
| 1638 | 19109135 | The simultaneous exposure of CD8(+) T cells to both TLR agonists had an additive effect on IFN-gamma production. |
| 1639 | 19097981 | After administration, whole lungs of C57Bl/6 mice were lavaged with saline; COX-2 expression and PGE(2) release by alveolar MØ and tumor necrosis factor (TNF)-alpha and nitric oxide levels in the lung lavage were monitored. |
| 1640 | 19095031 | Construction and characterization of a novel DNA vaccine that is potent antigen-specific tolerizing therapy for experimental arthritis by increasing CD4+CD25+Treg cells and inducing Th1 to Th2 shift in both cells and cytokines. |
| 1641 | 19095031 | The resulting recombinant plasmid pcDNA-CCOL2A1 was produced in Escherichia coli, purified, characterized and used as a tolerizing DNA vaccine for the treatment of collagen-induced arthritis (CIA). |
| 1642 | 19095031 | Furthermore, the action mechanism behind this efficacy can be at least partially attributed to increased CD4(+)CD25(+) T regulatory cells, which specifically down-modulate the T lymphocyte proliferative response to CCII, induce a shift of Th1 to Th2 cells, as well as down-regulate Th1-cytokine TNF-alpha, while up-regulating both Th2-cytokine IL-10 and Th3-cytokine TGF-beta. |
| 1643 | 19054933 | RT-PCR revealed that all allergen-treated mice had marked increase of IL-13, IL-4 and TNF-alpha gene expressions, slight increase of IL-5 gene expression, and absence of detectable IFN-gamma gene expression in comparison to the non-allergenic controls. |
| 1644 | 19036811 | We therefore expressed a viral protein that constitutively activates NF-kappaB, vFLIP from Kaposi's sarcoma-associated herpesvirus (KSHV), in a lentivector to mature DCs. vFLIP activated NF-kappaB in mouse bone marrow-derived DCs in vitro and matured these DCs to a similar extent as lipopolysaccharide; costimulatory markers CD80, CD86, CD40, and ICAM-1 were upregulated and tumor necrosis factor alpha and interleukin-12 secreted. |
| 1645 | 19036430 | At the lowest antigen dose (0.01 microg/mL), PK3-OVA-poly(I:C) microparticles also enhanced TNF-alpha and IL-2 production in CD8(+) T cells. |
| 1646 | 19027810 | To evaluate cytokines levels (TNFalpha, IFNgamma, IL6, IL10) we used real-time PCR. |
| 1647 | 19027322 | Peripheral blood samples were measured by ELISA for plasma levels of IL-2, IL-6, TNF-alpha, IFN-gamma, and IFN-alpha. |
| 1648 | 19027322 | Peripheral blood samples were measured by ELISA for plasma levels of IL-2, IL-6, TNF-alpha, IFN-gamma, and IFN-alpha. |
| 1649 | 19027322 | The pattern of production of IFN-gamma was opposite to that of TNF-alpha, but statistical significance was stronger in patients receiving ATT and Dzherelo+Anemin than in Dzherelo group: -34% (P=0.004), +31.9% (P=0.008), and +17.3% (P=0.33), respectively. |
| 1650 | 19027322 | The pattern of production of IFN-gamma was opposite to that of TNF-alpha, but statistical significance was stronger in patients receiving ATT and Dzherelo+Anemin than in Dzherelo group: -34% (P=0.004), +31.9% (P=0.008), and +17.3% (P=0.33), respectively. |
| 1651 | 19020113 | We previously reported that LPS-induced de novo expression of RelB is required for generating tolerance to interleukin-1beta (IL-1beta) and tumor necrosis factor alpha (TNF-alpha) expression. |
| 1652 | 19020113 | We previously reported that LPS-induced de novo expression of RelB is required for generating tolerance to interleukin-1beta (IL-1beta) and tumor necrosis factor alpha (TNF-alpha) expression. |
| 1653 | 19020113 | RelB represses transcription by binding with heterochromatic protein 1 alpha (HP1alpha) to the proximal promoters of IL-1beta and TNF-alpha. |
| 1654 | 19020113 | RelB represses transcription by binding with heterochromatic protein 1 alpha (HP1alpha) to the proximal promoters of IL-1beta and TNF-alpha. |
| 1655 | 19020113 | In contrast, we report herein that RelB is required for sustained expression of anti-inflammatory IkappaBalpha in LPS-tolerant THP-1 cells. |
| 1656 | 19020113 | In contrast, we report herein that RelB is required for sustained expression of anti-inflammatory IkappaBalpha in LPS-tolerant THP-1 cells. |
| 1657 | 19020113 | RelB transcription activation requires binding to the IkappaBalpha proximal promoter along with NF-kappaB p50 and is associated with an apparent dimer exchange with p65. |
| 1658 | 19020113 | RelB transcription activation requires binding to the IkappaBalpha proximal promoter along with NF-kappaB p50 and is associated with an apparent dimer exchange with p65. |
| 1659 | 19020105 | The lymphoproliferative and cytokine responses (interleukin-2 [IL-2], IL-4, IL-5, IL-10, gamma interferon, and tumor necrosis factor alpha) were assessed for 11 HIV-seropositive, Cryptosporidium-positive (group I) patients; 20 HIV-seropositive, Cryptosporidium-negative (group II) patients; 10 HIV-seronegative, Cryptosporidium-positive (group III) patients, including four post-renal transplant (group IIIa) and 6 presumably immunocompetent (group IIIb) patients; and 20 HIV-seronegative, Cryptosporidium-negative healthy individuals (group IV). |
| 1660 | 19017986 | Vaccine candidates that led to reduction in lung bacterial burden following challenge-induced pluripotent CD4 and CD8 T cells, including Th1 cell responses characterized by elevated levels of Ag-specific IgG2c, IFN-gamma, and TNF. |
| 1661 | 19017986 | Priority vaccine Ags elicited pluripotent CD4 and CD8 T responses in purified protein derivative-positive donor PBMCs. |
| 1662 | 19017955 | Targeting poly(I:C) to the TLR3-independent pathway boosts effector CD8 T cell differentiation through IFN-alpha/beta. |
| 1663 | 19017955 | A higher percentage of Ag-specific CD8 T cells became IFN-gamma and TNF-alpha producers in the absence of TLR3 signaling. |
| 1664 | 19017955 | Ultimately, however, the fundamental mechanism of CD8 effector T cell differentiation through the TLR3-independent pathway was shown to be completely IFN-alpha/beta-dependent. |
| 1665 | 19013492 | TLR4 and MyD88 control protection and pulmonary granulocytic recruitment in a murine intranasal RSV immunization and challenge model. |
| 1666 | 19013492 | TLR4 and MyD88 control protection and pulmonary granulocytic recruitment in a murine intranasal RSV immunization and challenge model. |
| 1667 | 19013492 | An intranasal vaccine composed of Toll-like receptor 2 (TLR2) ligand Neisseria meningitidis outer membrane proteins and Toll-like receptor 4 (TLR4) ligand Shigella flexneri lipopolysaccharide (LPS) (Protollin) and enriched respiratory syncytial virus (RSV) proteins (eRSV) has been demonstrated to promote balanced Th1/Th2 responses without eosinophil recruitment and to protect against challenge in mouse models. |
| 1668 | 19013492 | An intranasal vaccine composed of Toll-like receptor 2 (TLR2) ligand Neisseria meningitidis outer membrane proteins and Toll-like receptor 4 (TLR4) ligand Shigella flexneri lipopolysaccharide (LPS) (Protollin) and enriched respiratory syncytial virus (RSV) proteins (eRSV) has been demonstrated to promote balanced Th1/Th2 responses without eosinophil recruitment and to protect against challenge in mouse models. |
| 1669 | 19013492 | We used TLR2, TLR4 and myeloid differentiation factor 88 (MyD88) knock-out (-/-) mice to investigate the roles of these signalling pathways on immunogenicity, protection and pulmonary infiltrates following RSV immunization and challenge. |
| 1670 | 19013492 | We used TLR2, TLR4 and myeloid differentiation factor 88 (MyD88) knock-out (-/-) mice to investigate the roles of these signalling pathways on immunogenicity, protection and pulmonary infiltrates following RSV immunization and challenge. |
| 1671 | 19013492 | In contrast, an intact MyD88 pathway was crucial to elicit a balanced type 1:type 2 immune response, characterized by increased splenocyte production of antigen-induced IFNgamma and IL-10 with concomitant reduction of IL5, IgG2a isotype switching and abrogation of pulmonary eosinophil recruitment following challenge. |
| 1672 | 19013492 | In contrast, an intact MyD88 pathway was crucial to elicit a balanced type 1:type 2 immune response, characterized by increased splenocyte production of antigen-induced IFNgamma and IL-10 with concomitant reduction of IL5, IgG2a isotype switching and abrogation of pulmonary eosinophil recruitment following challenge. |
| 1673 | 19013492 | Both TLR4 and MyD88-signalling were required for optimal protection against challenge. |
| 1674 | 19013492 | Both TLR4 and MyD88-signalling were required for optimal protection against challenge. |
| 1675 | 19013492 | The upregulation of early signalling molecules IFN-beta, TNFalpha, CD40 and CD86 were studied in splenocytes isolated from naïve TLR2, TLR4 and MyD88-/- mice following stimulation with vaccine components. |
| 1676 | 19013492 | The upregulation of early signalling molecules IFN-beta, TNFalpha, CD40 and CD86 were studied in splenocytes isolated from naïve TLR2, TLR4 and MyD88-/- mice following stimulation with vaccine components. |
| 1677 | 19013492 | Splenocytes from TLR4-/- mice displayed reduced IFN-beta while those of MyD88-/- mice elicited less TNFalpha and lower expression of CD40 and CD86 on CD11c+ cells. |
| 1678 | 19013492 | Splenocytes from TLR4-/- mice displayed reduced IFN-beta while those of MyD88-/- mice elicited less TNFalpha and lower expression of CD40 and CD86 on CD11c+ cells. |
| 1679 | 19013492 | Together, our results suggest that optimal immunogenicity and protection against RSV without risk of enhanced pulmonary inflammation requires intact TLR4/MyD88-dependent signalling. |
| 1680 | 19013492 | Together, our results suggest that optimal immunogenicity and protection against RSV without risk of enhanced pulmonary inflammation requires intact TLR4/MyD88-dependent signalling. |
| 1681 | 19011222 | When assayed before vaccination, KGF-treated allo-BMT recipients have increased numbers of peripheral T cells, including CD8(+) T cells with vaccine-recognition potential. |
| 1682 | 19011222 | In response to vaccination, KGF-treated allo-BMT recipients, compared with control subjects, generate increased numbers of tumor-specific CD8(+) cells, as well as increased numbers of CD8(+) cells producing interferon-gamma (IFN-gamma) and tumor necrosis factor-alpha (TNF-alpha). |
| 1683 | 19009291 | Also, anti-inflammatory effects on LPS-stimulated monocytes (TNF-alpha is decreased) and costimulatory effects on anti-CD3 stimulated T cells, (enhanced T cell proliferation and proinflammatory cytokine production) are observed. |
| 1684 | 19009291 | Both drugs inhibit IL-2-mediated generation of FOXP3 positive CTLA-4 positive CD25high CD4+ T regulatory cells from PBMCs by upto 50%. |
| 1685 | 19009291 | Inhibition of T regulatory cell function was not due to changes in TGF-beta or IL-10 production but was associated with decreased T regulatory cell FOXP3 expression. |
| 1686 | 19006832 | Serum concentrations of cytokines (IFN-gamma, TNF-alpha, IL-2, IL-4, IL-6, IL-8) and antibody levels to influenza virus antigens were studied in adults vaccinated with split-vaccine against influenza. |
| 1687 | 19006832 | Serum concentrations of cytokines (IFN-gamma, TNF-alpha, IL-2, IL-4, IL-6, IL-8) and antibody levels to influenza virus antigens were studied in adults vaccinated with split-vaccine against influenza. |
| 1688 | 19006832 | Study of cytokine profile showed absence of significant changes of IFN-gamma, TNF-alpha, IL-2, IL-4 levels and considerable variability of IL-6 and IL-8 baseline levels as well as their dynamics after vaccination. |
| 1689 | 19006832 | Study of cytokine profile showed absence of significant changes of IFN-gamma, TNF-alpha, IL-2, IL-4 levels and considerable variability of IL-6 and IL-8 baseline levels as well as their dynamics after vaccination. |
| 1690 | 19006832 | Direct correlation between IL-6 and IL-8 levels was observed during whole period post-immunization. |
| 1691 | 19006832 | Direct correlation between IL-6 and IL-8 levels was observed during whole period post-immunization. |
| 1692 | 18991097 | These phenotypic changes were enhanced when the DC were loaded with apoptotic cells, leading to increased expression of the DC maturation-associated markers CD83, CD80 and the chemokine receptor CCR7. |
| 1693 | 18991097 | The CD8 T cells expressed augmented levels of perforin, IFN-gamma and TNF-alpha and mediated CTCL cell apoptosis. |
| 1694 | 18981522 | Hamsters were immunized with killed L. interrogans serovar Autumnalis before challenge to study cytokine mRNA expression levels (interferon [IFN]-gamma, tumor necrosis factor [TNF]-alpha, interleukin [IL]-10, and IL-4). |
| 1695 | 18981522 | Hamsters were immunized with killed L. interrogans serovar Autumnalis before challenge to study cytokine mRNA expression levels (interferon [IFN]-gamma, tumor necrosis factor [TNF]-alpha, interleukin [IL]-10, and IL-4). |
| 1696 | 18981522 | IFN-gamma and TNF-alpha mRNA expression levels correlated with the severity of infection and lung pathology, whereas IL-4 and IL-10 expression levels were significantly higher in vaccinated groups. |
| 1697 | 18981522 | IFN-gamma and TNF-alpha mRNA expression levels correlated with the severity of infection and lung pathology, whereas IL-4 and IL-10 expression levels were significantly higher in vaccinated groups. |
| 1698 | 18981239 | Ad5 IC induced more notable DC maturation, as indicated by increased CD86 expression, decreased endocytosis, and production of tumor necrosis factor and type I interferons. |
| 1699 | 18977270 | Our data show that all three proteins activate and mature DCs, induce secretion of cytokines IL-12p70, IL-10, TNF-alpha, IL-6 from DCs, and rVV protein-loaded DCs induce secretion of IFN-gamma and proliferation of T cells with selective expansion of effector memory T cells. |
| 1700 | 18945879 | Downregulation of CD40 ligand response in monocytes from sepsis patients. |
| 1701 | 18945879 | Here, the response of monocytes to CD40 ligand (CD40L) for patients with sepsis due to infection with gram-negative organisms has been analyzed. |
| 1702 | 18945879 | Compared to cells from controls, monocytes from septic patients showed significantly reduced production of tumor necrosis factor alpha, interleukin-1beta (IL-1beta), and IL-12 and were unable to acquire high levels of CD80 and CD86 molecules. |
| 1703 | 18945879 | In addition, costimulation of autologous CD4+ T lymphocytes by CD40L-activated monocytes from septic patients failed to induce cell proliferation and gamma interferon production. |
| 1704 | 18945465 | We demonstrated that VLP expressed by recombinant baculoviruses activate human PBMC to release pro-inflammatory (lL-6, TNF-alpha), anti-inflammatory (IL-10) and Th1-polarizing (IFN-gamma) cytokines as well as GM-CSF and MIP-1alpha in a dose-and time-dependent manner. |
| 1705 | 18945465 | Furthermore, VLP-induced monocyte activation was shown by upregulation of molecules involved in antigen presentation (MHC II, CD80, CD86) and cell adhesion (CD54). |
| 1706 | 18936231 | Vitamin A supplementation increased YFV- and TT-specific lymphocyte proliferation and YFV-specific interleukin (IL)-5, IL-10, and tumor necrosis factor-alpha production but inhibited development of a TT-specific IL-10 response. |
| 1707 | 18927587 | Hepatitis B virus core protein inhibits TRAIL-induced apoptosis of hepatocytes by blocking DR5 expression. |
| 1708 | 18927587 | TRAIL, the TNF-related apoptosis-inducing ligand, has recently been implicated in hepatocyte death during HBV infection. |
| 1709 | 18927587 | We report here that the HBV core protein (HBc) is a potent inhibitor of TRAIL-induced apoptosis. |
| 1710 | 18927587 | Overexpressing HBc significantly decreased TRAIL-induced apoptosis of human hepatoma cells, whereas knocking-down HBc expression in hepatoma cells transfected with HBV genome enhanced it. |
| 1711 | 18927587 | The resistance of HBc-expressing cells to TRAIL-induced apoptosis was associated with a significant reduction in death receptor 5 (DR5) expression. |
| 1712 | 18927587 | Upon transfection, HBc significantly repressed the promoter activity of the human DR5 gene. |
| 1713 | 18927587 | Importantly, HBc gene transfer inhibited hepatocyte death in a mouse model of HBV-induced hepatitis; and in patients with chronic hepatitis, DR5 expression in the liver was significantly reduced. |
| 1714 | 18927587 | These results indicate that HBc may prevent hepatocytes from TRAIL-induced apoptosis by blocking DR5 expression, which in turn contributes to the development of chronic hepatitis and HCC. |
| 1715 | 18926869 | We demonstrate that neutralizing tumor necrosis factor-alpha (TNFalpha) and gamma-interferon (IFNgamma) abrogates this protection at sub-optimal levels of F1- or LcrV-specific antibody, but not at optimal levels. |
| 1716 | 18926869 | We demonstrate that neutralizing tumor necrosis factor-alpha (TNFalpha) and gamma-interferon (IFNgamma) abrogates this protection at sub-optimal levels of F1- or LcrV-specific antibody, but not at optimal levels. |
| 1717 | 18926869 | We demonstrate that neutralizing tumor necrosis factor-alpha (TNFalpha) and gamma-interferon (IFNgamma) abrogates this protection at sub-optimal levels of F1- or LcrV-specific antibody, but not at optimal levels. |
| 1718 | 18926869 | Moreover, we demonstrate that endogenous TNFalpha and IFNgamma confer measurable protection in the complete absence of protective antibodies. |
| 1719 | 18926869 | Moreover, we demonstrate that endogenous TNFalpha and IFNgamma confer measurable protection in the complete absence of protective antibodies. |
| 1720 | 18926869 | Moreover, we demonstrate that endogenous TNFalpha and IFNgamma confer measurable protection in the complete absence of protective antibodies. |
| 1721 | 18926869 | These findings indicate that antibodies and cytokines independently protect against pneumonic plague and suggest that surrogate assays for plague vaccine efficacy should consider both the level of vaccine-induced antibody and the capacity of vaccine recipients to produce TNFalpha and IFNgamma upon exposure to Y. pestis. |
| 1722 | 18926869 | These findings indicate that antibodies and cytokines independently protect against pneumonic plague and suggest that surrogate assays for plague vaccine efficacy should consider both the level of vaccine-induced antibody and the capacity of vaccine recipients to produce TNFalpha and IFNgamma upon exposure to Y. pestis. |
| 1723 | 18926869 | These findings indicate that antibodies and cytokines independently protect against pneumonic plague and suggest that surrogate assays for plague vaccine efficacy should consider both the level of vaccine-induced antibody and the capacity of vaccine recipients to produce TNFalpha and IFNgamma upon exposure to Y. pestis. |
| 1724 | 18836718 | The immune attack against malignant tumors require the concerted action of CD8+ cytotoxic T lymphocytes (CTL) as well as CD4+ T helper cells. |
| 1725 | 18836718 | Antigen recognition by the T4H2 DN clone resulted in specific secretion of IFN-gamma and TNF. |
| 1726 | 18833003 | Detection of intracellular cytokine production (interleukin-2, interferon-gamma, and tumor necrosis factor-alpha) upon phorbol 12-myristate 13-acetate-ionomycin stimulation in CD8alphaalpha+ and CD8alphabeta+ T-cells revealed that CD8alphaalpha+ T-cells show a unique cytokine production pattern (tumor necrosis factor-alpha and interferon-gamma production) as compared with CD8alphabeta+ T-cells. |
| 1727 | 18832706 | CD8(+) T cell responses were more frequent and of a greater magnitude than CD4(+) T cell responses (p < 0.001). |
| 1728 | 18832706 | Polychromatic cytometry analysis indicated that the virus-specific T cells from the severe group tended to be a central memory phenotype (CD27(+)/CD45RO(+)) with a significantly higher frequency of polyfunctional CD4(+) T cells producing IFN-gamma, TNF-alpha, and IL-2, and CD8(+) T cells producing IFN-gamma, TNF-alpha, and CD107a (degranulation), as compared with the mild-moderate group. |
| 1729 | 18827195 | Throughout the infection (until 120 days), we monitored outcome (CFU), molecules involved in the development of immunoregulation (Foxp3, hemoxygenase 1, idoleamine 2,3-dioxygenase, and transforming growth factor beta [TGF-beta]), and indicators of cytokine balance (tumor necrosis factor, inducible nitric oxide synthase, interleukin-4 [IL-4], and IL-4delta2; an inhibitory splice variant of IL-4 associated with improved outcome in human TB). |
| 1730 | 18827195 | Oral M. vaccae had a significant effect on CFU and led to increased expression of Th1 markers and of IL-4delta2, while suppressing IL-4, Foxp3, and TGF-beta. |
| 1731 | 18827187 | The levels of proinflammatory cytokines (gamma interferon, tumor necrosis factor alpha, interleukin-1beta [IL-1beta], IL-2) and anti-inflammatory cytokines (IL-4, IL-10), in addition to those of IL-6, were assessed on days 1, 3, and 5 postinfection by enzyme-linked immunosorbent assay, and the ratios of proinflammatory cytokines to anti-inflammatory cytokines were calculated. |
| 1732 | 18819411 | Influence of immunomodulator of bacterial origin - purified staphylococcal toxoid (PST) - on the synthesisof proinlammatory (IL-1beta, IL-6, TNFalpha, IFN-gamma) and anti-inflammatory (IL- 10) cytokines, as well as cytokines directing the immune response to Th1 (IL-12) or Th2 (IL-4) type was studied in mice. |
| 1733 | 18819411 | Influence of immunomodulator of bacterial origin - purified staphylococcal toxoid (PST) - on the synthesisof proinlammatory (IL-1beta, IL-6, TNFalpha, IFN-gamma) and anti-inflammatory (IL- 10) cytokines, as well as cytokines directing the immune response to Th1 (IL-12) or Th2 (IL-4) type was studied in mice. |
| 1734 | 18819411 | Synthesis of several serum interleukins (IL-2, IL-10) did not changed 4 and 24 hours after inoculation irrespective from dose of PST. |
| 1735 | 18819411 | Synthesis of several serum interleukins (IL-2, IL-10) did not changed 4 and 24 hours after inoculation irrespective from dose of PST. |
| 1736 | 18819411 | For example, increase of number of cells secreting antibodies to sheep erythrocytes was registered both during increased synthesis of cytokines (4 hours, IL-1beta, IL-6, IL-12) and during period of its depression (IL-6, TNF-alpha, IFN-gamma), as well as during stable production of cytokines (IL-1beta, IL-6, IFN-gamma). |
| 1737 | 18819411 | For example, increase of number of cells secreting antibodies to sheep erythrocytes was registered both during increased synthesis of cytokines (4 hours, IL-1beta, IL-6, IL-12) and during period of its depression (IL-6, TNF-alpha, IFN-gamma), as well as during stable production of cytokines (IL-1beta, IL-6, IFN-gamma). |
| 1738 | 18810669 | In this study, DCs isolated from peripheral blood monocytes of three pediatric patients with advanced (stage IV) NPC were incubated with whole-tumor-antigen preparations and differentiated into immature DCs in the presence of granulocyte-macrophage colony-stimulating factor and interleukin-4, and then underwent maturation when exposed to tumor necrosis factor-alpha. |
| 1739 | 18807035 | ABT-737, a small molecule inhibitor of the antiapoptotic proteins Bcl-2, Bcl-w and Bcl-x(L), was tested for the ability to increase antitumor immune responses in two tumor immunotherapy animal models. |
| 1740 | 18807035 | However, the addition of ABT-737 to either a vaccine strategy involving priming with TRP-2 melanoma antigen peptide-pulsed DC and boosting with recombinant Listeria monocytogenes expressing the same melanoma antigen, or the adoptive transfer of TCR transgenic cells, did not result in superior antitumor activity against B16 murine melanoma. |
| 1741 | 18807035 | In vitro studies failed to demonstrate increased cytotoxic lytic activity when testing the combination of ABT-737 with lymphokine activated killer (LAK) cells, or the death receptor agonists Fas, TRAIL-ligand or TNF-alpha against the CT26 and B16 cell lines. |
| 1742 | 18806877 | Immunisation with this chimeric vaccine consistently generated strong HCMV-specific CD8(+) and CD4(+) T-cells which co-expressed IFN-gamma and TNF-alpha, while the humoral response induced by this vaccine showed strong virus neutralizing capacity. |
| 1743 | 18806877 | Furthermore, in vitro stimulation with this adenoviral chimeric vaccine rapidly expanded multiple antigen-specific human CD8(+) and CD4(+) T-cells from healthy virus carriers. |
| 1744 | 18802099 | Mice boosted intradermally make very strong splenic CD4 and CD8 Th1 cytokine responses to Ag 85A, but show no change in lung mycobacterial burden over BCG primed animals. |
| 1745 | 18802099 | In contrast, intranasally boosted mice show greatly reduced mycobacterial burden and make a much weaker splenic response but a very strong lung CD4 and CD8 response to Ag 85A and an increased response to purified protein derivative. |
| 1746 | 18802099 | This effect is associated with the presence in the lung of multifunctional T cells, with high median fluorescence intensity and integrated median fluorescence intensity for IFN-gamma, IL-2, and TNF. |
| 1747 | 18791167 | We reported previously that administration of MIP-1alpha mobilized a population of F4/80(-)B220(-)CD11c+ DC precursors into peripheral blood by the expression of CCR1 and CCR5. |
| 1748 | 18791167 | In this study, we identified a new subset of CCR6+CCR1(-)CCR5(-)B220(-)CD11c(+) cells in MIP-1alpha-administered mice. |
| 1749 | 18791167 | When cultured with GM-CSF, IL-4, and TNF-alpha, these cells differentiated into mature DCs, possessing the typical morphologic characteristics, phenotypes, and antigen-presenting function (termed CCR6+ DC precursors). |
| 1750 | 18791167 | Taken together, this study further demonstrates the mechanism of DC precursor mobilization induced by MIP-1alpha; that is, besides mobilizing DC precursors with CCR1 and CCR5 expressions, MIP-1alpha recruited F4/80+CD11c(-) monocyte/macrophage-producing MIP-3alpha, which finally mobilized the CCR6+ DC precursor subset to amplify the B220(-)CD11c+ DC precursor population. |
| 1751 | 18789542 | CD14+ cells are required for IL-12 response in bovine blood mononuclear cells activated with Toll-like receptor (TLR) 7 and TLR8 ligands. |
| 1752 | 18789542 | Single-stranded viral RNA (ssRNA) was recently identified as the natural ligand for TLR7 and TLR8. ssRNA sequences from viruses, as well as their synthetic analogues stimulate innate immune responses in immune cells from humans and mice, but their immunostimulatory activity has not been investigated in ruminants. |
| 1753 | 18789542 | In vitro incubation of bovine peripheral blood mononuclear cells (PBMCs) with ORN-induced production of IL-12, IFN-gamma and TNF-alpha. |
| 1754 | 18789542 | Depletion of CD14+ cells from PBMC abrogated the IL-12 response and consequently the IFN-gamma response, suggesting that CD14+ cells are required for PBMC immune activation with ORN. |
| 1755 | 18789542 | Consistent with these findings, the putative receptors for ORN (TLR7 and TLR8) were expressed at higher levels in the CD14+ fraction than the CD14- PBMC fraction. |
| 1756 | 18722475 | LIGHT is a member of the TNF superfamily and functions as a co-stimulatory molecule for T cell proliferation. |
| 1757 | 18716452 | Using these samples, RT-PCR and ELISA analysis were carried out for the comparative study of the cytokines, including TNF-alpha, INF-gamma, IL-2, IL-4, IL-10 and IL-12. |
| 1758 | 18716452 | Using these samples, RT-PCR and ELISA analysis were carried out for the comparative study of the cytokines, including TNF-alpha, INF-gamma, IL-2, IL-4, IL-10 and IL-12. |
| 1759 | 18716452 | Using these samples, RT-PCR and ELISA analysis were carried out for the comparative study of the cytokines, including TNF-alpha, INF-gamma, IL-2, IL-4, IL-10 and IL-12. |
| 1760 | 18716452 | Using these samples, RT-PCR and ELISA analysis were carried out for the comparative study of the cytokines, including TNF-alpha, INF-gamma, IL-2, IL-4, IL-10 and IL-12. |
| 1761 | 18716452 | In the Pohang-infected mice at 120 h, the liver showed a 53 times higher level of TNF-alpha and a 42 times higher level of IFN-gamma than the respective levels at the early time points after infection. |
| 1762 | 18716452 | In the Pohang-infected mice at 120 h, the liver showed a 53 times higher level of TNF-alpha and a 42 times higher level of IFN-gamma than the respective levels at the early time points after infection. |
| 1763 | 18716452 | In the Pohang-infected mice at 120 h, the liver showed a 53 times higher level of TNF-alpha and a 42 times higher level of IFN-gamma than the respective levels at the early time points after infection. |
| 1764 | 18716452 | In the Pohang-infected mice at 120 h, the liver showed a 53 times higher level of TNF-alpha and a 42 times higher level of IFN-gamma than the respective levels at the early time points after infection. |
| 1765 | 18716452 | The levels of TNF-alpha and IFN-gamma induced by LVS were 5 times lower than those induced by the Pohang isolate. |
| 1766 | 18716452 | The levels of TNF-alpha and IFN-gamma induced by LVS were 5 times lower than those induced by the Pohang isolate. |
| 1767 | 18716452 | The levels of TNF-alpha and IFN-gamma induced by LVS were 5 times lower than those induced by the Pohang isolate. |
| 1768 | 18716452 | The levels of TNF-alpha and IFN-gamma induced by LVS were 5 times lower than those induced by the Pohang isolate. |
| 1769 | 18716452 | Also, the organs from the Pohang-infected mice showed higher levels of TNF-alpha, IFN-gamma, IL-10 and IL-12 than the levels in the LVS-infected mice. |
| 1770 | 18716452 | Also, the organs from the Pohang-infected mice showed higher levels of TNF-alpha, IFN-gamma, IL-10 and IL-12 than the levels in the LVS-infected mice. |
| 1771 | 18716452 | Also, the organs from the Pohang-infected mice showed higher levels of TNF-alpha, IFN-gamma, IL-10 and IL-12 than the levels in the LVS-infected mice. |
| 1772 | 18716452 | Also, the organs from the Pohang-infected mice showed higher levels of TNF-alpha, IFN-gamma, IL-10 and IL-12 than the levels in the LVS-infected mice. |
| 1773 | 18716452 | The blood from the Pohang-infected mice at 120 h revealed about a 40 times increased level of IFN-gamma, and IL-10 was also increased by 4 times at 96 h compared to an early infection time point, while IL-4 was not induced during the whole infection period. |
| 1774 | 18716452 | The blood from the Pohang-infected mice at 120 h revealed about a 40 times increased level of IFN-gamma, and IL-10 was also increased by 4 times at 96 h compared to an early infection time point, while IL-4 was not induced during the whole infection period. |
| 1775 | 18716452 | The blood from the Pohang-infected mice at 120 h revealed about a 40 times increased level of IFN-gamma, and IL-10 was also increased by 4 times at 96 h compared to an early infection time point, while IL-4 was not induced during the whole infection period. |
| 1776 | 18716452 | The blood from the Pohang-infected mice at 120 h revealed about a 40 times increased level of IFN-gamma, and IL-10 was also increased by 4 times at 96 h compared to an early infection time point, while IL-4 was not induced during the whole infection period. |
| 1777 | 18713984 | The reprogrammed Tregs cease to express IL-10 and TGFbeta, fail to suppress T cell responses, and gain the ability to produce IFN-gamma, IL-17, and TNF-alpha. |
| 1778 | 18708593 | DnaK induced the activation of MAPKs and NF-kappaB in DC and the production of the proinflammatory cytokines IL-6, TNF-alpha, and IL-12 p40, as well as low levels of IL-10. |
| 1779 | 18708593 | DnaK induced phenotypic maturation of DC, as demonstrated by an up-regulation of costimulatory molecules CD40, CD80, and CD86. |
| 1780 | 18708593 | DnaK stimulated DC through TLR4 and the adapters MyD88 and Toll/IL-1R domain-containing adaptor-inducing IFN-beta (TRIF) that mediated differential responses. |
| 1781 | 18708593 | DnaK induced activation of MAPKs and NF-kappaB in a MyD88- or TRIF-dependent manner. |
| 1782 | 18708593 | In contrast, DnaK induced DC maturation in a TRIF-dependent, MyD88-independent manner. |
| 1783 | 18703465 | Recently, it has been demonstrated that interaction between dendritic cells (DCs) and thymic stromal lymphopoietin (TSLP), an IL-7-like cytokine, is essential for evoking T(h)2 responses in allergy. |
| 1784 | 18703465 | Recently, it has been demonstrated that interaction between dendritic cells (DCs) and thymic stromal lymphopoietin (TSLP), an IL-7-like cytokine, is essential for evoking T(h)2 responses in allergy. |
| 1785 | 18703465 | We demonstrated that BCG redirects TSLP-DCs away from inducing inflammatory T(h)2 cells that produce IL-4, IL-5, IL-13 and tumor necrosis factor (TNF)-alpha and toward regulatory T(h)1 cells that produce IFN-gamma and IL-10. |
| 1786 | 18703465 | We demonstrated that BCG redirects TSLP-DCs away from inducing inflammatory T(h)2 cells that produce IL-4, IL-5, IL-13 and tumor necrosis factor (TNF)-alpha and toward regulatory T(h)1 cells that produce IFN-gamma and IL-10. |
| 1787 | 18703465 | We also demonstrated that this functional alteration of TSLP-DCs by BCG depended on both production of IL-12 from DCs and down-regulation of OX40 ligand, a member of the TNF family, on DCs. |
| 1788 | 18703465 | We also demonstrated that this functional alteration of TSLP-DCs by BCG depended on both production of IL-12 from DCs and down-regulation of OX40 ligand, a member of the TNF family, on DCs. |
| 1789 | 18684965 | Vaccination without autoantigen protects against collagen II-induced arthritis via immune deviation and regulatory T cells. |
| 1790 | 18684965 | A Salmonella vector expressing colonization factor Ag I (CFA/I), shown to behave as an anti-inflammatory vaccine, stimulates the production of CD4(+)CD25(+) T cells and regulatory cytokines. |
| 1791 | 18684965 | In this work, we queried whether Salmonella-CFA/I can protect DBA/1 mice from collagen-induced arthritis. |
| 1792 | 18684965 | Clinical findings were accompanied by the suppression of inflammatory cytokines TNF-alpha, IL-1beta, IL-6, and IL-27. |
| 1793 | 18684965 | Vaccination evoked a multi-tier response consisting of IL-4 producing Th2 cells, an increased production of TGF-beta by CD4(+) T cells, and suppression of collagen II-specific CD4(+) T cell proliferation. |
| 1794 | 18684965 | To assess the contribution of Salmonella-CFA/I-primed CD4(+) T cells, adoptive transfer studies with total CD4(+), CD4(+)CD25(-), or CD4(+)CD25(+) T cells were performed 15 days postchallenge. |
| 1795 | 18684965 | Mice receiving either subset showed reduced disease incidence and low clinical scores; however, mice receiving total CD4(+) T cells showed delayed disease onset by 10 days with reduced clinical scores, reduced IL-17 and IL-27, but enhanced IL-4, IL-10, IL-13, and TGF-beta. |
| 1796 | 18684965 | Inhibition of TGF-beta or IL-4 compromised protective immunity. |
| 1797 | 18684965 | These data show that Salmonella-CFA/I vaccination of DBA/1 mice protects against collagen-induced arthritis by stimulating TGF-beta- and IL-4-producing regulatory CD4(+) T cells. |
| 1798 | 18683503 | Ex vivo production of interferon-gamma, tumor necrosis factor-alpha, and interleukin-6 by mouse macrophages during infection with M. bovis and M. tuberculosis H37Rv. |
| 1799 | 18683503 | Ex vivo production of interferon-gamma, tumor necrosis factor-alpha, and interleukin-6 by mouse macrophages during infection with M. bovis and M. tuberculosis H37Rv. |
| 1800 | 18683503 | Ex vivo production of interferon-gamma, tumor necrosis factor-alpha, and interleukin-6 by mouse macrophages during infection with M. bovis and M. tuberculosis H37Rv. |
| 1801 | 18683503 | Ex vivo production of IFN-gamma, TNF-alpha, and IL-6 by mouse peritoneal macrophages was studied during successive infection with the vaccine strain M. bovis BCG and virulent strain M. tuberculosis H37Rv. |
| 1802 | 18683503 | Ex vivo production of IFN-gamma, TNF-alpha, and IL-6 by mouse peritoneal macrophages was studied during successive infection with the vaccine strain M. bovis BCG and virulent strain M. tuberculosis H37Rv. |
| 1803 | 18683503 | Ex vivo production of IFN-gamma, TNF-alpha, and IL-6 by mouse peritoneal macrophages was studied during successive infection with the vaccine strain M. bovis BCG and virulent strain M. tuberculosis H37Rv. |
| 1804 | 18683503 | The increase in the concentrations of TNF-alpha and IL-6 did not depend on the sequence of macrophage infection with the vaccine or virulent strain, but was related to the presence of the vaccine strain M. bovis BCG in the medium. |
| 1805 | 18683503 | The increase in the concentrations of TNF-alpha and IL-6 did not depend on the sequence of macrophage infection with the vaccine or virulent strain, but was related to the presence of the vaccine strain M. bovis BCG in the medium. |
| 1806 | 18683503 | The increase in the concentrations of TNF-alpha and IL-6 did not depend on the sequence of macrophage infection with the vaccine or virulent strain, but was related to the presence of the vaccine strain M. bovis BCG in the medium. |
| 1807 | 18653385 | The effect of beta-interferon therapy on myelin basic protein-elicited CD4+ T cell proliferation and cytokine production in multiple sclerosis. |
| 1808 | 18653385 | We analysed the CD4+ T cell proliferation and cytokine responses elicited by myelin basic protein (MBP) and a foreign recall antigen, tetanus toxoid (TT), in mononuclear cell cultures from fourteen MS patients undergoing IFN-beta therapy. |
| 1809 | 18653385 | The MBP-elicited IFN-gamma-, TNF-alpha- and IL-10 production decreased during therapy (p<0.007-0.03), while the IL-6 production increased (p<0.03). |
| 1810 | 18653385 | No significant change was observed in the MBP-induced CD4+ T cell proliferation, or in the production of IL-4, IL-5 and brain-derived neurotrophic factor. |
| 1811 | 18653385 | In comparison, IFN-beta therapy reduced IFN-gamma and IL-4 responses to TT (p<0.003 and p<0.04). |
| 1812 | 18653385 | Thus, IFN-beta inhibits IFN-gamma production in general, presumably alleviating the detrimental influence of IFN-gamma in MS. |
| 1813 | 18653385 | However, the increase in proinflammatory IL-6 and the decrease in anti-inflammatory IL-10 responses suggest that IFN-beta has more diverse effects than previously assumed. |
| 1814 | 18650852 | Compared with the control-vaccinated mice, the MIF/TTX DNA-vaccinated mice also showed significantly lower serum tumor necrosis factor (TNF)-alpha protein levels and reduced mRNA expression of TNF-alpha, interleukin (IL)-1beta, IL-6, macrophage inflammatory protein-2 and Toll-like receptor-4 in the lungs. |
| 1815 | 18640169 | Since i.n. treatment with OMVs as well as killed whole-cell bacteria enhanced markers of innate immune response such as TNFalpha, IL-6 and CCL20, i.n. immunizations were performed with no adjuvant added. |
| 1816 | 18632918 | It is involved in the haptoglobin-mediated removal of free hemoglobin from plasma, has been identified as a naturally soluble plasma glycoprotein with potential anti-inflammatory properties, and is possibly linked to an individual's haptoglobin phenotype. |
| 1817 | 18632918 | In order to verify this, the relationships between sCD163 levels, malaria severity, and selected inflammatory mediators (tumor necrosis factor alpha [TNF-alpha], interleukin-6 [IL-6], and IL-10) were assessed by enzyme-linked immunosorbent assay using plasma samples obtained from pediatric malaria patients with uncomplicated malaria (UM [n = 38]), cerebral malaria (CM [n = 52]), and severe malarial anemia (SA [n = 55]) during two consecutive malaria transmission seasons (2002 and 2003). |
| 1818 | 18632652 | Here, we show that monocyte-derived immature human DCs stimulated with polyinosinic acid:polycytidylic acid, IFN-alpha, tumor necrosis factor-alpha (TNF-alpha), interleukin-1 beta (IL-1 beta), and IFN-gamma, alpha-type 1-polarized DC (alpha DC1), secrete profuse amounts of the CXCR3 ligand CXCL9/MIG and substantial amounts of CXCL10/IP-10 and CXCL11/I-TAC after withdrawal of maturation stimuli. |
| 1819 | 18632652 | Here, we show that monocyte-derived immature human DCs stimulated with polyinosinic acid:polycytidylic acid, IFN-alpha, tumor necrosis factor-alpha (TNF-alpha), interleukin-1 beta (IL-1 beta), and IFN-gamma, alpha-type 1-polarized DC (alpha DC1), secrete profuse amounts of the CXCR3 ligand CXCL9/MIG and substantial amounts of CXCL10/IP-10 and CXCL11/I-TAC after withdrawal of maturation stimuli. |
| 1820 | 18632652 | In sharp contrast, no measurable production of these chemokines was found in DCs after maturation with the current gold standard maturation cocktail for human DC-based cancer vaccines consisting of TNF-alpha, IL-1 beta, IL-6, and prostaglandin-E(2) (PGE(2)-DC). |
| 1821 | 18632652 | In sharp contrast, no measurable production of these chemokines was found in DCs after maturation with the current gold standard maturation cocktail for human DC-based cancer vaccines consisting of TNF-alpha, IL-1 beta, IL-6, and prostaglandin-E(2) (PGE(2)-DC). |
| 1822 | 18632652 | PGE(2)-DCs preferentially produced the Th2 and regulatory T-cell-attracting chemokines CCL17/TARC and CCL22/MDC, whereas only marginal levels of these chemokines were produced by alpha DC1s. |
| 1823 | 18632652 | PGE(2)-DCs preferentially produced the Th2 and regulatory T-cell-attracting chemokines CCL17/TARC and CCL22/MDC, whereas only marginal levels of these chemokines were produced by alpha DC1s. |
| 1824 | 18632652 | Functional studies in vitro showed that supernatants from mature alpha DC1s actively recruited CD3(-)CD56(+) NK cells and that adding anti-CXCL9/MIG antibodies to the alpha DC1 supernatant substantially reduced this recruitment. |
| 1825 | 18632652 | Functional studies in vitro showed that supernatants from mature alpha DC1s actively recruited CD3(-)CD56(+) NK cells and that adding anti-CXCL9/MIG antibodies to the alpha DC1 supernatant substantially reduced this recruitment. |
| 1826 | 18632652 | Finally, alpha DC1s were able to induce IFN-gamma production when cocultured with resting autologous NK cells, but only if concurrent CD40 ligation was provided. |
| 1827 | 18632652 | Finally, alpha DC1s were able to induce IFN-gamma production when cocultured with resting autologous NK cells, but only if concurrent CD40 ligation was provided. |
| 1828 | 18628832 | Such BVLPs up-regulated the level of CD40, CD80, CD86, CD83, and enhanced the secretion of IL-6, IL-10 and TNF-alpha in immature dendritic cells (DCs). |
| 1829 | 18628832 | Such BVLPs up-regulated the level of CD40, CD80, CD86, CD83, and enhanced the secretion of IL-6, IL-10 and TNF-alpha in immature dendritic cells (DCs). |
| 1830 | 18628832 | BVLPs showed a stronger ability to stimulate DCs in terms of cytokine induction as evidenced by 2 to 6 fold higher production of IL-6 and TNF-alpha. |
| 1831 | 18628832 | BVLPs showed a stronger ability to stimulate DCs in terms of cytokine induction as evidenced by 2 to 6 fold higher production of IL-6 and TNF-alpha. |
| 1832 | 18628832 | Further study indicated that IFN-gamma+ and IL-4+ populations in CD4+ T cells increased upon co-cultivation with DCs pre-exposed with BVLPs or SARS-CoV VLPs. |
| 1833 | 18628832 | Further study indicated that IFN-gamma+ and IL-4+ populations in CD4+ T cells increased upon co-cultivation with DCs pre-exposed with BVLPs or SARS-CoV VLPs. |
| 1834 | 18624356 | The Nlrp3 inflammasome is critical for aluminium hydroxide-mediated IL-1beta secretion but dispensable for adjuvant activity. |
| 1835 | 18624356 | Alum has recently been shown to promote caspase-1 activation and IL-1beta secretion, but the cellular pathways involved remain elusive. |
| 1836 | 18624356 | Here we report that the release of IL-1beta triggered by alum is abrogated in macrophages deficient in the NLR family, pyrin domain containing 3 (Nlrp3) protein and the apoptosis-associated speck-like protein containing a caspase recruitment domain (Asc) but not the NLR family, CARD domain containing 4 (Nlrc4) protein. |
| 1837 | 18624356 | The requirement of the Nlrp3 inflammasome was specific for IL-1beta in that secretion of TNF-alpha was independent of Nlrp3 or Asc. |
| 1838 | 18624356 | Consistently, processing of pro-caspase-1 induced by alum was abolished in macrophages lacking Nlrp3 or Asc. |
| 1839 | 18624356 | Unlike caspase-1 processing and IL-1beta secretion triggered by LPS, alum-mediated activation of the inflammasome did not require exogenous ATP. |
| 1840 | 18624356 | Importantly, induction of IgG production against human serum albumin by alum was unimpaired in mice deficient in Nlrp3. |
| 1841 | 18624356 | These results indicate that alum induces IL-1beta via the Nlrp3 inflammasome but this activity is dispensable for alum-mediated adjuvant activity. |
| 1842 | 18606649 | We investigated the expression and the functions of the TNF family cytokines, B cell-activating factor of the TNF family (BAFF) and a proliferation-inducing ligand (APRIL), and their receptors in newborn mice and found that TACI expression on B lymphocytes was dramatically reduced (p < 0.0001) in newborns as compared with adults. |
| 1843 | 18606649 | More importantly, TACI ligands BAFF or APRIL were unable to induce IgA/IgG/IgM secretion from newborn B lymphocytes. |
| 1844 | 18606649 | In vitro or in vivo exposure of newborn B lymphocytes to oligodeoxynucleotides (CpG ODN) led to up-regulation of TACI expression on newly formed, follicular, and marginal zone as well as B1 B lymphocyte populations, and rendered them responsive to BAFF- or APRIL-mediated CD138 expression and IgA/IgG secretion. |
| 1845 | 18600182 | Unmodified freeze-thaw tumor cell lysates inhibited the toll-like receptor-induced maturation and function of bone marrow-derived DCs, preventing up-regulation of CD40, CD86, and major histocompatibility complex class II, and reducing secretion of inflammatory cytokines [interleukin (IL)-12 p70, tumor necrosis factor-alpha, and IL-6]. |
| 1846 | 18600182 | Although IL-10 secretion was increased by lysate-pulsed DCs, this was not responsible for the observed suppression of IL-12. |
| 1847 | 18598175 | The CA-elicited production of the Th1 cytokines tumor necrosis factor (TNF)-alpha, interleukin (IL)-2, and interferon (IFN)-gamma was increased after Immunlina administration for 3 days (P < .001, < .03, and < .007, respectively), and increased IL-2 production persisted after 56 days (P < .004). |
| 1848 | 18598175 | The CA-elicited production of the Th1 cytokines tumor necrosis factor (TNF)-alpha, interleukin (IL)-2, and interferon (IFN)-gamma was increased after Immunlina administration for 3 days (P < .001, < .03, and < .007, respectively), and increased IL-2 production persisted after 56 days (P < .004). |
| 1849 | 18598175 | The CA-elicited production of the Th1 cytokines tumor necrosis factor (TNF)-alpha, interleukin (IL)-2, and interferon (IFN)-gamma was increased after Immunlina administration for 3 days (P < .001, < .03, and < .007, respectively), and increased IL-2 production persisted after 56 days (P < .004). |
| 1850 | 18598175 | The TNF-alpha, IFN-gamma, and IL-6 responses to TT were enhanced after 8 and 14 days (P < .002-.05), while IL-5 responses increased significantly within 3 days (P < .04) and fell below baseline levels after 14 days (P < .008). |
| 1851 | 18598175 | The TNF-alpha, IFN-gamma, and IL-6 responses to TT were enhanced after 8 and 14 days (P < .002-.05), while IL-5 responses increased significantly within 3 days (P < .04) and fell below baseline levels after 14 days (P < .008). |
| 1852 | 18598175 | The TNF-alpha, IFN-gamma, and IL-6 responses to TT were enhanced after 8 and 14 days (P < .002-.05), while IL-5 responses increased significantly within 3 days (P < .04) and fell below baseline levels after 14 days (P < .008). |
| 1853 | 18598175 | Upon addition to normal mononuclear cells in vitro, Immulina elicited strong TNF-alpha, IL-1beta, and IL-6 responses, indicating that it acts by inducing a pro-inflammatory state. |
| 1854 | 18598175 | Upon addition to normal mononuclear cells in vitro, Immulina elicited strong TNF-alpha, IL-1beta, and IL-6 responses, indicating that it acts by inducing a pro-inflammatory state. |
| 1855 | 18598175 | Upon addition to normal mononuclear cells in vitro, Immulina elicited strong TNF-alpha, IL-1beta, and IL-6 responses, indicating that it acts by inducing a pro-inflammatory state. |
| 1856 | 18591233 | However, contrarily to nMP65, rMP65 did not induce tumor necrosis factor alpha and interleukin-6 release from these cells. |
| 1857 | 18579590 | We assessed both the magnitude and the functional profile of the virus-specific CD8(+) T cells by measuring gamma interferon, interleukin-2, and tumor necrosis factor alpha production. |
| 1858 | 18579264 | The stimulated T cells produced higher amount of IL-4 and IL-10 than IFN-gamma, TNF-alpha, and IL-12 indicating a Th2 type of response bias. |
| 1859 | 18573897 | In addition, testing of TB patients' PBMC for secretion of proinflammatory cytokines (tumor necrosis factor alpha [TNF-alpha], interleukin 6 [IL-6], IL-8, and IL-1beta), Th1 cytokines (IFN-gamma, IL-2, and TNF-beta), and Th2 cytokines (IL-4, IL-5, and IL-10) showed differential effects of RD peptides in the secretion of IFN-gamma and IL-10, with high IFN-gamma/IL-10 ratios (32 to 5.0) in response to RD1, RD5, RD7, RD9, and RD10 and low IFN-gamma/IL-10 ratios (<1.0) in response to RD12, RD13, and RD15. |
| 1860 | 18573897 | In conclusion, our results suggest that M. tuberculosis RDs can be divided into two major groups--one group that activates PBMC to preferentially secrete IFN-gamma and another group that activates preferential secretion of IL-10--and that these two groups of RDs may have roles in protection against and pathogenesis of TB, respectively. |
| 1861 | 18572242 | Nine cytokine genes (IL-2, -4, -10, -12, -13, -18, TNFalpha, TGFbeta and IFNgamma) and Cox-2 were selected for analysis. |
| 1862 | 18566382 | Coligation of the hepatitis C virus receptor CD81 with CD28 primes naive T lymphocytes to acquire type 2 effector function. |
| 1863 | 18566382 | In this study, we describe for the first time that coligation of the tetraspanins CD81, CD82, or CD9 with the costimulatory molecule CD28 in vitro leads to proliferation of naive T cells. |
| 1864 | 18566382 | When activated through this pathway, both CD4+ and CD8+ naive T cells differentiate into type 2 effector cells, which produce IL-4, IL-5, IL-13, and IL-10, together with IL-2 and TNF-alpha, but little to no IFN-gamma. |
| 1865 | 18566382 | These effector cells descend from precursors that display early and strong production of IL-4, STAT6 phosphorylation, and up-regulation of the transcription factor GATA-3, suggesting a direct skewing toward Th2 differentiation without a Th0 intermediate. |
| 1866 | 18566382 | The hepatitis C virus envelope protein E2 is the only ligand known for CD81. |
| 1867 | 18562053 | CD40L expressed from the canarypox vector, ALVAC, can boost immunogenicity of HIV-1 canarypox vaccine in mice and enhance the in vitro expansion of viral specific CD8+ T cell memory responses from HIV-1-infected and HIV-1-uninfected individuals. |
| 1868 | 18562053 | CD40 ligand (CD40L), a member of the tumor necrosis factor superfamily (TNFSF), is a pivotal costimulatory molecule for immune responses. |
| 1869 | 18562053 | Co-immunization of mice with CD40L expressing canarypox and the canarypox vaccine expressing HIV-1 proteins, vCP1452, augmented HIV-1 specific cytotoxic T lymphocyte (CTL) responses in terms of frequency, polyfunctionality and interleukin (IL)-7 receptor alpha chain (IL-7Ralpha, CD127) expression. |
| 1870 | 18562053 | In addition, CD40L expressed from canarypox virus could significantly augment CD4+ T cell responses against HIV-1 in mice. |
| 1871 | 18562053 | CD40L expressed from canarypox virus matured human monocyte-derived dendritic cells (MDDCs) in a tumor necrosis factor-alpha (TNF-alpha) independent manner, which underwent less apoptosis, and could expand ex vivo Epstein-Barr virus (EBV)-specific CTL responses from healthy human individuals and ex vivo HIV-1-specific CTL responses from HIV-1-infected individuals in the presence or absence of CD4+ T cells. |
| 1872 | 18552348 | For example, aspartylglucosaminidase (AGA), PLA2, SIAT8B, GALNT7, or B3GAT1 metabolize chemical ligands to which the influenza virus, herpes simplex, cytomegalovirus (CMV), rubella, or Toxoplasma gondii bind. |
| 1873 | 18552348 | The epidermal growth factor receptor (EGR/EGFR) is used by the CMV to gain entry to cells, and a CMV gene codes for an interleukin (IL-10) mimic that binds the host cognate receptor, IL10R. |
| 1874 | 18552348 | The fibroblast growth factor receptor (FGFR1) is used by herpes simplex. |
| 1875 | 18552348 | KPNA3 and RANBP5 control the nuclear import of the influenza virus. |
| 1876 | 18552348 | Disrupted in schizophrenia 1 (DISC1) controls the microtubule network that is used by viruses as a route to the nucleus, while DTNBP1, MUTED, and BLOC1S3 regulate endosomal to lysosomal routing that is also important in viral traffic. |
| 1877 | 18552348 | Neuregulin 1 activates ERBB receptors releasing a factor, EBP1, known to inhibit the influenza virus transcriptase. |
| 1878 | 18552348 | Other viral or bacterial components bind to genes or proteins encoded by CALR, FEZ1, FYN, HSPA1B, IL2, HTR2A, KPNA3, MED12, MED15, MICB, NQO2, PAX6, PIK3C3, RANBP5, or TP53, while the cerebral infectivity of the herpes simplex virus is modified by Apolipoprotein E (APOE). |
| 1879 | 18552348 | Genes encoding for proteins related to the innate immune response, including cytokine related (CCR5, CSF2RA, CSF2RB, IL1B, IL1RN, IL2, IL3, IL3RA, IL4, IL10, IL10RA, IL18RAP, lymphotoxin-alpha, tumor necrosis factor alpha [TNF]), human leukocyte antigen (HLA) antigens (HLA-A10, HLA-B, HLA-DRB1), and genes involved in antigen processing (angiotensin-converting enzyme and tripeptidyl peptidase 2) are all concerned with defense against invading pathogens. |
| 1880 | 18552348 | Human microRNAs (Hsa-mir-198 and Hsa-mir-206) are predicted to bind to influenza, rubella, or poliovirus genes. |
| 1881 | 18550728 | C57BL/6 mice vaccinated with T. cruzi G1 (TcG1)-, TcG2-, or TcG4-encoding plasmids and cytokine (interleukin-12 and granulocyte-macrophage colony-stimulating factor) expression plasmids elicited a strong Th1-type antibody response dominated by immunoglobulin G2b (IgG2b)/IgG1 isotypes. |
| 1882 | 18550728 | Subsequently, the serum and cardiac levels of IFN-gamma and tumor necrosis factor alpha and infiltration of inflammatory infiltrate in the heart were decreased in vaccinated mice during the course of infection and chronic disease development. |
| 1883 | 18549647 | The function of exosomes in immunity was detected through block test after blocking some molecules (CD11a, CD11b, CD11c, CD54, MFG-E8 and CD83). |
| 1884 | 18549647 | The exosomes derived from mDC induced with different cytokines (LPS, TNF-alpha, CpG, CD40L) were no significant difference in concentrations but were different in effect. |
| 1885 | 18549647 | The immunity function of exosomes depended on CD11a, CD11b, CD11c, CD54, MFG-E8 and CD83 molecules, the effect of priming T cells is reduced when these molecules were blocked. |
| 1886 | 18549647 | Confocal microscopy and FACS assay showed that blocking CD11a and CD54 could inhibit exosome-targeted DC and DC-embedded exosomes. |
| 1887 | 18544042 | Membrane expressed TNF allowed a substantial recruitment of activated T cells and macrophages with granuloma formation and expression of bactericidal inducible nitric oxide synthase (iNOS). |
| 1888 | 18544042 | Membrane expressed TNF allowed a substantial recruitment of activated T cells and macrophages with granuloma formation and expression of bactericidal inducible nitric oxide synthase (iNOS). |
| 1889 | 18544042 | Infection in TNF(tm/tm) double transgenic mice with TNF-R1 or TNF-R2 suggest protection is mediated through TNF-R2 signalling. |
| 1890 | 18544042 | Infection in TNF(tm/tm) double transgenic mice with TNF-R1 or TNF-R2 suggest protection is mediated through TNF-R2 signalling. |
| 1891 | 18524883 | Our data show that the difference between the therapeutic administration of BCG and RUTI resides mainly in the stronger activation of IFN-gamma(+) CD4(+) cells and CD8(+) cells against tuberculin purified protein derivative, ESAT-6, and Ag85B that RUTI generates. |
| 1892 | 18524883 | Both vaccines also triggered a specific immune response against the M. tuberculosis structural antigens Ag16kDa and Ag38kDa and a marked mRNA expression of IFN-gamma, tumor necrosis factor, interleukin-12, inducible nitric oxide synthase, and RANTES in the lung. |
| 1893 | 18524823 | The samples were tested using a statistically qualified nine-color intracellular cytokine staining assay measuring interleukin-2 (IL-2), tumor necrosis factor alpha, macrophage inflammatory protein 1beta, and gamma interferon production and expression of CD107a. |
| 1894 | 18524823 | Both vaccine regimens induced CD4(+) and CD8(+) HIV gag-specific T-cell responses which variably expressed several intracellular markers. |
| 1895 | 18524823 | Several trends were observed in which the frequencies of HIV-1-specific CD4(+) T cells and IL-2 production from antigen-specific CD8(+) T cells in the DNA/Ad5 cohort were more pronounced than in the Ad5/Ad5 cohort. |
| 1896 | 18524682 | T cells expanded from adeno-HCV stimulated cultures were potent producers of HCV-specific IFN-gamma and TNF-alpha and efficiently lysed target cells pulsed with HCV peptides. |
| 1897 | 18523260 | Therapeutic vaccination with simian immunodeficiency virus (SIV)-DNA + IL-12 or IL-15 induces distinct CD8 memory subsets in SIV-infected macaques. |
| 1898 | 18523260 | Cytokines, such as IL-12 and IL-15, have been shown to be potent adjuvants for the induction and maintenance of cellular immune responses, in particular during HIV infection. |
| 1899 | 18523260 | In this study, we examined the ability of therapeutic vaccination with SIV-DNA+IL-12 or IL-15 as molecular adjuvants to improve DNA vaccine potency and to enhance memory immune responses in SIV-infected macaques. |
| 1900 | 18523260 | Our results demonstrate that incorporating IL-12 into the vaccine induces SIV-specific CD8 effector memory T cell (T(EM)) functional responses and enhances the capacity of IFN-gamma-producing CD8 T(EM) cells to produce TNF. |
| 1901 | 18523260 | Lower levels of PD-1 were expressed on T cells acquiring dual function upon vaccination as compared with mono-functional CD8 T(EM) cells. |
| 1902 | 18523260 | Finally, a boost with SIV-DNA+IL-15 triggered most T cell memory subsets in macaques primed with either DNA-SIV or placebo but only CD8 T(EM) in macaques primed with SIV-DNA+IL-12. |
| 1903 | 18523260 | These results indicate that plasmid IL-12 and IL-15 cytokines represent a significant addition to enhance the ability of therapeutic DNA vaccines to induce better immunity. |
| 1904 | 18505805 | Cytokine quantitation for the sera of SchuS4-challenged mice indicated that OMP and iLVS immunizations induced high levels of tumor necrosis factor alpha and interleukin-2 (IL-2) production, whereas only OMP immunization induced high levels of IL-10 production. |
| 1905 | 18505805 | By comparison, high levels of proinflammatory cytokines, including RANTES, granulocyte colony-stimulating factor, IL-6, IL-1alpha, IL-12p40, and KC, in nonvaccinated mice indicated that these cytokines may facilitate disease progression. |
| 1906 | 18495849 | Antibodies to proteinase 3 prime human oral, lung, and kidney epithelial cells to secrete proinflammatory cytokines upon stimulation with agonists to various Toll-like receptors, NOD1, and NOD2. |
| 1907 | 18495849 | In this study, anti-PR3 antibodies (Abs) and PR3 ANCA-containing sera from WG patients endowed human oral, lung, and kidney epithelial cells with responsiveness to PAMPs in terms of the production of proinflammatory cytokines, such as interleukin-6 (IL-6), IL-8, monocyte chemoattractant protein-1, and tumor necrosis factor alpha. |
| 1908 | 18495849 | Protease-activated receptor-2 (PAR-2) agonist peptides mimicked the priming effects of PR3 ANCA against PAMPs. |
| 1909 | 18495849 | Furthermore, the anti-PR3 Ab-mediated cell activation was significantly abolished by RNA interference targeting PAR-2 and NF-kappaB. |
| 1910 | 18490717 | We observed that radiosensitive and radioresistant cells played distinct roles in the innate response to flagellin, with the radiosensitive cells producing the majority of the TNF-alpha, IL-12, and IL-6 cytokines and the radioresistant cells most of the KC, IP-10, and MCP-1 cytokines. |
| 1911 | 18490717 | We observed that radiosensitive and radioresistant cells played distinct roles in the innate response to flagellin, with the radiosensitive cells producing the majority of the TNF-alpha, IL-12, and IL-6 cytokines and the radioresistant cells most of the KC, IP-10, and MCP-1 cytokines. |
| 1912 | 18490717 | Further studies revealed that hemopoietic and nonhemopoietic expression of the cytokines TNF-alpha and IL-6, but not IL-1, played an important role in promoting flagellin-induced Ab responses. |
| 1913 | 18490717 | Further studies revealed that hemopoietic and nonhemopoietic expression of the cytokines TNF-alpha and IL-6, but not IL-1, played an important role in promoting flagellin-induced Ab responses. |
| 1914 | 18484346 | This review focuses on the different vaccination strategies with cytokines (including Tumor Necrosis Factor (TNF)alpha, Interleukin-1beta (IL-1beta), IL-17) in different autoimmune diseases in preclinical studies; the benefit/risk ratio of such a strategy and the present development of clinical trials in some autoimmune diseases are also discussed. |
| 1915 | 18481222 | The secretion of Th type 1 (TNF, IFN-gamma and IL-2) and Th type 2 (IL-4 and IL-6) cytokines was tested in the medium fluid of purified PBL and splenocyte cultures; their absolute values were expressed in relative indexes. |
| 1916 | 18481222 | The secretion of Th type 1 (TNF, IFN-gamma and IL-2) and Th type 2 (IL-4 and IL-6) cytokines was tested in the medium fluid of purified PBL and splenocyte cultures; their absolute values were expressed in relative indexes. |
| 1917 | 18481222 | The PBL from FpgD1/313 immunized mice showed increased secretion of both T(H)1 (TNF) as well as T(H)2 (IL-4) cytokines (7-10-fold, respectively). |
| 1918 | 18481222 | The PBL from FpgD1/313 immunized mice showed increased secretion of both T(H)1 (TNF) as well as T(H)2 (IL-4) cytokines (7-10-fold, respectively). |
| 1919 | 18480235 | In addition to standard clinical and laboratory parameter testing, the levels of expression of interleukin-1beta (IL-1beta), IL-6, IL-8, and IL-10, tumor necrosis factor-alpha, FasL, and CCL2 mRNA were also measured by real-time reverse transcriptase PCR. |
| 1920 | 18479887 | Protracted depressive-like behavior, but not sickness behavior, was associated with sustained increase in plasma interferon-gamma and TNF-alpha concentrations and peripheral IDO activation. |
| 1921 | 18468738 | Moreover, mice receiving RT-ODCsig gene mounted a mixed Th1/Th2 response characterized by the in vitro secretion of IFN-gamma, IL-2, TNF-alpha, IL-4, and IL-10 upon stimulation of splenocytes with RT protein or RT derived peptides. |
| 1922 | 18462845 | The effects of IL-6 and TNF-alpha as molecular adjuvants on immune responses to FMDV and maturation of dendritic cells by DNA vaccination. |
| 1923 | 18462845 | The effects of IL-6 and TNF-alpha as molecular adjuvants on immune responses to FMDV and maturation of dendritic cells by DNA vaccination. |
| 1924 | 18462845 | The effects of IL-6 and TNF-alpha as molecular adjuvants on immune responses to FMDV and maturation of dendritic cells by DNA vaccination. |
| 1925 | 18462845 | In this study, we investigated whether co-inoculation of a construct expressing either IL-6 or TNF-alpha as the molecular adjuvant with FMDV DNA vaccine, pcD-VP1, can increase immune responses. |
| 1926 | 18462845 | In this study, we investigated whether co-inoculation of a construct expressing either IL-6 or TNF-alpha as the molecular adjuvant with FMDV DNA vaccine, pcD-VP1, can increase immune responses. |
| 1927 | 18462845 | In this study, we investigated whether co-inoculation of a construct expressing either IL-6 or TNF-alpha as the molecular adjuvant with FMDV DNA vaccine, pcD-VP1, can increase immune responses. |
| 1928 | 18462845 | Compared to the group immunized with pcD-VP1 alone, the co-inoculation with either molecular adjuvant induced a higher ratio of IgG2a/IgG1, higher levels of expression of IFN-gamma in CD4+ and CD8+ T cells, IL-4 in CD4+ T cells, and in vivo antigen-specific cytotoxic response. |
| 1929 | 18462845 | Compared to the group immunized with pcD-VP1 alone, the co-inoculation with either molecular adjuvant induced a higher ratio of IgG2a/IgG1, higher levels of expression of IFN-gamma in CD4+ and CD8+ T cells, IL-4 in CD4+ T cells, and in vivo antigen-specific cytotoxic response. |
| 1930 | 18462845 | Compared to the group immunized with pcD-VP1 alone, the co-inoculation with either molecular adjuvant induced a higher ratio of IgG2a/IgG1, higher levels of expression of IFN-gamma in CD4+ and CD8+ T cells, IL-4 in CD4+ T cells, and in vivo antigen-specific cytotoxic response. |
| 1931 | 18462845 | Together, the results demonstrate that IL-6 and TNF-alpha used as molecular adjuvants can enhance the antigen-specific cell-mediated responses elicited by VP1 DNA vaccine. |
| 1932 | 18462845 | Together, the results demonstrate that IL-6 and TNF-alpha used as molecular adjuvants can enhance the antigen-specific cell-mediated responses elicited by VP1 DNA vaccine. |
| 1933 | 18462845 | Together, the results demonstrate that IL-6 and TNF-alpha used as molecular adjuvants can enhance the antigen-specific cell-mediated responses elicited by VP1 DNA vaccine. |
| 1934 | 18456294 | The clinical signs correlated with the systemic TNF-alpha and IL-12 levels. |
| 1935 | 18456294 | ORF1 vaccination elevated T-helper (Th)1 (IFN-gamma; P<0.001) and Th2 (IL-13; P<0.05) cytokine levels on DPI 35, while ORF2 markedly elevated the expression of the humoral immunity- and Th-2-related cytokine IL-10 (P<0.001) on DPI 35. |
| 1936 | 18453582 | IL-12-impaired and IL-12-secreting dendritic cells produce IL-23 upon CD154 restimulation. |
| 1937 | 18453582 | However, upon restimulation with rhesus macaque CD154, GA/d-cAMP-activated DCs produced IL-12p40/IL-23. |
| 1938 | 18453582 | Additionally, DCs activated by proinflammatory cytokines following protocols for the generation of cells used in clinical studies secreted significantly more IL-23 upon CD154 restimulation than following prior activation. |
| 1939 | 18453582 | When similarly injected, GA/d-cAMP as well as cytokine-activated protein-loaded DCs induced comparable Th immune responses characterized by secretion of IFN-gamma, TNF, and IL-17, and transiently expanded FOXP3(+) regulatory T cells. |
| 1940 | 18450338 | The current "gold standard" for generation of dendritic cell (DC) used in DC-based cancer vaccine studies is maturation of monocyte-derived DCs with tumor necrosis factor-alpha (TNF-alpha)/IL-1beta/IL-6 and prostaglandin E(2) (PGE(2)). |
| 1941 | 18450338 | The current "gold standard" for generation of dendritic cell (DC) used in DC-based cancer vaccine studies is maturation of monocyte-derived DCs with tumor necrosis factor-alpha (TNF-alpha)/IL-1beta/IL-6 and prostaglandin E(2) (PGE(2)). |
| 1942 | 18450338 | Recently, a protocol for producing so-called alpha-Type-1 polarized dendritic cells (alphaDC1) in serum-free medium was published based on maturation of monocyte-derived DCs with TNF-alpha/IL-1-beta/polyinosinic:polycytidylic acid (poly-I:C)/interferon (IFN)-alpha and IFN-gamma. |
| 1943 | 18450338 | Recently, a protocol for producing so-called alpha-Type-1 polarized dendritic cells (alphaDC1) in serum-free medium was published based on maturation of monocyte-derived DCs with TNF-alpha/IL-1-beta/polyinosinic:polycytidylic acid (poly-I:C)/interferon (IFN)-alpha and IFN-gamma. |
| 1944 | 18450338 | We showed that alphaDC1 in this protocol induce lower up-regulation of CD83 and several other maturation markers, co-stimulatory molecules and CCR7 together with higher up-regulation of inhibitory molecules such as PD-L1, ILT2, ILT3 as compared to sDC. |
| 1945 | 18450338 | We showed that alphaDC1 in this protocol induce lower up-regulation of CD83 and several other maturation markers, co-stimulatory molecules and CCR7 together with higher up-regulation of inhibitory molecules such as PD-L1, ILT2, ILT3 as compared to sDC. |
| 1946 | 18442785 | Also, exposure of DCs to EP54 (50 microg/ml) induced the activation of genes specific for the Th1 cytokines IL-6, IL-12, INFgamma, and TNFalpha as well as the Th2 cytokine IL-4. |
| 1947 | 18435687 | Although both Th1 (IFN-gamma, TNF-alpha and IL-12) and Th2 (IL-4 and IL-10) cytokines were secreted by the PBMCs of the P. vivax-exposed individuals in response to PvTRAg, the overall response was more inclined towards Th2. |
| 1948 | 18433946 | Immunization with an HIV-1 immunogen induces CD4+ and CD8+ HIV-1-specific polyfunctional responses in patients with chronic HIV-1 infection receiving antiretroviral therapy. |
| 1949 | 18433946 | Fifty-four HIV-1 infected patients receiving antiretroviral treatment (ART) and immunization with an HIV-1 immunogen or placebo, periodically every 3 months throughout a period of 36 months, were evaluated for the purposes of analysing the development of HIV-1-specific CD4+ and CD8+ responses. |
| 1950 | 18433946 | A significant increase of proliferating and IFN-gamma producing CD8+ HIV-1-specific T cells, of HIV-1-specific precursor frequencies for CD8+ and for CD4+ T cells and of Gag/pol-specific memory CTL precursors (CTLp) was observed in the immunogen group in comparison to placebo. |
| 1951 | 18433946 | IL-2 intracellular expression and IFN-gamma and TNF-alpha co-expression in HIV-1-specific CD8+ T cells were also substantially increased in the immunized group. |
| 1952 | 18425373 | IL-15 exerts its effect on innate and acquired immunity with the most prominent action in NK cells and CD8(+) memory T cells. |
| 1953 | 18425373 | In our experiments, in a model of B78-H1 murine transplantable melanoma, tumor-bearing mice were treated with different cytokine-gene modified tumor cell vaccines (producing TNF-alpha, GM-CSF, IL-12 or IL-6/sIL-6R) followed by a series of IL-15 injections. |
| 1954 | 18425373 | Tumors treated with the combination of B78-H1 melanoma cells secreting IL-12 (B78/IL-12 vaccine) and IL-15 were heavily infiltrated by granulocytes. |
| 1955 | 18425373 | IL-15, either alone or in combination with the B78/IL-12 vaccine, influenced infiltration of tumors with CD3(+) lymphocytes, CD4(+)and CD8(+). |
| 1956 | 18414898 | IFNG +874T/A, IL10 -1082G/A and TNF -308G/A polymorphisms in association with tuberculosis susceptibility: a meta-analysis study. |
| 1957 | 18414898 | IFNG +874T/A, IL10 -1082G/A and TNF -308G/A polymorphisms in association with tuberculosis susceptibility: a meta-analysis study. |
| 1958 | 18414898 | IFNG +874T/A, IL10 -1082G/A and TNF -308G/A polymorphisms in association with tuberculosis susceptibility: a meta-analysis study. |
| 1959 | 18414898 | IFNG +874T/A, IL10 -1082G/A and TNF -308G/A polymorphisms in association with tuberculosis susceptibility: a meta-analysis study. |
| 1960 | 18414898 | In tuberculosis (TB), interferon-gamma (IFNgamma) is crucial to control intracellular growth of Mycobacterium tuberculosis while interleukin-10 (IL-10) has an antagonistic role. |
| 1961 | 18414898 | In tuberculosis (TB), interferon-gamma (IFNgamma) is crucial to control intracellular growth of Mycobacterium tuberculosis while interleukin-10 (IL-10) has an antagonistic role. |
| 1962 | 18414898 | In tuberculosis (TB), interferon-gamma (IFNgamma) is crucial to control intracellular growth of Mycobacterium tuberculosis while interleukin-10 (IL-10) has an antagonistic role. |
| 1963 | 18414898 | In tuberculosis (TB), interferon-gamma (IFNgamma) is crucial to control intracellular growth of Mycobacterium tuberculosis while interleukin-10 (IL-10) has an antagonistic role. |
| 1964 | 18414898 | Tumor necrosis factor (TNF) is a central mediator of granuloma formation and control of bacilli spread synergizing with IFNgamma to hamper M. tuberculosis infection. |
| 1965 | 18414898 | Tumor necrosis factor (TNF) is a central mediator of granuloma formation and control of bacilli spread synergizing with IFNgamma to hamper M. tuberculosis infection. |
| 1966 | 18414898 | Tumor necrosis factor (TNF) is a central mediator of granuloma formation and control of bacilli spread synergizing with IFNgamma to hamper M. tuberculosis infection. |
| 1967 | 18414898 | Tumor necrosis factor (TNF) is a central mediator of granuloma formation and control of bacilli spread synergizing with IFNgamma to hamper M. tuberculosis infection. |
| 1968 | 18414898 | The aim of this study was to determine the association of the interferon-gamma gene (IFNG) +874T/A, interleukin-10 gene (IL10) -1082G/A and tumor necrosis factor gene (TNF) -308G/A SNPs with TB in several populations using meta-analysis. |
| 1969 | 18414898 | The aim of this study was to determine the association of the interferon-gamma gene (IFNG) +874T/A, interleukin-10 gene (IL10) -1082G/A and tumor necrosis factor gene (TNF) -308G/A SNPs with TB in several populations using meta-analysis. |
| 1970 | 18414898 | The aim of this study was to determine the association of the interferon-gamma gene (IFNG) +874T/A, interleukin-10 gene (IL10) -1082G/A and tumor necrosis factor gene (TNF) -308G/A SNPs with TB in several populations using meta-analysis. |
| 1971 | 18414898 | The aim of this study was to determine the association of the interferon-gamma gene (IFNG) +874T/A, interleukin-10 gene (IL10) -1082G/A and tumor necrosis factor gene (TNF) -308G/A SNPs with TB in several populations using meta-analysis. |
| 1972 | 18414898 | Eleven studies were included in the IFNG +874T/A meta-analysis, while eight were used for the IL10 -1082G/A, and 10 were employed for TNF -308G/A. |
| 1973 | 18414898 | Eleven studies were included in the IFNG +874T/A meta-analysis, while eight were used for the IL10 -1082G/A, and 10 were employed for TNF -308G/A. |
| 1974 | 18414898 | Eleven studies were included in the IFNG +874T/A meta-analysis, while eight were used for the IL10 -1082G/A, and 10 were employed for TNF -308G/A. |
| 1975 | 18414898 | Eleven studies were included in the IFNG +874T/A meta-analysis, while eight were used for the IL10 -1082G/A, and 10 were employed for TNF -308G/A. |
| 1976 | 18389479 | DiC14-amidine liposomes also activated human DC, as shown by synthesis of IL-12p40 and TNF-alpha, accumulation of IL-6, IFN-beta and CXCL10 mRNA, and up-regulation of membrane expression of CD80 and CD86. |
| 1977 | 18389479 | DC stimulation by diC14-amidine liposomes was associated with activation of NF-kappaB, ERK1/2, JNK and p38 MAP kinases. |
| 1978 | 18389479 | Finally, we demonstrated in mouse and human cells that diC14-amidine liposomes use Toll-like receptor 4 to elicit both MyD88-dependent and Toll/IL-1R-containing adaptor inducing interferon IFN-beta (TRIF)-dependent responses. |
| 1979 | 18385234 | In contrast, the inflammatory response was better controlled by wild-type MV, as revealed by inhibition of interleukin-6 and tumor necrosis factor alpha transcription. |
| 1980 | 18378002 | Interleukin-1beta (IL-1beta), interleukin-8 (IL-8), tumor necrosis factor alpha 2 (TNF alpha 2) and heat shock protein 70 (Hsp70) gene expression in trout liver was monitored by real-time PCR using Acidic Ribosomal Phosphoprotein P0 (ARP) as internal standard. |
| 1981 | 18378002 | Interleukin-1beta (IL-1beta), interleukin-8 (IL-8), tumor necrosis factor alpha 2 (TNF alpha 2) and heat shock protein 70 (Hsp70) gene expression in trout liver was monitored by real-time PCR using Acidic Ribosomal Phosphoprotein P0 (ARP) as internal standard. |
| 1982 | 18378002 | This study also demonstrated the stimulatory properties of Ergosan on cytokine genes expression involved in innate immune response: liver IL-1beta, IL-8 and TNF alpha 2 gene expression was significantly (P<0.05) higher in trout fed on Ergosan compared to control, indicating a positive role of this feed additive in improving the immune responsiveness to AquaVac vaccine. |
| 1983 | 18378002 | This study also demonstrated the stimulatory properties of Ergosan on cytokine genes expression involved in innate immune response: liver IL-1beta, IL-8 and TNF alpha 2 gene expression was significantly (P<0.05) higher in trout fed on Ergosan compared to control, indicating a positive role of this feed additive in improving the immune responsiveness to AquaVac vaccine. |
| 1984 | 18363879 | Moraxella catarrhalis lipooligosaccharide selectively upregulates ICAM-1 expression on human monocytes and stimulates adjacent naïve monocytes to produce TNF-alpha through cellular cross-talk. |
| 1985 | 18363879 | Moraxella catarrhalis lipooligosaccharide selectively upregulates ICAM-1 expression on human monocytes and stimulates adjacent naïve monocytes to produce TNF-alpha through cellular cross-talk. |
| 1986 | 18363879 | Moraxella catarrhalis lipooligosaccharide selectively upregulates ICAM-1 expression on human monocytes and stimulates adjacent naïve monocytes to produce TNF-alpha through cellular cross-talk. |
| 1987 | 18363879 | ICAM-1 upregulation on human monocytes by the LOS required surface CD14, TLR4, NF-kappaB p65 and c-Jun N-terminal kinase (JNK) activity. |
| 1988 | 18363879 | ICAM-1 upregulation on human monocytes by the LOS required surface CD14, TLR4, NF-kappaB p65 and c-Jun N-terminal kinase (JNK) activity. |
| 1989 | 18363879 | ICAM-1 upregulation on human monocytes by the LOS required surface CD14, TLR4, NF-kappaB p65 and c-Jun N-terminal kinase (JNK) activity. |
| 1990 | 18363879 | Our study also revealed that the LOS-induced surface ICAM-1 expression was partially mediated through a TNF-alpha dependent autocrine mechanism and could be further augmented by lipopolysaccharide-binding protein in serum. |
| 1991 | 18363879 | Our study also revealed that the LOS-induced surface ICAM-1 expression was partially mediated through a TNF-alpha dependent autocrine mechanism and could be further augmented by lipopolysaccharide-binding protein in serum. |
| 1992 | 18363879 | Our study also revealed that the LOS-induced surface ICAM-1 expression was partially mediated through a TNF-alpha dependent autocrine mechanism and could be further augmented by lipopolysaccharide-binding protein in serum. |
| 1993 | 18363879 | In addition, M. catarrhalis LOS also stimulated human monocytes to produce pro-inflammatory cytokines in both TLR4- and CD14-dependent pathways. |
| 1994 | 18363879 | In addition, M. catarrhalis LOS also stimulated human monocytes to produce pro-inflammatory cytokines in both TLR4- and CD14-dependent pathways. |
| 1995 | 18363879 | In addition, M. catarrhalis LOS also stimulated human monocytes to produce pro-inflammatory cytokines in both TLR4- and CD14-dependent pathways. |
| 1996 | 18363879 | Furthermore, the LOS-activated human monocytes secreted a significantly high level of IL-8, and could stimulate adjacent naïve monocytes to produce TNF-alpha which was partially mediated via membrane ICAM-1 and IL-8/IL-8RA. |
| 1997 | 18363879 | Furthermore, the LOS-activated human monocytes secreted a significantly high level of IL-8, and could stimulate adjacent naïve monocytes to produce TNF-alpha which was partially mediated via membrane ICAM-1 and IL-8/IL-8RA. |
| 1998 | 18363879 | Furthermore, the LOS-activated human monocytes secreted a significantly high level of IL-8, and could stimulate adjacent naïve monocytes to produce TNF-alpha which was partially mediated via membrane ICAM-1 and IL-8/IL-8RA. |
| 1999 | 18362335 | IL-15 as a mediator of CD4+ help for CD8+ T cell longevity and avoidance of TRAIL-mediated apoptosis. |
| 2000 | 18362335 | CD4+ helper T cells contribute to the induction and maintenance of antigen-specific CD8+ T cells. |
| 2001 | 18362335 | Their absence results in short-lived antigen-specific CD8+ T cells and defective secondary CD8+ T cell responses because of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-mediated apoptosis. |
| 2002 | 18362335 | Here, we show that IL-15 codelivered with vaccines can overcome CD4+ T cell deficiency for promoting longevity of antigen-specific CD8+ T cells and avoidance of TRAIL-mediated apoptosis. |
| 2003 | 18362335 | In both priming and secondary responses, IL-15 down-regulates proapoptotic Bax, an intermediate in TRAIL-mediated apoptosis, and increases anti-apoptotic Bcl-X(L) in CD8+ T cells. |
| 2004 | 18362335 | Thus, IL-15 is sufficient to mimic CD4+ T cell help. |
| 2005 | 18362335 | Antigen-specific CD4+ T cells induce dendritic cells (DCs) to produce IL-15. |
| 2006 | 18362335 | Therefore, IL-15 codelivered with vaccines can overcome CD4+ helper T cell deficiency for induction of functionally efficient CD8+ T cells and maintenance of CD8+ cytotoxic T lymphocytes (CTLs), and IL-15 is probably one of the natural mediators of help. |
| 2007 | 18354173 | Assessment of Bet v 1-specific CD4+ T cell responses in allergic and nonallergic individuals using MHC class II peptide tetramers. |
| 2008 | 18354173 | In this study, we used HLA-DRB1*0101, DRB1*0401, and DRB1*1501 peptide tetramers combined with cytokine surface capture assays to characterize CD4(+) T cell responses against the immunodominant T cell epitope (peptide 141-155) from the major birch pollen allergen Bet v 1, in both healthy and allergic individuals. |
| 2009 | 18354173 | Analysis at a single-cell level revealed that allergen-specific CD4(+) T cells from healthy individuals secrete IFN-gamma and IL-10 in response to the allergen, whereas cells from allergic patients are bona fide Th2 cells (producing mostly IL-5, some IL-10, but no IFN-gamma), as corroborated by patterns of cytokines produced by T cell clones. |
| 2010 | 18354173 | A fraction of Bet v 1-specific cells isolated from healthy, but not allergic, individuals also expresses CTLA-4, glucocorticoid-induced TNF receptor, and Foxp 3, indicating that they represent regulatory T cells. |
| 2011 | 18354157 | Pulsing DCs with a lysate of L. major did not affect DC maturation with TNF-alpha or LPS+anti-CD40. |
| 2012 | 18354157 | When the expression of different Notch ligands on DCs was analyzed, we found increased expression of Th2-promoting Jagged2 in TNF-DCs, whereas LPS+CD40-DCs up-regulated the Th1-inducing Delta4 and Jagged1 molecules. |
| 2013 | 18338832 | In the present study, we used attenuated S. typhimurium as a carrier to deliver a eukaryotic expression vector (pSNhTS) that contains the second mitochondria-derived activator of caspases (Smac) and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) genes under the control of the hTERT promoter. |
| 2014 | 18338832 | The results of in vitro experiments showed that Smac could enhance TRAIL-induced apoptosis in tumor cells and the hTERT promoter could drive specific gene expression in tumor cells, but not in normal cells. |
| 2015 | 18338832 | /SNhTS was due to the synergistic antitumoral properties of Smac and TRAIL-recombinant proteins. |
| 2016 | 18337575 | While rAd5-Gag induced primarily gamma interferon-positive (IFN-gamma(+)) and IFN-gamma(+)/tumor necrosis factor alpha(+) (TNF-alpha(+)) T-lymphocyte responses, rAd26-Gag and rAd48-Gag induced higher proportions of interleukin-2(+) (IL-2(+)) and polyfunctional IFN-gamma(+)/TNF-alpha(+)/IL-2(+) T-lymphocyte responses. |
| 2017 | 18337575 | These data demonstrate that the rare serotype rAd vectors elicited T-lymphocyte responses that were phenotypically distinct from those elicited by rAd5 vectors and suggest the functional relevance of polyfunctional CD8(+) and CD4(+) T-lymphocyte responses. |
| 2018 | 18322193 | We report that, in sharp contrast to the effector cells (CTLs) that kill DCs in a granzyme B- and perforin-dependent mechanism, memory CD8(+) T cells enhance the ability of DCs to produce IL-12 and to induce functional Th1 and CTL responses in naive CD4(+) and CD8(+) T cell populations. |
| 2019 | 18322193 | Moreover, memory CD8(+) T cells that release the DC-activating factor TNF-alpha before the release of cytotoxic granules induce DC expression of an endogenous granzyme B inhibitor PI-9 and protect DCs from CTL killing with similar efficacy as CD4(+) Th cells. |
| 2020 | 18322193 | The currently identified DC-protective function of memory CD8(+) T cells helps to explain the phenomenon of CD8(+) T cell memory, reduced dependence of recall responses on CD4(+) T cell help, and the importance of delayed administration of booster doses of vaccines for the optimal outcome of immunization. |
| 2021 | 18321614 | HSP-70 and PFR-2 also produced an increase of the TNF-alpha transcripts abundance. |
| 2022 | 18321614 | No measurable induction of IL-10 was observed and low levels of IL-4 mRNA were produced in response to the three mentioned recombinant antigens. |
| 2023 | 18319583 | The results revealed that IFN-gamma and IL-6 were upregulated during the first week post-vaccination. |
| 2024 | 18319583 | Low level expressions of IL-1alpha, IL-1beta, TNFalpha and IL-10 and no expression of IL-2 and IL-4 were observed compared with the control camels. |
| 2025 | 18317362 | Given the perceived need to augment antitumor type-1 immunity (TC1 and Th1) as a therapeutic end point, and the known functional plasticity of DC populations that may display heterogeneous capacity to promote T-cell responses, we sought to identify a preferred DC preparation with this capacity. |
| 2026 | 18317362 | We compared 2 different preparations of monocyte-derived DC using interferon-alpha (IFN-alpha) (IFN-DC and alphaDC1) with classic DCs "matured" (mDCs) using interleukin-1beta/interleukin-6/tumor necrosis factor-alpha/prostaglandin E2, for their ability to promote autologous TC1 antitumor responses from RCC patients in vitro. |
| 2027 | 18317362 | IFN-alpha-conditioned DC promoted significantly higher numbers of RCC-specific CD8+ T cells exhibiting a cytotoxic phenotype after in vitro stimulation (IVS) than cytokine cocktail-mDCs. |
| 2028 | 18313150 | Results from a protein cytokine array showed significant elevations over time in interleukin (IL)-1alpha, IL-1beta, IL-6, IL-12, MCP-1, IFNgamma, TNFalpha, MIP-1alpha, and RANTES in homogenized brain samples of infected mice. |
| 2029 | 18311150 | In this study, the zinc-finger A20, a negative regulator of the Toll-like receptor and tumor necrosis factor receptor signaling pathways, was found to play a crucial part in controlling the maturation, cytokine production and immunostimulatory potency of dendritic cells (DCs). |
| 2030 | 18311150 | A20-silenced DCs showed spontaneous and enhanced expression of costimulatory molecules and proinflammatory cytokines and had different effects on T cell subsets: they inhibited T(reg) cells and hyperactivated tumor-infiltrating cytotoxic T lymphocytes and T helper cells that produced interleukin-6 and tumor necrosis factor-alpha and were refractory to T(reg) cell-mediated suppression. |
| 2031 | 20401320 | To measure the interferon gamma (IFN-γ) and tumor necrosis factor (TNF) anti-viral cytokines produced by peripheral CD4+ cells that recognize VP6 epitopes, whole blood cells from one infected macaque were stimulated in vitro with VP6 peptides. |
| 2032 | 18305406 | Upon recognition of the heat-denatured tumor antigens, macrophages and dendritic cells were found to acutely upregulate the expression of co-stimulatory molecules such as B7.2, as well as the secretion of inflammatory cytokines such as IL-12 and TNF-alpha. |
| 2033 | 18299457 | Expression of NadA on the surface on Escherichia coli does not increase bacterial-monocyte association, but a NadA-positive strain induced a significantly higher amount of TNF-alpha and IL-8 compared with the parental NadA-negative strain, suggesting that NadA has an intrinsic stimulatory action on these cells. |
| 2034 | 18299457 | Expression of NadA on the surface on Escherichia coli does not increase bacterial-monocyte association, but a NadA-positive strain induced a significantly higher amount of TNF-alpha and IL-8 compared with the parental NadA-negative strain, suggesting that NadA has an intrinsic stimulatory action on these cells. |
| 2035 | 18299457 | Consistently, highly pure, soluble NadA(Delta351-405), a proposed component of an antimeningococcal vaccine, efficiently stimulates monocytes/macrophages to secrete a selected pattern of cytokines and chemotactic factors characterized by high levels of IL-8, IL-6, MCP-1, and MIP-1alpha and low levels of the main vasoactive mediators TNF-alpha and IL-1. |
| 2036 | 18299457 | Consistently, highly pure, soluble NadA(Delta351-405), a proposed component of an antimeningococcal vaccine, efficiently stimulates monocytes/macrophages to secrete a selected pattern of cytokines and chemotactic factors characterized by high levels of IL-8, IL-6, MCP-1, and MIP-1alpha and low levels of the main vasoactive mediators TNF-alpha and IL-1. |
| 2037 | 18292584 | Ex vivo stimulation of whole blood with BCG for 12 h induced expression of predominantly IFN-gamma, IL-2, and TNF-alpha in CD4+ T cells in seven distinct cytokine combinations. |
| 2038 | 18292584 | Ex vivo stimulation of whole blood with BCG for 12 h induced expression of predominantly IFN-gamma, IL-2, and TNF-alpha in CD4+ T cells in seven distinct cytokine combinations. |
| 2039 | 18292584 | IL-4 and IL-10 expression was detected in CD4+ T cells at low frequencies and only in cells that did not coexpress type 1 cytokines. |
| 2040 | 18292584 | IL-4 and IL-10 expression was detected in CD4+ T cells at low frequencies and only in cells that did not coexpress type 1 cytokines. |
| 2041 | 18292584 | Specific CD8+ T cells were less frequent than CD4+ T cells and produced mainly IFN-gamma and/or IL-2 and less TNF-alpha, IL-4, and IL-10. |
| 2042 | 18292584 | Specific CD8+ T cells were less frequent than CD4+ T cells and produced mainly IFN-gamma and/or IL-2 and less TNF-alpha, IL-4, and IL-10. |
| 2043 | 18292584 | Importantly, many mycobacteria-specific CD4+ and CD8+ T cells did not produce IFN-gamma. |
| 2044 | 18292584 | Importantly, many mycobacteria-specific CD4+ and CD8+ T cells did not produce IFN-gamma. |
| 2045 | 18292584 | Among five phenotypic patterns of CD4+ T cells, central memory cells were more likely to be IL-2+ and effector cells were more likely to be IFN-gamma+. |
| 2046 | 18292584 | Among five phenotypic patterns of CD4+ T cells, central memory cells were more likely to be IL-2+ and effector cells were more likely to be IFN-gamma+. |
| 2047 | 18286194 | In addition, we found a higher frequency of triple-positive IFN-gamma, TNF-alpha and IL-2 secreting E3-specific CD8+ T-cells 8 weeks after vaccination with MVA lacking B15R. |
| 2048 | 18266272 | AdC7 and AdC9 elicited strong immunogenicity ( approximately 20% of CD8(+) T cells in spleen), equivalent to or outperforming AdH5 and inducing sterile protection in 92% (C9), 83% (H5 and C7) and 67% (C6) of the mice, providing the first evidence of single-dose protection to Plasmodium berghei. |
| 2049 | 18266272 | Multifunctional CD8(+) T cell responses (co-expressing IFN-gamma, TNF-alpha and IL-2) were also induced by the Ad in higher percentages than the poxviral vectors. |
| 2050 | 18258343 | RTS,S/AS01B-induced high specific antibody titers and increased the frequency of mouse CD4(+) and CD8(+) T cells expressing IFN-gamma, and of monkey CD4(+) T cells expressing IL-2 and/or IFN-gamma and/or TNF-alpha upon stimulation with vaccine antigens. |
| 2051 | 18256207 | This work aimed at evaluating the degree of anemia and the plasmatic profile of the cytokines tumor necrosis factor alpha (TNF-alpha), gamma interferon (IFN-gamma), interleukin-12 (IL-12), migration inhibitory factor (MIF), and IL-10 and the monocyte chemotactic protein-1 (MCP-1) chemokine, as well as evaluating the presence of antibodies directed to components of the normal erythrocyte membrane and to cardiolipin in individuals with malaria from the Brazilian Amazon. |
| 2052 | 18256207 | This work aimed at evaluating the degree of anemia and the plasmatic profile of the cytokines tumor necrosis factor alpha (TNF-alpha), gamma interferon (IFN-gamma), interleukin-12 (IL-12), migration inhibitory factor (MIF), and IL-10 and the monocyte chemotactic protein-1 (MCP-1) chemokine, as well as evaluating the presence of antibodies directed to components of the normal erythrocyte membrane and to cardiolipin in individuals with malaria from the Brazilian Amazon. |
| 2053 | 18256207 | This work aimed at evaluating the degree of anemia and the plasmatic profile of the cytokines tumor necrosis factor alpha (TNF-alpha), gamma interferon (IFN-gamma), interleukin-12 (IL-12), migration inhibitory factor (MIF), and IL-10 and the monocyte chemotactic protein-1 (MCP-1) chemokine, as well as evaluating the presence of antibodies directed to components of the normal erythrocyte membrane and to cardiolipin in individuals with malaria from the Brazilian Amazon. |
| 2054 | 18256207 | Significant increases in the concentrations of TNF-alpha, IFN-gamma, MIF, and MCP-1 were observed in patients with P. falciparum and P. vivax malaria, whereas the concentrations of IL-10 was increased only in patients with P. vivax infection. |
| 2055 | 18256207 | Significant increases in the concentrations of TNF-alpha, IFN-gamma, MIF, and MCP-1 were observed in patients with P. falciparum and P. vivax malaria, whereas the concentrations of IL-10 was increased only in patients with P. vivax infection. |
| 2056 | 18256207 | Significant increases in the concentrations of TNF-alpha, IFN-gamma, MIF, and MCP-1 were observed in patients with P. falciparum and P. vivax malaria, whereas the concentrations of IL-10 was increased only in patients with P. vivax infection. |
| 2057 | 18256207 | Higher concentrations of IL-12 and IL-10 were observed in the P. falciparum anemic patients, while for TNF-alpha this profile was observed in the nonanemic ones. |
| 2058 | 18256207 | Higher concentrations of IL-12 and IL-10 were observed in the P. falciparum anemic patients, while for TNF-alpha this profile was observed in the nonanemic ones. |
| 2059 | 18256207 | Higher concentrations of IL-12 and IL-10 were observed in the P. falciparum anemic patients, while for TNF-alpha this profile was observed in the nonanemic ones. |
| 2060 | 18256187 | The T cells simultaneously make IFN-gamma, tumor necrosis factor (TNF)-alpha, and IL-2, and in high amounts for prolonged periods. |
| 2061 | 18256187 | The adjuvant role of poly IC requires Toll-like receptor (TLR) 3 and melanoma differentiation-associated gene-5 (MDA5) receptors, but its analog poly IC(12)U requires only TLR3. |
| 2062 | 18250467 | MoDC, the most common inflammatory cell type in infected lungs, induce robust naive T cell proliferation and produce NO synthase 2 (NOS2), whereas exMACs produce high levels of TNF-alpha and NOS2 and stimulate the proliferation of memory T cells. |
| 2063 | 18248757 | On the other hand, rBCG-Pertussis induces higher PT-specific IFN-gamma production and an increase in both IFN-gamma(+) and TNF-alpha(+)-CD4(+)-T cells than the whole cell pertussis vaccine and confers protection against a lethal intracerebral challenge with B. pertussis. |
| 2064 | 18245488 | Our results show the induction of an immune response against a newly defined PSCA epitope that is mediated primarily by CD8 T cells. |
| 2065 | 18245488 | The prostates of PSCA-vaccinated mice were infiltrated by CD4-positive, CD8-positive, CD11b-positive, and CD11c-positive cells. |
| 2066 | 18245488 | Vaccination induced MHC class I expression and cytokine production [IFN-gamma, tumor necrosis factor-alpha, interleukin 2 (IL-2), IL-4, and IL-5] within prostate tumors. |
| 2067 | 18240963 | The individual vaccines induced CD8(+) and CD4(+) T cells specific for the vaccine-expressed antigens in BALB/c mice. |
| 2068 | 18240963 | Th1 cytokine IFN-gamma and TNF-alpha levels from HIV-specific CD8(+) and CD4(+) T cells increased 20- and 8-fold, respectively, with a SAAVI MVA-C boost. |
| 2069 | 18237828 | Gene expression in fish vaccinated at 15 degrees C (the protected fish) was up-regulated with regard to the pro-inflammatory cytokines IFN-gamma, TNF-alpha, IL-6 and the anti-inflammatory cytokines IL-10 and TGF-beta, the cell receptors TcR, CD8alpha, CD4, C5aR and the teleost specific immunoglobulin IgT. |
| 2070 | 18202769 | DCs adenovirally transduced with the CEA gene were cultured under various conditions with tumor necrosis factor (TNF)-alpha, lipopolysaccharide (LPS), or OK-432. |
| 2071 | 18202769 | DCs adenovirally transduced with the CEA gene were cultured under various conditions with tumor necrosis factor (TNF)-alpha, lipopolysaccharide (LPS), or OK-432. |
| 2072 | 18202769 | In all groups (immature DCs, TNF-alpha/DCs, LPS/DCs, OK-432/DCs), CEA-specific CTLs were generated. |
| 2073 | 18202769 | In all groups (immature DCs, TNF-alpha/DCs, LPS/DCs, OK-432/DCs), CEA-specific CTLs were generated. |
| 2074 | 18202769 | OK-432-stimulated DCs (HLA-A24) induced the most potent cytotoxic activity against CEA-expressing targets (A24) but not against controls. |
| 2075 | 18202769 | OK-432-stimulated DCs (HLA-A24) induced the most potent cytotoxic activity against CEA-expressing targets (A24) but not against controls. |
| 2076 | 18202753 | Recently, we have demonstrated up-regulation of a new member of the LOX family, lysyl oxidase-like 4 (LOXL4), in invasive HNC revealed a significant correlation between LOXL4 expression and local lymph node metastases and higher tumour stages. |
| 2077 | 18202753 | The successfully transfected immature dendritic cells (DCs) were induced to mature with GM-CSF, IL-4, IL-1beta, TNF-alpha, IL-6, and PGE2, and then used to stimulate T cell enriched non-adherent fraction of PBMC. |
| 2078 | 18202753 | LOXL4 specific T cell stimulation induced cytotoxic T lymphocyte (CTL) response was monitored using IFN-gamma secretion from the non-adherent PBMC fraction exposed to mature, LOXL4 transfected DCs acting as the antigen presenting target cells. |
| 2079 | 18178854 | Neither hexaacylated nor pentaacylated synthetic lipid A induced NF-kappaB activity in wild-type transfectants under the identical transfection conditions used for LPS; however, increasing human MD-2 expression rescued responsiveness to hexaacylated lipid A only, while murine MD-2 was required to elicit a response to pentaacylated lipid A. |
| 2080 | 18178854 | Adherent PBMC of healthy volunteers were also compared for LPS-induced TNF-alpha, IL-6, IL-1beta, and IL-10 production. |
| 2081 | 18165707 | With regard to the cellular response, ScLL 50 and 100 microgram/animal stimulated the delayed-type hypersensitivity (DTH) reaction significantly (P < 0.05) higher than SLA or SLA plus ScLL 10 weeks after the challenge infection. |
| 2082 | 18165707 | The detection of high levels of IgG2a and the expression of mRNA cytokines, such as IFN-gamma, IL-12, and TNF-alpha (Th1 profiles), corroborated the protective role of this lectin against cutaneous leishmaniasis. |
| 2083 | 18165156 | Cells were stimulated with live or heat-killed Mycobacterium tuberculosis, and/or with recombinant guinea pig (rgp) TNF-alpha and/or rgp IFN-gamma. |
| 2084 | 18165156 | Cells were stimulated with live or heat-killed Mycobacterium tuberculosis, and/or with recombinant guinea pig (rgp) TNF-alpha and/or rgp IFN-gamma. |
| 2085 | 18165156 | Cells were stimulated with live or heat-killed Mycobacterium tuberculosis, and/or with recombinant guinea pig (rgp) TNF-alpha and/or rgp IFN-gamma. |
| 2086 | 18165156 | Cells were stimulated with live or heat-killed Mycobacterium tuberculosis, and/or with recombinant guinea pig (rgp) TNF-alpha and/or rgp IFN-gamma. |
| 2087 | 18165156 | In PM from BCG-vaccinated guinea pigs, IL-12p40 mRNA was significantly up-regulated; however, the level of IL-10 mRNA was not affected by prior vaccination. rgp TNF-alpha or rgp IFN-gamma, both alone and together, induced a significant increase of H(2)O(2) production in PM from BCG-vaccinated animals. |
| 2088 | 18165156 | In PM from BCG-vaccinated guinea pigs, IL-12p40 mRNA was significantly up-regulated; however, the level of IL-10 mRNA was not affected by prior vaccination. rgp TNF-alpha or rgp IFN-gamma, both alone and together, induced a significant increase of H(2)O(2) production in PM from BCG-vaccinated animals. |
| 2089 | 18165156 | In PM from BCG-vaccinated guinea pigs, IL-12p40 mRNA was significantly up-regulated; however, the level of IL-10 mRNA was not affected by prior vaccination. rgp TNF-alpha or rgp IFN-gamma, both alone and together, induced a significant increase of H(2)O(2) production in PM from BCG-vaccinated animals. |
| 2090 | 18165156 | In PM from BCG-vaccinated guinea pigs, IL-12p40 mRNA was significantly up-regulated; however, the level of IL-10 mRNA was not affected by prior vaccination. rgp TNF-alpha or rgp IFN-gamma, both alone and together, induced a significant increase of H(2)O(2) production in PM from BCG-vaccinated animals. |
| 2091 | 18165156 | MHC class II expression was dramatically up-regulated in PM from BCG-vaccinated animals stimulated with both rgp TNF-alpha and rgp IFN-gamma. |
| 2092 | 18165156 | MHC class II expression was dramatically up-regulated in PM from BCG-vaccinated animals stimulated with both rgp TNF-alpha and rgp IFN-gamma. |
| 2093 | 18165156 | MHC class II expression was dramatically up-regulated in PM from BCG-vaccinated animals stimulated with both rgp TNF-alpha and rgp IFN-gamma. |
| 2094 | 18165156 | MHC class II expression was dramatically up-regulated in PM from BCG-vaccinated animals stimulated with both rgp TNF-alpha and rgp IFN-gamma. |
| 2095 | 18165156 | The levels of IL-10 and IL-12p40 mRNA were significantly enhanced in PM stimulated with combinations of rgp TNF-alpha and rgp IFN-gamma, and those cells suppressed the intracellular accumulation of viable, virulent M. tuberculosis. |
| 2096 | 18165156 | The levels of IL-10 and IL-12p40 mRNA were significantly enhanced in PM stimulated with combinations of rgp TNF-alpha and rgp IFN-gamma, and those cells suppressed the intracellular accumulation of viable, virulent M. tuberculosis. |
| 2097 | 18165156 | The levels of IL-10 and IL-12p40 mRNA were significantly enhanced in PM stimulated with combinations of rgp TNF-alpha and rgp IFN-gamma, and those cells suppressed the intracellular accumulation of viable, virulent M. tuberculosis. |
| 2098 | 18165156 | The levels of IL-10 and IL-12p40 mRNA were significantly enhanced in PM stimulated with combinations of rgp TNF-alpha and rgp IFN-gamma, and those cells suppressed the intracellular accumulation of viable, virulent M. tuberculosis. |
| 2099 | 18164706 | After B. microti infection, the levels of interleukin (IL)-2, IL-4, IL-5, IL-10, IL-12p70, and tumor necrosis factor (TNF)-alpha in the treated group were significantly lower than in the control group. |
| 2100 | 18164561 | Both vaccines were able to induce a non-significant secretion of gamma interferon and did not induce the secretion of IL-4 or tumor necrosis factor (TNF)-alpha. |
| 2101 | 19578511 | Human monocytes were cultured with GM-CSF and IL-4 for 6 days under standard conditions, followed by another 2 days in the presence of M1, M4, T-cadinol or calamenene. |
| 2102 | 19578511 | The expression levels of CD1a, CD80, CD83, CD86 and HLA-DR on M1-primed DC, M4-primed DC, T-cadinol-primed DC and calamenene-primed DC were enhanced with a concomitant decrease in endocytic activity. |
| 2103 | 19578511 | Naïve T cells co-cultured with allogeneic M1-primed DC, M4-primed DC, T-cadinol-primed DC or calamenene-primed DC turned into typical Th1 cells, which produced large quantities of IFN-gamma and released small amounts of IL-4 depending on IL-12 secretion. |
| 2104 | 19578511 | In the CTL assay (cytotoxic T-lymphocyte assay), the production of IFN-gamma and (51)Cr release on M4-primed DC was more augmented than of immature DC or TNF-alpha-primed DC. |
| 2105 | 18160013 | Immunogenicity in macaques of the clinical product for a clade B DNA/MVA HIV vaccine: elicitation of IFN-gamma, IL-2, and TNF-alpha coproducing CD4 and CD8 T cells. |
| 2106 | 18160013 | Both CD4 and CD8 T cell responses had high frequencies of cytokine coproducing cells with >50% of the memory cells coproducing multiple cytokines including IL-2. |
| 2107 | 18156495 | Activin-A: a novel dendritic cell-derived cytokine that potently attenuates CD40 ligand-specific cytokine and chemokine production. |
| 2108 | 18156495 | Human monocyte-derived DCs (MoDCs) and the CD1c(+) and CD123(+) peripheral blood DC populations express both activin-A and the type I and II activin receptors. |
| 2109 | 18156495 | Furthermore, MoDCs and CD1c(+) myeloid DCs rapidly secrete high levels of activin-A after exposure to bacteria, specific toll-like receptor (TLR) ligands, or CD40 ligand (CD40L). |
| 2110 | 18156495 | Blocking autocrine activin-A signaling in DCs using its antagonist, follistatin, enhanced DC cytokine (IL-6, IL-10, IL-12p70, and tumor necrosis factor-alpha [TNF-alpha]) and chemokine (IL-8, IP-10, RANTES, and MCP-1) production during CD40L stimulation, but not TLR-4 ligation. |
| 2111 | 18156414 | However, production of cytokines, interferon-gamma, interleukin-12, and tumor necrosis factor alpha, was numerically increased in spleen cell cultures stimulated with mitogens from FOS:inulin-fed mice 1 and 4 wk postimmunization. |
| 2112 | 18085063 | The activation of memory T cells results in cascades of inflammatory cytokines, including tumor necrosis factor-alpha, interleukins (IL-2, IL-6, and IL-8), and other chemical mediators that increase vascular endothelial permeability or trigger death of target cells through apoptosis. |
| 2113 | 18068748 | Efficient inhibition of SIV replication in rhesus CD4+ T-cell clones by autologous immortalized SIV-specific CD8+ T-cell clones. |
| 2114 | 18068748 | We investigated the capacity of SIV-specific CTL clones (effectors), immortalized by transduction with human telomerase reverse transcriptase (hTERT), to suppress SIV replication in autologous hTERT immortalized CD4(+) T-cell clones (targets). |
| 2115 | 18068748 | Our in vitro assays of inhibition of viral replication, using T-cell clones as effectors and targets, provide a well-defined approach for evaluating possible mechanisms of CTL-mediated control of viral production which may involve direct killing of infected target cells and/or release of proinflammatory cytokines such as IFN-gamma and TNF-alpha. |
| 2116 | 18040852 | The splenocytes from protected mice and morphine low concentration-treated infected-PM, elaborated significantly (p < 0.05) enhanced levels of interleukin-12, interferon-gamma, tumor necrosis factor-alpha, granulocyte-macrophage colony-stimulating factor and nitrite in the culture medium; a high dose/concentration suppressed their elaboration. |
| 2117 | 18040852 | Curiously, only morphine high dose/concentration-treated infected mice splenocytes and infected PM, produced significantly (p < 0.05) increased quantity of transforming growth factor-beta1. |
| 2118 | 18032570 | Real-time PCR analysis of the acquired RNA clearly demonstrated that primary tubercles from BCG-vaccinated guinea pigs were overwhelmed with mRNA from the anti-inflammatory cytokine, transforming growth factor (TGF)-beta, with some IFN-gamma and IL-12p40 mRNA. |
| 2119 | 18032570 | The cytokine mRNA profile of secondary lesions from unimmunized animals was strikingly similar to the profile of primary lesions from BCG-vaccinated guinea pigs (i.e., a predominance of TGF-beta mRNA with some IL-12p40 and IFN-gamma mRNA), indicating that the lung lobes from which these lesions were retrieved had been naturally "vaccinated" by the time the bloodborne bacilli returned to the lung at 3 to 4 weeks after infection. |
| 2120 | 18032570 | Furthermore, cytokine mRNA analysis of splenic granulomas from nonvaccinated and vaccinated animals showed close resemblance to primary granulomas recovered from the lungs of the same animal, that is, high levels of TNF-alpha mRNA in unimmunized animals, and mostly TGF-beta mRNA in BCG-vaccinated guinea pigs. |
| 2121 | 18025217 | Differential requirements by CD4+ and CD8+ T cells for soluble and membrane TNF in control of Francisella tularensis live vaccine strain intramacrophage growth. |
| 2122 | 18025217 | Differential requirements by CD4+ and CD8+ T cells for soluble and membrane TNF in control of Francisella tularensis live vaccine strain intramacrophage growth. |
| 2123 | 18025217 | Differential requirements by CD4+ and CD8+ T cells for soluble and membrane TNF in control of Francisella tularensis live vaccine strain intramacrophage growth. |
| 2124 | 18025217 | Differential requirements by CD4+ and CD8+ T cells for soluble and membrane TNF in control of Francisella tularensis live vaccine strain intramacrophage growth. |
| 2125 | 18025217 | Generation of CD44(high) memory T cells and clearance of bacteria were similar, although more IFN-gamma and IL-12(p40) were produced by memTNF mice. |
| 2126 | 18025217 | Generation of CD44(high) memory T cells and clearance of bacteria were similar, although more IFN-gamma and IL-12(p40) were produced by memTNF mice. |
| 2127 | 18025217 | Generation of CD44(high) memory T cells and clearance of bacteria were similar, although more IFN-gamma and IL-12(p40) were produced by memTNF mice. |
| 2128 | 18025217 | Generation of CD44(high) memory T cells and clearance of bacteria were similar, although more IFN-gamma and IL-12(p40) were produced by memTNF mice. |
| 2129 | 18025217 | LVS-immune CD4(+) and CD8(+) T cells isolated from WT and memTNF mice exhibited comparable control of LVS growth in either normal or TNF-alpha knockout macrophages. |
| 2130 | 18025217 | LVS-immune CD4(+) and CD8(+) T cells isolated from WT and memTNF mice exhibited comparable control of LVS growth in either normal or TNF-alpha knockout macrophages. |
| 2131 | 18025217 | LVS-immune CD4(+) and CD8(+) T cells isolated from WT and memTNF mice exhibited comparable control of LVS growth in either normal or TNF-alpha knockout macrophages. |
| 2132 | 18025217 | LVS-immune CD4(+) and CD8(+) T cells isolated from WT and memTNF mice exhibited comparable control of LVS growth in either normal or TNF-alpha knockout macrophages. |
| 2133 | 18025217 | Although the magnitude of CD4(+) T cell-induced macrophage NO production clearly depended on TNF, control of LVS growth by both CD4(+) and CD8(+) T cells did not correlate with levels of nitrite. |
| 2134 | 18025217 | Although the magnitude of CD4(+) T cell-induced macrophage NO production clearly depended on TNF, control of LVS growth by both CD4(+) and CD8(+) T cells did not correlate with levels of nitrite. |
| 2135 | 18025217 | Although the magnitude of CD4(+) T cell-induced macrophage NO production clearly depended on TNF, control of LVS growth by both CD4(+) and CD8(+) T cells did not correlate with levels of nitrite. |
| 2136 | 18025217 | Although the magnitude of CD4(+) T cell-induced macrophage NO production clearly depended on TNF, control of LVS growth by both CD4(+) and CD8(+) T cells did not correlate with levels of nitrite. |
| 2137 | 18025217 | Importantly, intramacrophage LVS growth control by CD8(+) T cells, but not CD4(+) T cells, was almost entirely dependent on T cell-expressed TNF, and required stimulation through macrophage TNFRs. |
| 2138 | 18025217 | Importantly, intramacrophage LVS growth control by CD8(+) T cells, but not CD4(+) T cells, was almost entirely dependent on T cell-expressed TNF, and required stimulation through macrophage TNFRs. |
| 2139 | 18025217 | Importantly, intramacrophage LVS growth control by CD8(+) T cells, but not CD4(+) T cells, was almost entirely dependent on T cell-expressed TNF, and required stimulation through macrophage TNFRs. |
| 2140 | 18025217 | Importantly, intramacrophage LVS growth control by CD8(+) T cells, but not CD4(+) T cells, was almost entirely dependent on T cell-expressed TNF, and required stimulation through macrophage TNFRs. |
| 2141 | 18025215 | Similar to levels induced by bacterial cells, MV-stimulated macrophages and dendritic cells displayed increased surface expression of MHC-II and CD86 and enhanced production of the proinflammatory mediators NO, TNF-alpha, and IL-12. |
| 2142 | 18019188 | Correlates of protection involve robust CD4+ and CD8+ T cell responses, and the production of IFN-gamma, TNF-alpha, and IL-12. |
| 2143 | 18003817 | The cytokines analyzed in this study were gamma interferon, vascular endothelial growth factor, tumor necrosis factor alpha, interleukin-6 (IL-6), macrophage inflammatory protein 1beta, monocyte chemoattractant protein 1, IL-12p40, and IL-4. |
| 2144 | 17998917 | Single oral immunization with live BCG also invoked an interleukin-2 response (but not TNF-alpha or IL-4), although the magnitude was not elevated by multiple immunizations. |
| 2145 | 17989340 | Modulation of type 1 diabetes susceptibility by tumor necrosis factor alpha -308 G/A and lymphotoxin alpha +249 A/G haplotypes and lack of linkage disequilibrium with predisposing DQB1-DRB1 haplotypes in Bahraini patients. |
| 2146 | 17989340 | Modulation of type 1 diabetes susceptibility by tumor necrosis factor alpha -308 G/A and lymphotoxin alpha +249 A/G haplotypes and lack of linkage disequilibrium with predisposing DQB1-DRB1 haplotypes in Bahraini patients. |
| 2147 | 17989340 | Modulation of type 1 diabetes susceptibility by tumor necrosis factor alpha -308 G/A and lymphotoxin alpha +249 A/G haplotypes and lack of linkage disequilibrium with predisposing DQB1-DRB1 haplotypes in Bahraini patients. |
| 2148 | 17989340 | Modulation of type 1 diabetes susceptibility by tumor necrosis factor alpha -308 G/A and lymphotoxin alpha +249 A/G haplotypes and lack of linkage disequilibrium with predisposing DQB1-DRB1 haplotypes in Bahraini patients. |
| 2149 | 17989340 | Tumor necrosis factor alpha (TNF-alpha) -308 G/A and lymphotoxin alpha (LTalpha) +249 A/G single-nucleotide polymorphisms were investigated in 228 type 1 diabetes mellitus (T1DM) patients and 240 controls. |
| 2150 | 17989340 | Tumor necrosis factor alpha (TNF-alpha) -308 G/A and lymphotoxin alpha (LTalpha) +249 A/G single-nucleotide polymorphisms were investigated in 228 type 1 diabetes mellitus (T1DM) patients and 240 controls. |
| 2151 | 17989340 | Tumor necrosis factor alpha (TNF-alpha) -308 G/A and lymphotoxin alpha (LTalpha) +249 A/G single-nucleotide polymorphisms were investigated in 228 type 1 diabetes mellitus (T1DM) patients and 240 controls. |
| 2152 | 17989340 | Tumor necrosis factor alpha (TNF-alpha) -308 G/A and lymphotoxin alpha (LTalpha) +249 A/G single-nucleotide polymorphisms were investigated in 228 type 1 diabetes mellitus (T1DM) patients and 240 controls. |
| 2153 | 17989340 | Only LTalpha +249G allele and +249G/+249G genotype frequencies were higher among patients, and no linkage disequilibrium was found between TNF-alpha/LTalpha alleles and susceptible/protective DRB1-DQB1 haplotypes. |
| 2154 | 17989340 | Only LTalpha +249G allele and +249G/+249G genotype frequencies were higher among patients, and no linkage disequilibrium was found between TNF-alpha/LTalpha alleles and susceptible/protective DRB1-DQB1 haplotypes. |
| 2155 | 17989340 | Only LTalpha +249G allele and +249G/+249G genotype frequencies were higher among patients, and no linkage disequilibrium was found between TNF-alpha/LTalpha alleles and susceptible/protective DRB1-DQB1 haplotypes. |
| 2156 | 17989340 | Only LTalpha +249G allele and +249G/+249G genotype frequencies were higher among patients, and no linkage disequilibrium was found between TNF-alpha/LTalpha alleles and susceptible/protective DRB1-DQB1 haplotypes. |
| 2157 | 17989340 | TNF-alpha/LTalpha T1DM-susceptible (-308G/+249G) and protective (-308G/+249A) haplotypes were identified. |
| 2158 | 17989340 | TNF-alpha/LTalpha T1DM-susceptible (-308G/+249G) and protective (-308G/+249A) haplotypes were identified. |
| 2159 | 17989340 | TNF-alpha/LTalpha T1DM-susceptible (-308G/+249G) and protective (-308G/+249A) haplotypes were identified. |
| 2160 | 17989340 | TNF-alpha/LTalpha T1DM-susceptible (-308G/+249G) and protective (-308G/+249A) haplotypes were identified. |
| 2161 | 17989338 | Both BM- and PB-pDCs responded ex vivo to synthetic CpG oligodeoxynucleotides and inactivated influenza virus by upregulating HLA-DR and CD86 and secreting cytokines; however, stimulated BM-pDCs secreted less alpha interferon and tumor necrosis factor alpha per cell than did PB-pDCs. |
| 2162 | 17962945 | In turn, the onset of the immunological eclipse was coincidental with the onset of a systemic inflammatory condition characterized by a high number of circulating and splenic polymorphonucleated neutrophils (PMN) displaying activation and Gr1(+)Mac1(+) phenotype and an increasing serum concentration of the pro-inflammatory cytokines TNF-alpha, IL-1beta and IL-6 cytokines and C-reactive protein (CRP) and serum A amyloid (SAA) phase acute proteins. |
| 2163 | 17954572 | Adjuvanting a DNA vaccine with a TLR9 ligand plus Flt3 ligand results in enhanced cellular immunity against the simian immunodeficiency virus. |
| 2164 | 17954572 | Rhesus macaques were injected with Fms-like tyrosine kinase 3 (Flt3)-ligand (FL) to expand dendritic cells (DCs) and were primed with a DNA vaccine encoding immunodeficiency virus antigens mixed with ligands for TLR9 or TLR7/8. |
| 2165 | 17954572 | TLR9-L (CpG DNA) mediated activation of DCs in vivo and enhanced the magnitude of antigen-specific CD8(+) interferon (IFN) gamma(+) T cells and polyfunctional CD8(+) T cells producing IFN-gamma, tumor necrosis factor alpha, and interleukin 2. |
| 2166 | 17948267 | Promisingly, antigen 85A-specific CD4(+) T cells were found to be highly polyfunctional, producing IFN-gamma, TNF-alpha, IL-2 and MIP-1beta. |
| 2167 | 17948267 | Surface staining showed the responding CD4(+) T cells to be relatively immature (CD45RO(+) CD27(int)CD57(-)); this observation was supported by the robust proliferative responses observed following antigenic stimulation. |
| 2168 | 17945538 | In addition to the effect of abatacept on proliferation, T-cell cytokines, IL-2, TNFalpha and IFNgamma were also reduced. |
| 2169 | 17929411 | In the study, concentrations of IFN-gamma/Il-2 and 1l-4/Il-5 in supernatants of cultured mice splenocytes have been determined to evaluate differences in Th1 or Th2 lymphocytes subpopulation response. |
| 2170 | 17929411 | Simultaneously, studies of intracellular expression of genes encoding of Il-2, Il-12, IFN-gamma and Il-4, Il-5, Il-10, Il-13 in mice splenocytes, and genes encoding factors involved in inflammatory process in the lung tissue (GM-CSF, TNF-alpha, Il-1beta, Il-6 i TGF-beta) have been performed on RNA level. |
| 2171 | 17924971 | The production of both the pro- and the anti-inflammatory cytokines, tumour necrosis factor (TNF)-alpha and interleukin (IL)-10, was higher in cultures of capillary blood compared with venous blood. |
| 2172 | 17924971 | We found no other difference in the levels of IL-5 or IFN-gamma between venous and capillary blood. |
| 2173 | 17913827 | TRAIL is a novel antiviral protein against dengue virus. |
| 2174 | 17913827 | Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), one of the common response genes, was identified as a key link between type I and type II interferon response genes. |
| 2175 | 17908769 | Genetic polymorphisms in immunoresponse genes TNFA, IL6, IL10, and TLR4 are associated with recurrent acute otitis media. |
| 2176 | 17898182 | We examined B. burgdorferi infection of brain microvascular barriers during A. phagocytophilum coinfection and showed that coinfection enhanced reductions in transendothelial electrical resistance and enhanced or synergistically increased production of MMPs (MMP-1, -3, -7, -8, and -9), cytokines (interleukin 6 [IL-6], IL-10, and tumor necrosis factor alpha), and chemokines (IL-8 and macrophage inflammatory protein 1alpha) known to affect vascular permeability and inflammatory responses. |
| 2177 | 17894638 | However when the 3D4 cell line was incubated overnight in the presence of porcine serum, it efficiently responded to the wild-type strain and the ssrA mutant but not to the noninvasive hilA mutant as measured by mRNA quantification of TNF-alpha, IL-8 and GM-CSF by the real-time RT-PCR. |
| 2178 | 17886372 | Suppression of APF was observed along with suppression of proinflammatory cytokines (IL-1beta, IL-6, TNF-alpha) as well as B-lymphocytes growth factor (IL-4). |
| 2179 | 17868958 | Antigen-specific CD4(+) and CD8(+) T-cell responses to amplicon and adenovirus (rAd5) vectors encoding HIV-1 gp120 were assessed following immunization of mice, by performing intracellular cytokine staining for IFNgamma, IL2 and TNFalpha, following stimulation of splenocytes with a HIV-1 Env peptide pool. |
| 2180 | 17850592 | T-cell response to cytomegalovirus (CMV), varicella zoster virus (VZV) and tetanus toxoid (TT) was determined by flow cytometry analysis for CD69, TNFalpha, IFNgamma, IL-4 expression and cell proliferation. |
| 2181 | 17850592 | In spite of a general reduction of the CD4/CD8 ratio following transplantation, recovery of antigen specific CD4(+) T cells reactivity generally occurred prior to CD8(+) recovery and often to a higher level. |
| 2182 | 17828746 | Safety studies were carried out by measuring the levels of alkaline phosphatase (ALP), lactate dehydrogenase (LDH) and tumor necrosis factor alpha (TNF-alpha) in bronchoalveolar lavage (BAL) fluid. |
| 2183 | 17785828 | After priming with IFN-gamma and stimulation with NadADelta351-405, mo-DCs strongly up-regulated maturation markers CD83, CD86, CD80, and HLA-DR, secreted moderate quantities of TNF-alpha, IL-6, and IL-8, and produced a slight, although significant, amount of IL-12p70. |
| 2184 | 17785828 | After priming with IFN-gamma and stimulation with NadADelta351-405, mo-DCs strongly up-regulated maturation markers CD83, CD86, CD80, and HLA-DR, secreted moderate quantities of TNF-alpha, IL-6, and IL-8, and produced a slight, although significant, amount of IL-12p70. |
| 2185 | 17785828 | After priming with IFN-gamma and stimulation with NadADelta351-405, mo-DCs strongly up-regulated maturation markers CD83, CD86, CD80, and HLA-DR, secreted moderate quantities of TNF-alpha, IL-6, and IL-8, and produced a slight, although significant, amount of IL-12p70. |
| 2186 | 17785828 | Costimulation of mo-DCs with NadADelta351-405 and the imidoazoquinoline drug R-848, believed to mimic bacterial RNA, increased CD86 in an additive way, but strongly synergized the secretion of IL-12p70, IL-1, IL-6, TNF-alpha, and MIP-1alpha, especially after IFN-gamma priming. |
| 2187 | 17785828 | Costimulation of mo-DCs with NadADelta351-405 and the imidoazoquinoline drug R-848, believed to mimic bacterial RNA, increased CD86 in an additive way, but strongly synergized the secretion of IL-12p70, IL-1, IL-6, TNF-alpha, and MIP-1alpha, especially after IFN-gamma priming. |
| 2188 | 17785828 | Costimulation of mo-DCs with NadADelta351-405 and the imidoazoquinoline drug R-848, believed to mimic bacterial RNA, increased CD86 in an additive way, but strongly synergized the secretion of IL-12p70, IL-1, IL-6, TNF-alpha, and MIP-1alpha, especially after IFN-gamma priming. |
| 2189 | 17785828 | CD86/CD80 overexpression correlated with the occupation of high-(kd approximately 80 nM) and low-(kd approximately 4 muM) affinity binding sites for NadADelta351-405. |
| 2190 | 17785828 | CD86/CD80 overexpression correlated with the occupation of high-(kd approximately 80 nM) and low-(kd approximately 4 muM) affinity binding sites for NadADelta351-405. |
| 2191 | 17785828 | CD86/CD80 overexpression correlated with the occupation of high-(kd approximately 80 nM) and low-(kd approximately 4 muM) affinity binding sites for NadADelta351-405. |
| 2192 | 17785828 | Alternatively, secretion of IL-12p70 and TNF-alpha, IL-6, and IL-8 corresponded to the occupation of high- or low-affinity receptors, respectively. |
| 2193 | 17785828 | Alternatively, secretion of IL-12p70 and TNF-alpha, IL-6, and IL-8 corresponded to the occupation of high- or low-affinity receptors, respectively. |
| 2194 | 17785828 | Alternatively, secretion of IL-12p70 and TNF-alpha, IL-6, and IL-8 corresponded to the occupation of high- or low-affinity receptors, respectively. |
| 2195 | 17785828 | Mo-DCs matured by IFN-gamma and NadADelta351-405 supported the proliferation of naive CD4+ T lymphocytes, inducing the differentiation of both IFN-gamma and IL-4 producing phenotypes. |
| 2196 | 17785828 | Mo-DCs matured by IFN-gamma and NadADelta351-405 supported the proliferation of naive CD4+ T lymphocytes, inducing the differentiation of both IFN-gamma and IL-4 producing phenotypes. |
| 2197 | 17785828 | Mo-DCs matured by IFN-gamma and NadADelta351-405 supported the proliferation of naive CD4+ T lymphocytes, inducing the differentiation of both IFN-gamma and IL-4 producing phenotypes. |
| 2198 | 17728221 | Here, we evaluate the cytokine coexpression profiles of human immunodeficiency virus (HIV)-specific CD4 T cells for the expression of the cytokines gamma interferon (IFN-gamma), interleukin-2, and tumor necrosis factor alpha. |
| 2199 | 17725100 | For this purpose, eighteen patients with relapsed or refractory cancer were vaccinated with peripheral monocyte-derived DCs generated with GM-CSF and IL-4, and pulsed consequently with 100 microg/ml of tumor lysate before maturation in culture in the presence of IL-1beta, PGE2 and TNF alpha for two days. |
| 2200 | 17714025 | In this review, the authors discuss a number of novel biological response modifiers that work as general stimulants of the immune system, through varied mechanisms including induction of stimulatory cytokines (such as IFN-alpha, TNF-alpha and IL-12) and activation of T cells and the antigen-presenting dendritic cells. |
| 2201 | 17709416 | Elevated numbers of granulocytes, CD8+ cells, and TCR1+ cells and mRNA expression rates for interleukin 12 (IL-12), IL-18, tumor necrosis factor alpha factor, and iNOS in cecum correlated well with the invasiveness of serovars in the lamina propria. |
| 2202 | 17709416 | In contrast, changes in numbers of TCR2+ and CD4+ cells and IL-2 mRNA expression seemed to be more dependent on infection of epithelial cells. |
| 2203 | 17704295 | A role for TNF in limiting the duration of CTL effector phase and magnitude of CD8 T cell memory. |
| 2204 | 17704295 | A role for TNF in limiting the duration of CTL effector phase and magnitude of CD8 T cell memory. |
| 2205 | 17704295 | A role for TNF in limiting the duration of CTL effector phase and magnitude of CD8 T cell memory. |
| 2206 | 17704295 | A role for TNF in limiting the duration of CTL effector phase and magnitude of CD8 T cell memory. |
| 2207 | 17704295 | A role for TNF in limiting the duration of CTL effector phase and magnitude of CD8 T cell memory. |
| 2208 | 17704295 | A role for TNF in limiting the duration of CTL effector phase and magnitude of CD8 T cell memory. |
| 2209 | 17704295 | A role for TNF in limiting the duration of CTL effector phase and magnitude of CD8 T cell memory. |
| 2210 | 17704295 | To better understand the cellular mechanisms underlying the regulation of T cells by TNF, we have analyzed the role of TNF in regulating various facets of the antigen-specific CD8 T cell response to lymphocytic choriomeningitis virus (LCMV) in mice. |
| 2211 | 17704295 | To better understand the cellular mechanisms underlying the regulation of T cells by TNF, we have analyzed the role of TNF in regulating various facets of the antigen-specific CD8 T cell response to lymphocytic choriomeningitis virus (LCMV) in mice. |
| 2212 | 17704295 | To better understand the cellular mechanisms underlying the regulation of T cells by TNF, we have analyzed the role of TNF in regulating various facets of the antigen-specific CD8 T cell response to lymphocytic choriomeningitis virus (LCMV) in mice. |
| 2213 | 17704295 | To better understand the cellular mechanisms underlying the regulation of T cells by TNF, we have analyzed the role of TNF in regulating various facets of the antigen-specific CD8 T cell response to lymphocytic choriomeningitis virus (LCMV) in mice. |
| 2214 | 17704295 | To better understand the cellular mechanisms underlying the regulation of T cells by TNF, we have analyzed the role of TNF in regulating various facets of the antigen-specific CD8 T cell response to lymphocytic choriomeningitis virus (LCMV) in mice. |
| 2215 | 17704295 | To better understand the cellular mechanisms underlying the regulation of T cells by TNF, we have analyzed the role of TNF in regulating various facets of the antigen-specific CD8 T cell response to lymphocytic choriomeningitis virus (LCMV) in mice. |
| 2216 | 17704295 | To better understand the cellular mechanisms underlying the regulation of T cells by TNF, we have analyzed the role of TNF in regulating various facets of the antigen-specific CD8 T cell response to lymphocytic choriomeningitis virus (LCMV) in mice. |
| 2217 | 17704295 | We show that expansion and differentiation of virus-specific effector CD8 T cells and LCMV clearance are not dependent on TNF. |
| 2218 | 17704295 | We show that expansion and differentiation of virus-specific effector CD8 T cells and LCMV clearance are not dependent on TNF. |
| 2219 | 17704295 | We show that expansion and differentiation of virus-specific effector CD8 T cells and LCMV clearance are not dependent on TNF. |
| 2220 | 17704295 | We show that expansion and differentiation of virus-specific effector CD8 T cells and LCMV clearance are not dependent on TNF. |
| 2221 | 17704295 | We show that expansion and differentiation of virus-specific effector CD8 T cells and LCMV clearance are not dependent on TNF. |
| 2222 | 17704295 | We show that expansion and differentiation of virus-specific effector CD8 T cells and LCMV clearance are not dependent on TNF. |
| 2223 | 17704295 | We show that expansion and differentiation of virus-specific effector CD8 T cells and LCMV clearance are not dependent on TNF. |
| 2224 | 17704295 | Instead, we demonstrate that TNF limits the duration of the effector phase of the CD8 T cell response by regulating apoptosis and not proliferation of effector cells in vivo. |
| 2225 | 17704295 | Instead, we demonstrate that TNF limits the duration of the effector phase of the CD8 T cell response by regulating apoptosis and not proliferation of effector cells in vivo. |
| 2226 | 17704295 | Instead, we demonstrate that TNF limits the duration of the effector phase of the CD8 T cell response by regulating apoptosis and not proliferation of effector cells in vivo. |
| 2227 | 17704295 | Instead, we demonstrate that TNF limits the duration of the effector phase of the CD8 T cell response by regulating apoptosis and not proliferation of effector cells in vivo. |
| 2228 | 17704295 | Instead, we demonstrate that TNF limits the duration of the effector phase of the CD8 T cell response by regulating apoptosis and not proliferation of effector cells in vivo. |
| 2229 | 17704295 | Instead, we demonstrate that TNF limits the duration of the effector phase of the CD8 T cell response by regulating apoptosis and not proliferation of effector cells in vivo. |
| 2230 | 17704295 | Instead, we demonstrate that TNF limits the duration of the effector phase of the CD8 T cell response by regulating apoptosis and not proliferation of effector cells in vivo. |
| 2231 | 17704295 | We further show that attenuation of effector cell apoptosis induced by TNF deficiency led to a substantial increase in the number of virus-specific memory CD8 T cells without affecting their function. |
| 2232 | 17704295 | We further show that attenuation of effector cell apoptosis induced by TNF deficiency led to a substantial increase in the number of virus-specific memory CD8 T cells without affecting their function. |
| 2233 | 17704295 | We further show that attenuation of effector cell apoptosis induced by TNF deficiency led to a substantial increase in the number of virus-specific memory CD8 T cells without affecting their function. |
| 2234 | 17704295 | We further show that attenuation of effector cell apoptosis induced by TNF deficiency led to a substantial increase in the number of virus-specific memory CD8 T cells without affecting their function. |
| 2235 | 17704295 | We further show that attenuation of effector cell apoptosis induced by TNF deficiency led to a substantial increase in the number of virus-specific memory CD8 T cells without affecting their function. |
| 2236 | 17704295 | We further show that attenuation of effector cell apoptosis induced by TNF deficiency led to a substantial increase in the number of virus-specific memory CD8 T cells without affecting their function. |
| 2237 | 17704295 | We further show that attenuation of effector cell apoptosis induced by TNF deficiency led to a substantial increase in the number of virus-specific memory CD8 T cells without affecting their function. |
| 2238 | 17704295 | The enhancement in the number of memory CD8 T cells in TNF-deficient (TNF-/-) mice was not associated with up-regulation of IL-7Ralpha or Bcl-2 in effector cells, which indicated that TNF might limit differentiation of memory cells from IL-7R(lo) effector cells. |
| 2239 | 17704295 | The enhancement in the number of memory CD8 T cells in TNF-deficient (TNF-/-) mice was not associated with up-regulation of IL-7Ralpha or Bcl-2 in effector cells, which indicated that TNF might limit differentiation of memory cells from IL-7R(lo) effector cells. |
| 2240 | 17704295 | The enhancement in the number of memory CD8 T cells in TNF-deficient (TNF-/-) mice was not associated with up-regulation of IL-7Ralpha or Bcl-2 in effector cells, which indicated that TNF might limit differentiation of memory cells from IL-7R(lo) effector cells. |
| 2241 | 17704295 | The enhancement in the number of memory CD8 T cells in TNF-deficient (TNF-/-) mice was not associated with up-regulation of IL-7Ralpha or Bcl-2 in effector cells, which indicated that TNF might limit differentiation of memory cells from IL-7R(lo) effector cells. |
| 2242 | 17704295 | The enhancement in the number of memory CD8 T cells in TNF-deficient (TNF-/-) mice was not associated with up-regulation of IL-7Ralpha or Bcl-2 in effector cells, which indicated that TNF might limit differentiation of memory cells from IL-7R(lo) effector cells. |
| 2243 | 17704295 | The enhancement in the number of memory CD8 T cells in TNF-deficient (TNF-/-) mice was not associated with up-regulation of IL-7Ralpha or Bcl-2 in effector cells, which indicated that TNF might limit differentiation of memory cells from IL-7R(lo) effector cells. |
| 2244 | 17704295 | The enhancement in the number of memory CD8 T cells in TNF-deficient (TNF-/-) mice was not associated with up-regulation of IL-7Ralpha or Bcl-2 in effector cells, which indicated that TNF might limit differentiation of memory cells from IL-7R(lo) effector cells. |
| 2245 | 17704295 | Collectively, these data are strongly suggestive of a role for TNF in down-regulating CD8 T cell responses and the establishment of CD8 T cell memory during an acute viral infection. |
| 2246 | 17704295 | Collectively, these data are strongly suggestive of a role for TNF in down-regulating CD8 T cell responses and the establishment of CD8 T cell memory during an acute viral infection. |
| 2247 | 17704295 | Collectively, these data are strongly suggestive of a role for TNF in down-regulating CD8 T cell responses and the establishment of CD8 T cell memory during an acute viral infection. |
| 2248 | 17704295 | Collectively, these data are strongly suggestive of a role for TNF in down-regulating CD8 T cell responses and the establishment of CD8 T cell memory during an acute viral infection. |
| 2249 | 17704295 | Collectively, these data are strongly suggestive of a role for TNF in down-regulating CD8 T cell responses and the establishment of CD8 T cell memory during an acute viral infection. |
| 2250 | 17704295 | Collectively, these data are strongly suggestive of a role for TNF in down-regulating CD8 T cell responses and the establishment of CD8 T cell memory during an acute viral infection. |
| 2251 | 17704295 | Collectively, these data are strongly suggestive of a role for TNF in down-regulating CD8 T cell responses and the establishment of CD8 T cell memory during an acute viral infection. |
| 2252 | 17698589 | Memory CD8+ T cells mediate antibacterial immunity via CCL3 activation of TNF/ROI+ phagocytes. |
| 2253 | 17698589 | Memory CD8+ T cells mediate antibacterial immunity via CCL3 activation of TNF/ROI+ phagocytes. |
| 2254 | 17698589 | Cytolysis, interferon gamma and tumor necrosis factor (TNF) alpha secretion are major effector mechanisms of memory CD8+ T cells that are believed to be required for immunological protection in vivo. |
| 2255 | 17698589 | Cytolysis, interferon gamma and tumor necrosis factor (TNF) alpha secretion are major effector mechanisms of memory CD8+ T cells that are believed to be required for immunological protection in vivo. |
| 2256 | 17698261 | The observed post-challenge results paralleled increasing production of IFN-gamma and IL-6, but only limited changes to proinflammatory mediators TNF-alpha or IL-1beta from BCG-stimulated splenocytes. |
| 2257 | 17682046 | CD40 ligation has also been shown to trigger autophagic elimination of T. gondii independent of IFN-gamma and p47 GTPases. |
| 2258 | 17682046 | Here we demonstrate that IFN-gamma/p47 GTPase-dependent elimination of T. gondii by strain CPS vaccine-primed macrophages is independent of CD40/tumor necrosis factor signaling. |
| 2259 | 17682046 | Similar to wild-type controls, both CD40-deficient and tumor necrosis factor receptor 1/2 (TNFR1/2)-deficient macrophages can efficiently eliminate invaded strain GFP-PTG and restrain its replication following priming. |
| 2260 | 17682046 | Thus, CD40 and IFN-gamma-induced pathogen elimination might represent two independent resistance pathways, the latter of which plays a primary role in anti-Toxoplasma immunity in mice. |
| 2261 | 17681535 | CrmE shares significant sequence similarity with mammalian type 2 TNF receptors (TNFSFR1B, p75; TNFR type 2). |
| 2262 | 17681535 | CrmE shares significant sequence similarity with mammalian type 2 TNF receptors (TNFSFR1B, p75; TNFR type 2). |
| 2263 | 17681535 | The structure confirms that CrmE adopts the canonical TNFR fold but only one of the two "ligand-binding" loops of TNFRSF1A is conserved in CrmE, suggesting a mechanism for the higher affinity of poxvirus TNFRs for TNFalpha over lymphotoxin-alpha. |
| 2264 | 17681535 | The structure confirms that CrmE adopts the canonical TNFR fold but only one of the two "ligand-binding" loops of TNFRSF1A is conserved in CrmE, suggesting a mechanism for the higher affinity of poxvirus TNFRs for TNFalpha over lymphotoxin-alpha. |
| 2265 | 17675478 | Lipopeptide recalled D(b)PA(224)-specific CTL produced lower levels of IFN-gamma and TNF-alpha, but produced similar levels of IL-2 when compared with D(b)PA(224)-specific CTL recalled after virus infection. |
| 2266 | 17658618 | 'B-cell activating factor belonging to the TNF family' (BAFF) represents a cytokine produced by antigen presenting cells promoting B-cell maturation, activation and immunoglobulin class switching. |
| 2267 | 17658618 | In the present study, we demonstrate expression of BAFF on cultured monocyte-derived dendritic cells, which is further enhanced by interferon-alpha or interferon-gamma treatment. |
| 2268 | 17643559 | Peripheral blood mononuclear cell cultures from both groups showed CD4(+), CD8(+) and remarkable gammadelta(+) T cell BCG-specific proliferation, without significant differences. |
| 2269 | 17643559 | Also, IL-10, IL-12, IFN-gamma and TNF-alpha concentrations in culture supernatants, measured by ELISA, were similar. |
| 2270 | 17641838 | Peripheral blood monocytes were cultured in vitro with GM-CSF, IL-4 for 6 days, then TNF-(the TNF-group) or TNF-, IL-1, IL-6, PGE2 (the cytokine mixture group) were added to promote maturation. |
| 2271 | 17641838 | Peripheral blood monocytes were cultured in vitro with GM-CSF, IL-4 for 6 days, then TNF-(the TNF-group) or TNF-, IL-1, IL-6, PGE2 (the cytokine mixture group) were added to promote maturation. |
| 2272 | 17641838 | Peripheral blood monocytes were cultured in vitro with GM-CSF, IL-4 for 6 days, then TNF-(the TNF-group) or TNF-, IL-1, IL-6, PGE2 (the cytokine mixture group) were added to promote maturation. |
| 2273 | 17641838 | Cell number was counted by hematology analyzer, and phenotype study (CD1a, CD14, CD83) was carried out by flow cytometry, and the function of DCs was examined by mixed lymphocyte reaction. |
| 2274 | 17641838 | Cell number was counted by hematology analyzer, and phenotype study (CD1a, CD14, CD83) was carried out by flow cytometry, and the function of DCs was examined by mixed lymphocyte reaction. |
| 2275 | 17641838 | Cell number was counted by hematology analyzer, and phenotype study (CD1a, CD14, CD83) was carried out by flow cytometry, and the function of DCs was examined by mixed lymphocyte reaction. |
| 2276 | 17641838 | The phenotypes were as follows: CD1a+ (74.65+/-4.45)%, CD83+ (39.50+/-4.16)%, CD14+ (2.90+/-1.76)% in TNF-alpha group, and CD1a+ (81.86+/-5.87)%, CD83+ (81.65+/-6.36)%, CD14+ (2.46+/-1.68)% in the cytokine mixture group. |
| 2277 | 17641838 | The phenotypes were as follows: CD1a+ (74.65+/-4.45)%, CD83+ (39.50+/-4.16)%, CD14+ (2.90+/-1.76)% in TNF-alpha group, and CD1a+ (81.86+/-5.87)%, CD83+ (81.65+/-6.36)%, CD14+ (2.46+/-1.68)% in the cytokine mixture group. |
| 2278 | 17641838 | The phenotypes were as follows: CD1a+ (74.65+/-4.45)%, CD83+ (39.50+/-4.16)%, CD14+ (2.90+/-1.76)% in TNF-alpha group, and CD1a+ (81.86+/-5.87)%, CD83+ (81.65+/-6.36)%, CD14+ (2.46+/-1.68)% in the cytokine mixture group. |
| 2279 | 17641838 | It was concluded that leucapheresis may be a feasible way to provide large number of peripheral blood monocytes for DC generation, and combined administration of TNF-, IL-1, IL-6, and PGE2 may greatly promote maturity. |
| 2280 | 17641838 | It was concluded that leucapheresis may be a feasible way to provide large number of peripheral blood monocytes for DC generation, and combined administration of TNF-, IL-1, IL-6, and PGE2 may greatly promote maturity. |
| 2281 | 17641838 | It was concluded that leucapheresis may be a feasible way to provide large number of peripheral blood monocytes for DC generation, and combined administration of TNF-, IL-1, IL-6, and PGE2 may greatly promote maturity. |
| 2282 | 17629376 | The Th(1) (TNF-alpha, IL-12p70, IFN-gamma, IL-2) and Th(2) (IL-10, IL-4 and IL-5) cytokine profiles were analyzed after stimulation of spleen cells from mice immunized with purified RF-412 protein. |
| 2283 | 17628695 | Expression of IFN-gamma, TNF-alpha, iNOS and IL-4 by PBMC increased in response to infection, whereas, IL-10 expression decreased. |
| 2284 | 17628695 | Expression of IFN-gamma, TNF-alpha, iNOS and IL-4 by PBMC increased in response to infection, whereas, IL-10 expression decreased. |
| 2285 | 17628695 | Cells from animals in the high pathology group expressed more IFN-gamma, TNF-alpha, iNOS and IL-4 than did animals in the low pathology group at early time points. |
| 2286 | 17628695 | Cells from animals in the high pathology group expressed more IFN-gamma, TNF-alpha, iNOS and IL-4 than did animals in the low pathology group at early time points. |
| 2287 | 17628695 | IFN-gamma and iNOS gene expression were significantly greater in tissues from infected animals compared to tissues from uninfected animals. |
| 2288 | 17628695 | IFN-gamma and iNOS gene expression were significantly greater in tissues from infected animals compared to tissues from uninfected animals. |
| 2289 | 17582562 | Typhi oral vaccines include lymphoproliferation; production of type 1 cytokines (e.g., interferon- gamma and tumor necrosis factor- alpha ); and classical major histocompatibility complex (MHC) class Ia-restricted and novel, nonclassical MHC class Ib (human leukocyte antigen [HLA]-E)-restricted CD8(+) cytotoxic T cell responses. |
| 2290 | 17606603 | Analysis of the cellular immune responses of immunized, uninfected mice demonstrated that the vaccine induced a significant increase in CD4(+) T cells producing gamma interferon, interleukin 2, and tumor necrosis factor cytokines, indicating a Th1-type immune response. |
| 2291 | 17599092 | Each gene encoded a cell surface chimeric protein made up of extracellular single-chain immunoglobulin anti-erbB2 linked to an intracellular TLR-signaling component composed of either myeloid differentiation factor 88, interleukin-1 receptor-associated kinase-1 (IRAK-1) or the cytoplasmic domain of TLR4. |
| 2292 | 17599092 | However, only the chimera containing IRAK-1 was able to mediate interleukin-12 and tumor necrosis factor-alpha secretion. |
| 2293 | 17599092 | We found that JAWS II cells triggered through chimeric anti-erbB2-IRAK-1 displayed an enhanced ability to stimulate ovalbumin-specific OT-II CD4(+) T cells. |
| 2294 | 17590425 | More than 120 primary immunodeficiencies were defined at a molecular level, and biological agents such as TNF-alpha antagonists and IFN-alpha were shown to have therapeutic use. |
| 2295 | 17576158 | Higher doses of lentivirus, however, resulted in upregulation of adhesion, costimulatory, and HLA molecules, as well as in increased allostimulatory capacity and secretion of interleukin (IL)-6, IL-8, and tumor necrosis factor-alpha. |
| 2296 | 17576158 | Production of IL-12 p70, IL-10, and interferon-alpha was observed only at extremely high doses. |
| 2297 | 17576158 | A Toll-like receptor (TLR)-driven luciferase reporter assay showed dose-dependent activation of TLR2, TLR3, and TLR8, which was independent of the pseudotype, production, or transduction protocol and was abrogated on heat inactivation. |
| 2298 | 17570767 | A combined DNA vaccine encoding BCSP31, SOD, and L7/L12 confers high protection against Brucella abortus 2308 by inducing specific CTL responses. |
| 2299 | 17570767 | We constructed a combined DNA vaccine comprising genes encoding the antigens BCSP31, superoxide dismutase (SOD), and L7/L12 and evaluated its immunogenicity and protective efficacy. |
| 2300 | 17570767 | Cytokine profiling performed at the same time showed a biased Th1-type immune response with significantly increased interferon-gamma and tumor necrosis factor-alpha stimulation. |
| 2301 | 17570767 | CD8(+), but not CD4(+), T cells accumulated at significantly higher levels after administration of the vaccine. |
| 2302 | 17570767 | Granzyme B-producing CD8(+) T cells were significantly higher in number in samples prepared from combined DNA-vaccinated mice compared with S19-vaccinated mice, demonstrating that the cytotoxicity lysis pathway is involved in the response to Brucella infection. |
| 2303 | 17565610 | Similarly, total, non-adherent and adherent lung digest cells from BCG-vaccinated guinea pigs showed IFN-gamma and tumour necrosis factor (TNF)-alpha mRNA expression in response to ConA, lipopolysaccharide or PPD by reverse transcription-polymerase chain reaction followed by release of TNF protein but not IFN. |
| 2304 | 17563737 | PBMC were collected at 6, 9 and 15 months after transplantation and stimulated with a combination of CD2 and CD28 monoclonal antibodies, with PHA or with tetanus toxoid as recall antigen. |
| 2305 | 17563737 | PBMC were collected at 6, 9 and 15 months after transplantation and stimulated with a combination of CD2 and CD28 monoclonal antibodies, with PHA or with tetanus toxoid as recall antigen. |
| 2306 | 17563737 | A multiplex enzyme linked immunoassay was used to determine levels of Th1 cytokines IL-2, IFN-gamma and tumour-necrosis factor-alpha (TNF-alpha), Th2 cytokines IL-4, IL-5 and IL-13, the regulatory cytokine IL-10 and the proinflammatory cytokines IL-1alpha, IL-1beta, IL-6 and the chemokine IL-8. |
| 2307 | 17563737 | A multiplex enzyme linked immunoassay was used to determine levels of Th1 cytokines IL-2, IFN-gamma and tumour-necrosis factor-alpha (TNF-alpha), Th2 cytokines IL-4, IL-5 and IL-13, the regulatory cytokine IL-10 and the proinflammatory cytokines IL-1alpha, IL-1beta, IL-6 and the chemokine IL-8. |
| 2308 | 17563737 | Production of Th2 cytokines IL-5 and IL-13 was superior to production of Th1 cytokines IFN-gamma and TNF-alpha. |
| 2309 | 17563737 | Production of Th2 cytokines IL-5 and IL-13 was superior to production of Th1 cytokines IFN-gamma and TNF-alpha. |
| 2310 | 17561317 | In vitro restimulation of lymphocytes from the Protollin-eRSV immunized mice with F (MHC-I) and G (MHC-II) peptides elicited F peptide-specific CD8(+) T cells and supernatant IFNgamma, TNFalpha, IL-2 and IL-10 while the formalin-inactivated RSV (FI-RSV) vaccine elicited predominantly IL-5. |
| 2311 | 17558415 | Here, using multiparameter flow cytometry to assess the immune responses after immunization, we show that the degree of protection against Leishmania major infection in mice is predicted by the frequency of CD4+ T cells simultaneously producing interferon-gamma, interleukin-2 and tumor necrosis factor. |
| 2312 | 17553885 | Virus-specific CD4 T cells are endowed with multiple functions, such as cytokine production, CD40 ligand (CD40L) expression (associated with the costimulation of CD8 and B cells), and degranulation (associated with cytotoxic potential). |
| 2313 | 17553885 | CD4 T cells specific for each of the viruses produced all seven possible combinations of the cytokines gamma interferon (IFN-gamma), interleukin-2, and tumor necrosis factor alpha. |
| 2314 | 17544551 | Co-immunisation with DNA encoding RANK/RANKL or 4-1BBL costimulatory molecules does not enhance effector or memory CTL responses afforded by immunisation with a tumour antigen-encoding DNA vaccine. |
| 2315 | 17544551 | This 'second signalling' occurs through the B7 molecules CD80/86 expressed by DCs, and importantly through members of the TNF ligand/TNF receptor superfamilies. |
| 2316 | 17544551 | We have previously shown that co-expression of RANK/RANKL or 41BB-L in addition to tumour antigen in dendritic cells augmented cognate effector and memory tumour antigen-directed cytotoxic T cell responses when the DCs were used to immunise mice. |
| 2317 | 17538120 | Upregulated genes included the immune regulatory molecules interleukin 1beta (IL-1beta), CIAS-1, tumor necrosis factor alpha, PDE4B, PTGS2, IL-8, CXCL2, CCL4, ICAM-1, CD83, GOS-2, IER3 (IEX-1), and TNFAIP3 (A20). |
| 2318 | 17538120 | Plasma levels of IL-1beta and IL-8 were elevated during measles virus infection. |
| 2319 | 17538120 | Downregulated genes mainly involved three gene ontology biological processes, transcription, signal transduction, and the immune response, and included IL-16 and cell surface receptors IL-4R, IL-6R, IL-7R, IL-27RA, CCR2, and CCR7. |
| 2320 | 17535971 | Vaccinia virus-specific CD8(+) T cells induced by both MVA and Dryvax were highly polyfunctional; they degranulated and produced interferon gamma, interleukin 2, macrophage inflammatory protein 1beta, and tumor necrosis factor alpha after antigenic stimulation. |
| 2321 | 17535971 | Responding CD8(+) T cells exhibited an unusual phenotype (CD45RO(-)CD27(intermediate)). |
| 2322 | 17523874 | In the first set of experiments, PBMCs were stimulated in vitro with tinctures alone and assayed for proliferation and production of interleukin-10 (IL-10), IL-12, and tumor necrosis factor-alpha (TNF-alpha). |
| 2323 | 17523874 | In the first set of experiments, PBMCs were stimulated in vitro with tinctures alone and assayed for proliferation and production of interleukin-10 (IL-10), IL-12, and tumor necrosis factor-alpha (TNF-alpha). |
| 2324 | 17523874 | PBMCs from vaccinated individuals were stimulated in vitro with Echinacea tinctures and influenza virus; cytokine production (IL-2, IL-10, and interferon-gamma [IFN-gamma]) was compared prevaccination and postvaccination. |
| 2325 | 17523874 | PBMCs from vaccinated individuals were stimulated in vitro with Echinacea tinctures and influenza virus; cytokine production (IL-2, IL-10, and interferon-gamma [IFN-gamma]) was compared prevaccination and postvaccination. |
| 2326 | 17523874 | In the first experiments, (1) tinctures from E. angustifolia, E. pallida, E. paradoxa, and E. tennesseensis stimulated proliferation and tended to increase IL-10, (2) E. sanguinea and E. simulata stimulated only proliferation, (3) E. purpurea stimulated only IL-10, and (4) none of the extracts influenced IL-12 or TNF-alpha. |
| 2327 | 17523874 | In the first experiments, (1) tinctures from E. angustifolia, E. pallida, E. paradoxa, and E. tennesseensis stimulated proliferation and tended to increase IL-10, (2) E. sanguinea and E. simulata stimulated only proliferation, (3) E. purpurea stimulated only IL-10, and (4) none of the extracts influenced IL-12 or TNF-alpha. |
| 2328 | 17523874 | In the second experiments, (1) tinctures from E. pallida, E. paradoxa, E. sanguinea, and E. simulata diminished influenza-specific IL-2, and (2) none of the extracts influenced influenza-specific IL-10 or IFN-gamma. |
| 2329 | 17523874 | In the second experiments, (1) tinctures from E. pallida, E. paradoxa, E. sanguinea, and E. simulata diminished influenza-specific IL-2, and (2) none of the extracts influenced influenza-specific IL-10 or IFN-gamma. |
| 2330 | 17512528 | Spleen adherent cells secreted high levels of IFN-gamma and IL-12. |
| 2331 | 17512528 | Specific T-cells were essential for NO, IFN-gamma and TNF-alpha production. |
| 2332 | 17504117 | The presence of a background mixed IFN-gamma and Th2 response to mycobacterial antigens before infection with M. tuberculosis (Mtb), and the development of a large IL-4 response during progressive TB, are characteristics of individuals in the locations where BCG fails, which are also seen in animal models in the same countries. |
| 2333 | 17504117 | The presence of a background mixed IFN-gamma and Th2 response to mycobacterial antigens before infection with M. tuberculosis (Mtb), and the development of a large IL-4 response during progressive TB, are characteristics of individuals in the locations where BCG fails, which are also seen in animal models in the same countries. |
| 2334 | 17504117 | We outline how IL-4 (and IL-13) can undermine Th1-mediated immunity and drive inappropriate alternative activation of macrophages. |
| 2335 | 17504117 | We outline how IL-4 (and IL-13) can undermine Th1-mediated immunity and drive inappropriate alternative activation of macrophages. |
| 2336 | 17504117 | The mechanisms of the effects of IL-4 include impaired antimicrobial activity due to reduced TNF-alpha-mediated apoptosis of infected cells, reduced activity of iNOS, increased availability of iron to intracellular Mtb, and increased proliferation of antigen-specific FOXP-3+ regulatory T cells. |
| 2337 | 17504117 | The mechanisms of the effects of IL-4 include impaired antimicrobial activity due to reduced TNF-alpha-mediated apoptosis of infected cells, reduced activity of iNOS, increased availability of iron to intracellular Mtb, and increased proliferation of antigen-specific FOXP-3+ regulatory T cells. |
| 2338 | 17504117 | IL-4 also increases the toxicity of TNF-alpha and drives pulmonary fibrosis, thus enhancing immunopathology. |
| 2339 | 17504117 | IL-4 also increases the toxicity of TNF-alpha and drives pulmonary fibrosis, thus enhancing immunopathology. |
| 2340 | 17499850 | B cell activating factor belonging to the tumor necrosis factor (TNF) family (BAFF) is critical for B cell survival, maturation and T cell activation by acting through its three receptors, BAFF-R, BCMA and TACI. |
| 2341 | 17498851 | The effect was determined in the form of protective anti-HBsAg titers, neutralizing antibodies (IgG1 and IgG2a), spleen cell lymphocyte proliferation by using MTT assay, Th1 (IFN-gamma and TNF-alpha) and Th2 (IL-4) cytokines as well as T-lymphocyte subsets (CD4/CD8) and intracellular cytokines (IFN-gamma/IL-4), these responses were highest in BOS 2000 immunized mice. |
| 2342 | 17498851 | In contrast, BOS 2000 was associated with production of both IFN-gamma and IL-4. |
| 2343 | 17459080 | S. typhimurium CM induced potent tumour necrosis factor (TNF)-alpha responses from DCs accompanied by significant up-regulation of CD80 and CD86 expression. |
| 2344 | 17453679 | At the 45th day after first immunization, animals were sacrificed and a series of examinations such as HE stain, assay of TNF-alpha by ELISA and assay of inducible nitric oxide synthase (iNOS) mRNA by in-situ hybridization (ISH) were taken. |
| 2345 | 17453679 | The results of macropathology, histopathology and iNOS ISH also revealed the same tendency. |
| 2346 | 17451739 | Here we describe extensive studies to optimize and quantitatively validate the 8-color ICS assay for use in clinical trials of candidate vaccines, which includes measurement of viable IFN-gamma, IL-2, TNF-alpha and IL-4 producing CD4+ and CD8+ T cells. |
| 2347 | 17446350 | The mast-cell-derived cytokines TNF-alpha and IL-1beta play an important role in this process. |
| 2348 | 17440051 | SIV-specific CD8+ T cells express high levels of PD1 and cytokines but have impaired proliferative capacity in acute and chronic SIVmac251 infection. |
| 2349 | 17440051 | Programmed death-1 (PD-1) is a critical mediator of virus-specific CD8+ T-cell exhaustion. |
| 2350 | 17440051 | Here, we examined the expression of PD-1 on simian immunodeficiency virus (SIV)-specific CD8+ T cells and its possible involvement in regulation of cytokine production, proliferation, and survival of these cells. |
| 2351 | 17440051 | The majority of SIV-specific CD8+ T cells expressed a PD-1(high) phenotype, independent of their differentiation status, in all tissues tested. |
| 2352 | 17440051 | PD-1 expression gradually declined on CD8+ T cells specific for SIV-derived epitopes that had undergone mutational escape, indicating that antigen-specific TCR stimulation is the primary determinant of PD-1 expression. |
| 2353 | 17440051 | SIV-specific PD-1(high)CD8+ T cells produced IFN-gamma, TNF-alpha, and IL-2 under cognate peptide stimulation. |
| 2354 | 17440051 | While CD8+ T cells that proliferated in response to antigen had a PD-1(high) phenotype, it was determined that there was a reduced proliferative capacity of PD-1(high) compared with PD-1(low) SIV-specific CD8+ T cells. |
| 2355 | 17440051 | PD-1(high) SIV-specific CD8+ T cells were highly susceptible to cell death leading to loss of such cells after in vitro stimulation. |
| 2356 | 17440051 | Thus, PD-1 is a negative regulator of SIV-specific CD8+ T cells, operating predominantly through the induction of cell death. |
| 2357 | 17440051 | Manipulation of the interaction of PD-1 with its ligands could thus potentially restore the CD8+ T-cell responses in SIV infection. |
| 2358 | 17428947 | Five days after infection, these animals produced a potent, innate antiviral immune response by inducing the transcription of signature genes from the interferon (IFN) pathway with demonstrated antiviral activity, such as myxoprotein, 2',5'-oligoadenylate synthetase, phospholipid scramblase 1, and viperin. |
| 2359 | 17428947 | Unexpectedly, no up-regulation of IFN-alpha, -beta, or -gamma genes was detected. |
| 2360 | 17428947 | Transcription of the genes of interleukin-10 (IL-10), IL-8, IL-6, and tumor necrosis factor alpha was neither up-regulated nor down-regulated. |
| 2361 | 17425690 | PDT-cell lysates plus ODN coinjection for protection against E7-expressing tumors as well as specific immune responses were evaluated with the following tests: heat shock protein 70 (HSP70) enzyme-linked immunosorbent assay, in vitro and in vivo tumor growth inhibition, interferon-gamma (IFN-gamma) and tumor necrosis factor-alpha (TNF-alpha) assay, cytotoxic T-lymphocyte assay, and fluorescence activated cell sorting (FACS) analysis. |
| 2362 | 17420241 | When it was examined for binding to murine bone marrow-derived dendritic cells (DCs), the dltA mutant exhibited 200- to 400-fold less binding than the parent but similar levels of binding were shown for Toll-like receptor 2 (TLR2) knockout DCs and HEp-2 cells. |
| 2363 | 17420241 | LTA purified from the bacteria induced tumor necrosis factor-alpha and IL-6 production from wild-type DCs but not from TLR2 knockout DCs, and the mutant LTA induced a significantly smaller amount of these two cytokines. |
| 2364 | 17412460 | Mannosylated OVA failed to stimulate TNF-alpha and IL-12 production from dendritic cells. |
| 2365 | 17400535 | Pulmonary levels of TNFalpha, IL-6, IL-1 beta, MIP-1 alpha, KC, MCP-1/JE and MIP-2 cytokines were determined up to 48 hours post-infection. |
| 2366 | 17400535 | Pulmonary levels of TNFalpha, IL-6, IL-1 beta, MIP-1 alpha, KC, MCP-1/JE and MIP-2 cytokines were determined up to 48 hours post-infection. |
| 2367 | 17400535 | The only cytokines showing a greater increase in vaccinated mice compare to control animals were IL-1 beta, KC and MCP-1. |
| 2368 | 17400535 | The only cytokines showing a greater increase in vaccinated mice compare to control animals were IL-1 beta, KC and MCP-1. |
| 2369 | 17400535 | Production of TNFalpha and IL-6 was lower in vaccinated animals than in controls. |
| 2370 | 17400535 | Production of TNFalpha and IL-6 was lower in vaccinated animals than in controls. |
| 2371 | 17400535 | At variance with the previous bacteria strain-induced cytokine profile, infection with the P15986 strain induced a strong inflammatory response, with a substantial increase in all the cytokine tested, which was similar in vaccinated and in naïve, control animals, except for MIP-1 alpha, which was the only mediator significantly more produced by vaccinated animals than by naïve, control mice following P15986 infection. |
| 2372 | 17400535 | At variance with the previous bacteria strain-induced cytokine profile, infection with the P15986 strain induced a strong inflammatory response, with a substantial increase in all the cytokine tested, which was similar in vaccinated and in naïve, control animals, except for MIP-1 alpha, which was the only mediator significantly more produced by vaccinated animals than by naïve, control mice following P15986 infection. |
| 2373 | 17397028 | Compared with the native peptide, the agonist (i) bound to HLA-A2 molecules at lower peptide concentrations, (ii) demonstrated a higher stability of the peptide HLA-A2 complex, (iii) induced higher levels of production of IFN-gamma, Granzyme B, TNF-alpha, IL-2 and lymphotactin by PAGE4-specific T-cell lines and (iv) T-cell lines generated against the agonist peptide were more efficient to lyse HLA-A2 human tumor cells expressing native PAGE4. |
| 2374 | 17395728 | Aerosol and intranasal mouse infection models have yielded essentially equivalent results and have implicated an important role for Th1-type immune responses in protection, including IFN-gamma, TNF-alpha, and IL-12. |
| 2375 | 17386405 | IFN-gamma, TNF-alpha, IL-12P40 and IL-12P70 in the supernatants were assayed by ELISA, and the frequency as well as phenotype of IFN-gamma-producing cells were detected by ELISpot and FACS, respectively. |
| 2376 | 17386405 | The results showed that PBMCs from the HBV carriers secreted less IFN-gamma and IL-12 than those from the healthy controls. |
| 2377 | 17386405 | Exogenous IL-12 in combination with HBV specific antigens promoted PBMCs from the HBV carriers to secret more IFN-gamma by augmenting the frequency of CD8(+) IFN-gamma(+) T cells. |
| 2378 | 17383632 | It appears that TLR2/4 agonists induce a well controlled tumor necrosis factor-alpha (TNF-alpha) secretion, at plasma levels known to permeabilize neoangiogenic tumor vessels to the passage of cytotoxic drugs. |
| 2379 | 17383632 | Moreover, TLR2/4 agonists induce inducible nitric oxide synthase (iNOS) expression, and nitric oxide is able to induce apoptosis of chemotherapy-resistant tumor cell clones. |
| 2380 | 17371976 | These events were dependent on CD8 T cells, TNF-alpha, IFN-gamma, and type I IFNs. |
| 2381 | 17371976 | BM cells up-regulated Fas, and there was a significant increase in the number of CD8+ T cells that correlated with a loss of CD19+ and Ab-secreting cells in the BM. |
| 2382 | 17371857 | Markedly different effects on the immune system were observed; an IS901-negative strain (WAg 207) induced significant up-regulation of cell surface activation markers (major histocompatibility complex II, CD80, and CD86) on in vitro-derived dendritic cells and induced the release of proinflammatory monokines (interleukin-1beta [IL-1beta], IL-6, and tumor necrosis factor alpha) in dendritic cell-macrophage cocultures following direct in vitro contact of cells with bacteria. |
| 2383 | 17369012 | Human monocyte-derived macrophages produced more tumor necrosis factor alpha (TNFalpha), interleukin (IL)-1beta, IL-6, and IL-12 p40 following exposure to the variant, designated the activating variant (ACV). |
| 2384 | 17347551 | After being fed with the low casein diet, the guinea pigs were infected with Mycobacterium (M.) tuberculosis Kurono strain by aerosol infection, and seven weeks later were subjected to histopathologic examination, colony-forming unit (CFU) assay, fluorescence-activated cell sorter (FACS) analysis and real-time reverse transcriptase-polymerase chain reaction (RT-PCR) for interferon (IFN)-gamma, tumor necrosis factor (TNF)-alpha, interleukin (IL)-12 and inducible nitric oxide synthase (iNOS) mRNA. |
| 2385 | 17347551 | After being fed with the low casein diet, the guinea pigs were infected with Mycobacterium (M.) tuberculosis Kurono strain by aerosol infection, and seven weeks later were subjected to histopathologic examination, colony-forming unit (CFU) assay, fluorescence-activated cell sorter (FACS) analysis and real-time reverse transcriptase-polymerase chain reaction (RT-PCR) for interferon (IFN)-gamma, tumor necrosis factor (TNF)-alpha, interleukin (IL)-12 and inducible nitric oxide synthase (iNOS) mRNA. |
| 2386 | 17347551 | Pan T-, CD4-, CD8- and Mac antigen-positive cells were also recognized in the infected lung tissues of low casein-fed guinea pigs and Pan T-, CD4- and Mac antigen-positive cells increased after vaccination with BCG Tokyo. |
| 2387 | 17347551 | Pan T-, CD4-, CD8- and Mac antigen-positive cells were also recognized in the infected lung tissues of low casein-fed guinea pigs and Pan T-, CD4- and Mac antigen-positive cells increased after vaccination with BCG Tokyo. |
| 2388 | 17347551 | Expression of IFN-gamma, TNF-alpha, IL-12 and iNOS mRNA was also recognized in the infected lung tissues of low casein-fed guinea pigs and IFN-gamma and TNF-alpha mRNA expression was enhanced with BCG vaccination. |
| 2389 | 17347551 | Expression of IFN-gamma, TNF-alpha, IL-12 and iNOS mRNA was also recognized in the infected lung tissues of low casein-fed guinea pigs and IFN-gamma and TNF-alpha mRNA expression was enhanced with BCG vaccination. |
| 2390 | 17342333 | Supplementation with both anti-CD40 and OK432 resulted in induction of activated DCs with higher surface expression of CD80, CD83, CD86 and major histocompatibility complex class II antigens, compared with other mature DCs that were induced by the combination of anti-CD40 with tumor necrosis factor-alpha or lipopolysaccharide. |
| 2391 | 17339357 | Supernatants were assayed for interleukin-12p70 (IL-12p70), IL-10, IL-6, transforming growth factor beta (TGF-beta), NO, and tumor necrosis factor alpha (TNF-alpha). |
| 2392 | 17339357 | Supernatants were assayed for interleukin-12p70 (IL-12p70), IL-10, IL-6, transforming growth factor beta (TGF-beta), NO, and tumor necrosis factor alpha (TNF-alpha). |
| 2393 | 17339357 | Our results indicate that the addition of MAX upregulates the cytokines associated with a type 2 response (IL-10, IL-6, and TGF-beta) but downregulates type 1 cytokines (IL-12p70 and TNF-alpha) and NO. |
| 2394 | 17339357 | Our results indicate that the addition of MAX upregulates the cytokines associated with a type 2 response (IL-10, IL-6, and TGF-beta) but downregulates type 1 cytokines (IL-12p70 and TNF-alpha) and NO. |
| 2395 | 17339355 | The threshold for interleukin-1beta (IL-1beta) production by wild-type Mphi was significantly lower than that required for tumor necrosis factor alpha expression. |
| 2396 | 17332250 | Functional specialization of human circulating CD16 and CD1c myeloid dendritic-cell subsets. |
| 2397 | 17332250 | Functional specialization of human circulating CD16 and CD1c myeloid dendritic-cell subsets. |
| 2398 | 17332250 | Functional specialization of human circulating CD16 and CD1c myeloid dendritic-cell subsets. |
| 2399 | 17332250 | Human blood contains 2 populations of dendritic cells (DCs): plasmacytoid and myeloid (mDC). mDCs are subdivided into 3 subsets using the surface markers CD16, CD1c, and BDCA-3. |
| 2400 | 17332250 | Human blood contains 2 populations of dendritic cells (DCs): plasmacytoid and myeloid (mDC). mDCs are subdivided into 3 subsets using the surface markers CD16, CD1c, and BDCA-3. |
| 2401 | 17332250 | Human blood contains 2 populations of dendritic cells (DCs): plasmacytoid and myeloid (mDC). mDCs are subdivided into 3 subsets using the surface markers CD16, CD1c, and BDCA-3. |
| 2402 | 17332250 | Among 31 cytokines tested, both subsets produce CXCL8 (IL-8)/tumor necrosis factor-alpha (TNF-alpha)/IL-6/CCL3 (MIP-1 alpha)/CCL4 (MIP-1beta)/IL-1 beta. |
| 2403 | 17332250 | Among 31 cytokines tested, both subsets produce CXCL8 (IL-8)/tumor necrosis factor-alpha (TNF-alpha)/IL-6/CCL3 (MIP-1 alpha)/CCL4 (MIP-1beta)/IL-1 beta. |
| 2404 | 17332250 | Among 31 cytokines tested, both subsets produce CXCL8 (IL-8)/tumor necrosis factor-alpha (TNF-alpha)/IL-6/CCL3 (MIP-1 alpha)/CCL4 (MIP-1beta)/IL-1 beta. |
| 2405 | 17332250 | CXCL8 (IL-8) is the predominant cytokine produced by CD1c-mDCs on TLR engagement, whereas all other cytokines, particularly TNF-alpha, are secreted in 10-fold to 100-fold higher amounts by CD16-mDCs. |
| 2406 | 17332250 | CXCL8 (IL-8) is the predominant cytokine produced by CD1c-mDCs on TLR engagement, whereas all other cytokines, particularly TNF-alpha, are secreted in 10-fold to 100-fold higher amounts by CD16-mDCs. |
| 2407 | 17332250 | CXCL8 (IL-8) is the predominant cytokine produced by CD1c-mDCs on TLR engagement, whereas all other cytokines, particularly TNF-alpha, are secreted in 10-fold to 100-fold higher amounts by CD16-mDCs. |
| 2408 | 17332250 | CD16-mDCs cocultured with human umbilical vein endothelial cells induce a significantly higher production of CXCL10 (IP-10), granulocyte-macrophage colony-stimulating factor, and granulocyte colony-stimulating factor than CD1c-mDCs. |
| 2409 | 17332250 | CD16-mDCs cocultured with human umbilical vein endothelial cells induce a significantly higher production of CXCL10 (IP-10), granulocyte-macrophage colony-stimulating factor, and granulocyte colony-stimulating factor than CD1c-mDCs. |
| 2410 | 17332250 | CD16-mDCs cocultured with human umbilical vein endothelial cells induce a significantly higher production of CXCL10 (IP-10), granulocyte-macrophage colony-stimulating factor, and granulocyte colony-stimulating factor than CD1c-mDCs. |
| 2411 | 17332250 | In addition, interleukin-3 and type I interferons are stimuli specifically for DC maturation rather than cytokine secretion, whereas TNF-alpha is almost ineffective in inducing either function, suggesting a mechanism of T-cell-DC crosstalk and of rapid induction of antigen-presenting cell function during viral infection rather than inflammation. |
| 2412 | 17332250 | In addition, interleukin-3 and type I interferons are stimuli specifically for DC maturation rather than cytokine secretion, whereas TNF-alpha is almost ineffective in inducing either function, suggesting a mechanism of T-cell-DC crosstalk and of rapid induction of antigen-presenting cell function during viral infection rather than inflammation. |
| 2413 | 17332250 | In addition, interleukin-3 and type I interferons are stimuli specifically for DC maturation rather than cytokine secretion, whereas TNF-alpha is almost ineffective in inducing either function, suggesting a mechanism of T-cell-DC crosstalk and of rapid induction of antigen-presenting cell function during viral infection rather than inflammation. |
| 2414 | 17325890 | Monocyte-derived DC cultured in the presence of granulocyte-macrophage colony-stimulating factor, interleukin (IL)-4 and tumor necrosis factor (TNF)-alpha expressed maturation markers, produced IL-12 and loaded apoptotic bodies to a similar extent to normal DC. |
| 2415 | 17325890 | Monocyte-derived DC cultured in the presence of granulocyte-macrophage colony-stimulating factor, interleukin (IL)-4 and tumor necrosis factor (TNF)-alpha expressed maturation markers, produced IL-12 and loaded apoptotic bodies to a similar extent to normal DC. |
| 2416 | 17325890 | Patients' circulating T and NK lymphocytes were normally represented and, after stimulation, were capable of producing TNF-alpha and interferon-gamma to a similar extent to control lymphocytes. |
| 2417 | 17325890 | Patients' circulating T and NK lymphocytes were normally represented and, after stimulation, were capable of producing TNF-alpha and interferon-gamma to a similar extent to control lymphocytes. |
| 2418 | 17311933 | It is noteworthy that in response to heat stress, mature DC produced higher levels of IL-12p70 and TNF-alpha, which are two cytokines involved in the stimulation of inflammatory reaction, whereas IL-10 production remained low. |
| 2419 | 17311933 | After heat-stress exposure, mature DC have the full ability to stimulate naive T cells with Th1 response polarization (high IFN-gamma and low IL-4 production) in an allogeneic MLR. |
| 2420 | 17306360 | These should be directed at the level of gene selection and delivery, in order to identify the optimal cytokine and achieve efficient and durable cytokine expression, and at the level of improving immune stimulation, i.e. by co-administration of co-stimulatory molecules including B7 and CD40, or boosting the expression of tumor antigens or MHC class I molecules. |
| 2421 | 17306360 | Interestingly, some of the cytokines which have shown encouraging anti-tumor activity, including IFNs, IL-4, IL-12 and TNF-alpha, are endowed with anti-angiogenic or vasculotoxic effects, which may significantly contribute to local tumor control. |
| 2422 | 17296747 | Survival of vaccinated mice after live bacterial challenge was correlated with reduced bacterial burden, decreased pulmonary inflammation, increased serum antibody titers, and lower levels of gamma interferon (IFN-gamma), tumor necrosis factor alpha, and IL-6 in the lungs, livers, and spleens. |
| 2423 | 17296747 | Whereas NK cells were primarily responsible for the production of IFN-gamma in unvaccinated, challenged animals, vaccinated mice had increased levels of lung IFN-gamma+ CD4+ T cells after challenge. |
| 2424 | 17283172 | Two delivery systems, cDNA delivered by gene gun and Venezuelan equine encephalitis virus-like replicon particles (VRP), both encoding mouse STEAP (mSTEAP) and three vaccination strategies were used. |
| 2425 | 17283172 | Our results show that mSTEAP-based vaccination was able to induce a specific CD8 T-cell response against a newly defined mSTEAP epitope that prolonged the overall survival rate in tumor-challenged mice very significantly. |
| 2426 | 17283172 | Surprisingly, CD4 T cells that produced IFNgamma, tumor necrosis factor-alpha (TNF-alpha), and interleukin-2 (IL-2) played the main role in tumor rejection in our model as shown by using CD4- and CD8-deficient mice. |
| 2427 | 17273752 | Levels of 22 cytokines consisting of interleukin (IL)-1alpha, -1beta, -2, -4, -5, -6, -7, -8, -10, -12, -13, -15, -17, IFN-gamma, G-CSF, GM-CSF, TNF-alpha, IP-10, MIP-1alpha, RANTES, eotaxin and monocyte chemotactic protein-1 (MCP-1) were assessed. |
| 2428 | 17273752 | MCP-1, eotaxin, RANTES and GM-CSF levels were significantly elevated in BCa (P<0.009) and IL-1alpha and IL-4 levels were significantly decreased in BCa (P<0.015). |
| 2429 | 17273752 | Cytokine levels were generally elevated in NN patients compared to NP patients with the exception of eotaxin and IL-13, which were increased in NP patients. |
| 2430 | 17273752 | Three cytokines, IL-6, MIP-1alpha and G-CSF reached statistical significance (P<0.05). |
| 2431 | 17273752 | In 34 vaccinated BCa, MCP-1, eotaxin and IL-13 were significantly elevated post-vaccination with MCP-1 demonstrating the most significant response (median, 145.8-217.0 pg/ml, P=0.003). |
| 2432 | 17267590 | Tumor necrosis factor alpha (TNF-alpha), interleukin-6, and neutrophil responses were earlier and more pronounced in the bolus trial compared with the infusion trial results, whereas lymphocytes increased after endotoxin bolus injection as well as infusion without any difference between groups. |
| 2433 | 17257077 | The mature human DCs generated from peripheral blood mononuclear cells (PBMCs) in the presence of granulocyte macrophage-colony-stimulating factor (GM-CSF), interleukin (IL)-4, and tumor necrosis factor (TNF)-alpha have widely contributed to their growing use in cancer vaccination trials. |
| 2434 | 17257077 | The mature human DCs generated from peripheral blood mononuclear cells (PBMCs) in the presence of granulocyte macrophage-colony-stimulating factor (GM-CSF), interleukin (IL)-4, and tumor necrosis factor (TNF)-alpha have widely contributed to their growing use in cancer vaccination trials. |
| 2435 | 17257077 | Our data show that mature DCs can be generated from PBMCs in both Dulbecco's modified Eagle's medium plus 10% FCS and serum-free AIM-V medium containing GM-CSF (100 ng/mL), IL-4 (100 ng/mL), and TNF-alpha (10 ng/mL). |
| 2436 | 17257077 | Our data show that mature DCs can be generated from PBMCs in both Dulbecco's modified Eagle's medium plus 10% FCS and serum-free AIM-V medium containing GM-CSF (100 ng/mL), IL-4 (100 ng/mL), and TNF-alpha (10 ng/mL). |
| 2437 | 17255244 | In CYD-infected DCs, we observed an up-regulation of HLA-DR, CD80, CD86, and CD83. |
| 2438 | 17255244 | In CYD-infected DCs, we observed an up-regulation of HLA-DR, CD80, CD86, and CD83. |
| 2439 | 17255244 | Cells exposed to CYD secreted type I interferons, monocyte chemoattractant protein 1 (MCP-1)/CC chemokine ligand 2 (CCL-2), interleukin-6 (IL-6), and low amounts of tumor necrosis factor-alpha (TNF-alpha), but no IL-10, IL-12, or IL-1alpha. |
| 2440 | 17255244 | Cells exposed to CYD secreted type I interferons, monocyte chemoattractant protein 1 (MCP-1)/CC chemokine ligand 2 (CCL-2), interleukin-6 (IL-6), and low amounts of tumor necrosis factor-alpha (TNF-alpha), but no IL-10, IL-12, or IL-1alpha. |
| 2441 | 17255244 | Parental dengue viruses induced a similar array of cytokines, but more TNF-alpha, less IL-6, and less MCP-1/CCL-2 than induced by CYD. |
| 2442 | 17255244 | Parental dengue viruses induced a similar array of cytokines, but more TNF-alpha, less IL-6, and less MCP-1/CCL-2 than induced by CYD. |
| 2443 | 17242926 | Results showed that vaccination with GFT cells resulted in increased serum antibody to a PAIII cell lysate; reduced weight of the prostate/seminal vesicle complex and reduced incidence of prostate cancer in nude mice; increased splenocyte supernatant levels of TNF-alpha, IL-2, IFN-gamma and IL-12, cytokines associated with Th1 immunity; and increased splenocyte supernatant levels of IL-4 and IL-10, cytokines associated with Th2 immunity. |
| 2444 | 17242058 | The levels of gamma interferon, interleukin-1beta (IL-1beta), IL-6, tumor necrosis factor alpha, macrophage inflammatory protein 1alpha, KC, interferon-inducible protein 10, and monocyte chemotactic protein 1 were elevated from day 2 postinoculation onward. |
| 2445 | 17239501 | Chlamydia-specific cytokines including tumour necrosis factor-alpha (TNF-alpha) interleukin-10 (IL-10), interleukin-4 (IL-4), interleukin-12 (IL-12) and interferon-gamma (IFN-gamma) were detected in mice immunized either with selected DNA clones in spleen cells (0.2-135.2 pg/mL) or lymph nodes (0.15-84.9 pg/mL). |
| 2446 | 17235318 | Moreover, Ad5:CaPi-treated DCs were activated to express the maturation surface molecules CD40 and CD86, and to secrete proinflammatory cytokines tumor necrosis factor-alpha and interleukin 6. |
| 2447 | 17235318 | Ad5:CaPi also transduced human DC more efficiently than Ad5 alone, similar to a genetically modified vector (Ad5f35) targeted to the CD46 receptor. |
| 2448 | 17230439 | Although phosphoantigen activated immediately a strong release of systemic Th1 cytokines (IL-2, IL-6, IFN-gamma, TNF-alpha), it further anergized blood gammadelta T lymphocytes selectively. |
| 2449 | 17229643 | Anti-idiotypic T cells were analyzed in myeloma patients (n=18) vaccinated with idiotypic protein together with the adjuvant cytokines granulocyte-macrophage colony-stimulating factor (GM-CSF) and/or interleukin-12 (IL-12). |
| 2450 | 17229643 | In the group given IL-12/GM-CSF, 78% developed idiotype specific T cells as compared to 22% in the group given only IL-12 (proliferation/ELISPOT assays) (p<0.05). |
| 2451 | 17229643 | A predominance of a Th1 (IFN-gamma/TNF-alpha) immune response was noted in the IL-12 group while a Th2 (IL-5) response prevailed in the IL-12/GM-CSF group (p=0.053). |
| 2452 | 17224216 | This led us to study bacterial clearance, lung pathology, lung TNF-alpha expression, and parameters of immediate hypersensitivity (IH), being serum IgE levels, eosinophil numbers in the bronchoalveolar lavage fluid, and ex vivo IL-4, IL-5, IL-10, IL-13, and IFN-gamma production by the bronchial lymph node cells. |
| 2453 | 17223980 | In this study, we investigated human CC- [macrophage-derived chemokine (MDC), monocyte chemoattractant protein (MCP)-1, macrophage inflammatory protein (MIP)-1alpha and eosinophil chemoattractant activity (eotaxin)] and CXC-interferon-inducible protein (IP)-10 chemokine production in response to BCG stimulation. |
| 2454 | 17223980 | In this study, we investigated human CC- [macrophage-derived chemokine (MDC), monocyte chemoattractant protein (MCP)-1, macrophage inflammatory protein (MIP)-1alpha and eosinophil chemoattractant activity (eotaxin)] and CXC-interferon-inducible protein (IP)-10 chemokine production in response to BCG stimulation. |
| 2455 | 17223980 | Although BCG induced no or marginal chemokines from urothelial SV-HUC-1, RT4 and T24 cells, BCG-derived cytokines [interleukin (IL)-1beta, interferon (IFN)-gamma and tumour necrosis factor (TNF)-alpha] induced all chemokines tested except eotaxin from these cell lines. |
| 2456 | 17223980 | Although BCG induced no or marginal chemokines from urothelial SV-HUC-1, RT4 and T24 cells, BCG-derived cytokines [interleukin (IL)-1beta, interferon (IFN)-gamma and tumour necrosis factor (TNF)-alpha] induced all chemokines tested except eotaxin from these cell lines. |
| 2457 | 17223980 | MCP-1 and MIP-1alpha emerged at 4-5 h post-BCG exposure (early chemokines); IP-10 elevated at day 1 and peaked at day 2 (intermediate chemokine); and MDC elevated at day 1 and peaked at day 7 (late chemokine). |
| 2458 | 17223980 | MCP-1 and MIP-1alpha emerged at 4-5 h post-BCG exposure (early chemokines); IP-10 elevated at day 1 and peaked at day 2 (intermediate chemokine); and MDC elevated at day 1 and peaked at day 7 (late chemokine). |
| 2459 | 17223980 | This kinetic pattern was paralleled with that of BCG-induced cytokines [early: TNF-alpha; intermediate: IL-6 and IL-10; and late: IFN-gamma and granulocyte-macrophage colony-stimulating factor (GM-CSF)]. |
| 2460 | 17223980 | This kinetic pattern was paralleled with that of BCG-induced cytokines [early: TNF-alpha; intermediate: IL-6 and IL-10; and late: IFN-gamma and granulocyte-macrophage colony-stimulating factor (GM-CSF)]. |
| 2461 | 17223975 | Infection of Balb/c mice with M. tuberculosis SO2 was associated with comparatively lower levels of interferon (IFN)-gamma, interleukin (IL)-4 and tumour necrosis factor (TNF)-alpha and higher levels of inducible nitric oxide synthase (iNOS) during the late stage of infection, when compared with M. tuberculosis MT103 infection. |
| 2462 | 17223970 | Production of interleukin (IL)-5 and IL-10 accompanies T helper cell type 1 (Th1) cytokine responses to a major thyroid self-antigen, thyroglobulin, in health and autoimmune thyroid disease. |
| 2463 | 17223970 | Production of interleukin (IL)-5 and IL-10 accompanies T helper cell type 1 (Th1) cytokine responses to a major thyroid self-antigen, thyroglobulin, in health and autoimmune thyroid disease. |
| 2464 | 17223970 | Production of interleukin (IL)-5 and IL-10 accompanies T helper cell type 1 (Th1) cytokine responses to a major thyroid self-antigen, thyroglobulin, in health and autoimmune thyroid disease. |
| 2465 | 17223970 | Production of interleukin (IL)-5 and IL-10 accompanies T helper cell type 1 (Th1) cytokine responses to a major thyroid self-antigen, thyroglobulin, in health and autoimmune thyroid disease. |
| 2466 | 17223970 | Production of interleukin (IL)-5 and IL-10 accompanies T helper cell type 1 (Th1) cytokine responses to a major thyroid self-antigen, thyroglobulin, in health and autoimmune thyroid disease. |
| 2467 | 17223970 | Tumour necrosis factor (TNF)-alpha and interferon (IFN)-gamma exert detrimental effects in organ-specific autoimmune disease, while both destructive and protective roles have been demonstrated for interleukin (IL)-10, IL-4 and IL-5. |
| 2468 | 17223970 | Tumour necrosis factor (TNF)-alpha and interferon (IFN)-gamma exert detrimental effects in organ-specific autoimmune disease, while both destructive and protective roles have been demonstrated for interleukin (IL)-10, IL-4 and IL-5. |
| 2469 | 17223970 | Tumour necrosis factor (TNF)-alpha and interferon (IFN)-gamma exert detrimental effects in organ-specific autoimmune disease, while both destructive and protective roles have been demonstrated for interleukin (IL)-10, IL-4 and IL-5. |
| 2470 | 17223970 | Tumour necrosis factor (TNF)-alpha and interferon (IFN)-gamma exert detrimental effects in organ-specific autoimmune disease, while both destructive and protective roles have been demonstrated for interleukin (IL)-10, IL-4 and IL-5. |
| 2471 | 17223970 | Tumour necrosis factor (TNF)-alpha and interferon (IFN)-gamma exert detrimental effects in organ-specific autoimmune disease, while both destructive and protective roles have been demonstrated for interleukin (IL)-10, IL-4 and IL-5. |
| 2472 | 17223970 | Initially, TNF-alpha and IL-2 were produced in all three groups, accompanied by IL-10. |
| 2473 | 17223970 | Initially, TNF-alpha and IL-2 were produced in all three groups, accompanied by IL-10. |
| 2474 | 17223970 | Initially, TNF-alpha and IL-2 were produced in all three groups, accompanied by IL-10. |
| 2475 | 17223970 | Initially, TNF-alpha and IL-2 were produced in all three groups, accompanied by IL-10. |
| 2476 | 17223970 | Initially, TNF-alpha and IL-2 were produced in all three groups, accompanied by IL-10. |
| 2477 | 17223970 | Release of IFN-gamma, IL-4 and, notably, IL-5 ensued. |
| 2478 | 17223970 | Release of IFN-gamma, IL-4 and, notably, IL-5 ensued. |
| 2479 | 17223970 | Release of IFN-gamma, IL-4 and, notably, IL-5 ensued. |
| 2480 | 17223970 | Release of IFN-gamma, IL-4 and, notably, IL-5 ensued. |
| 2481 | 17223970 | Release of IFN-gamma, IL-4 and, notably, IL-5 ensued. |
| 2482 | 17223970 | Both patient groups exhibited increased TNF-alpha, IL-2, IFN-gamma and IL-10 responses, and PBMC from HT patients secreted lower amounts of IL-5 than male, but not female, controls. |
| 2483 | 17223970 | Both patient groups exhibited increased TNF-alpha, IL-2, IFN-gamma and IL-10 responses, and PBMC from HT patients secreted lower amounts of IL-5 than male, but not female, controls. |
| 2484 | 17223970 | Both patient groups exhibited increased TNF-alpha, IL-2, IFN-gamma and IL-10 responses, and PBMC from HT patients secreted lower amounts of IL-5 than male, but not female, controls. |
| 2485 | 17223970 | Both patient groups exhibited increased TNF-alpha, IL-2, IFN-gamma and IL-10 responses, and PBMC from HT patients secreted lower amounts of IL-5 than male, but not female, controls. |
| 2486 | 17223970 | Both patient groups exhibited increased TNF-alpha, IL-2, IFN-gamma and IL-10 responses, and PBMC from HT patients secreted lower amounts of IL-5 than male, but not female, controls. |
| 2487 | 17223970 | Conversely, higher production of TNF-alpha and IL-5 occurred in the presence of autologous sera than in the presence of pooled normal sera in both patient groups, indicating a dependency on serum constituents. |
| 2488 | 17223970 | Conversely, higher production of TNF-alpha and IL-5 occurred in the presence of autologous sera than in the presence of pooled normal sera in both patient groups, indicating a dependency on serum constituents. |
| 2489 | 17223970 | Conversely, higher production of TNF-alpha and IL-5 occurred in the presence of autologous sera than in the presence of pooled normal sera in both patient groups, indicating a dependency on serum constituents. |
| 2490 | 17223970 | Conversely, higher production of TNF-alpha and IL-5 occurred in the presence of autologous sera than in the presence of pooled normal sera in both patient groups, indicating a dependency on serum constituents. |
| 2491 | 17223970 | Conversely, higher production of TNF-alpha and IL-5 occurred in the presence of autologous sera than in the presence of pooled normal sera in both patient groups, indicating a dependency on serum constituents. |
| 2492 | 17223970 | Complement appeared to promote the production of IL-2 and particularly IL-5, the levels of which were reduced by neutralization of complement by heat- or zymosan treatment. |
| 2493 | 17223970 | Complement appeared to promote the production of IL-2 and particularly IL-5, the levels of which were reduced by neutralization of complement by heat- or zymosan treatment. |
| 2494 | 17223970 | Complement appeared to promote the production of IL-2 and particularly IL-5, the levels of which were reduced by neutralization of complement by heat- or zymosan treatment. |
| 2495 | 17223970 | Complement appeared to promote the production of IL-2 and particularly IL-5, the levels of which were reduced by neutralization of complement by heat- or zymosan treatment. |
| 2496 | 17223970 | Complement appeared to promote the production of IL-2 and particularly IL-5, the levels of which were reduced by neutralization of complement by heat- or zymosan treatment. |
| 2497 | 17223970 | The production of IFN-gamma and IL-2 of the three groups together correlated directly with the serum anti-Tg activity. |
| 2498 | 17223970 | The production of IFN-gamma and IL-2 of the three groups together correlated directly with the serum anti-Tg activity. |
| 2499 | 17223970 | The production of IFN-gamma and IL-2 of the three groups together correlated directly with the serum anti-Tg activity. |
| 2500 | 17223970 | The production of IFN-gamma and IL-2 of the three groups together correlated directly with the serum anti-Tg activity. |
| 2501 | 17223970 | The production of IFN-gamma and IL-2 of the three groups together correlated directly with the serum anti-Tg activity. |
| 2502 | 17223970 | Moreover, TNF-alpha, IFN-gamma, IL-5 and IL-10 responses were markedly inhibited by partial denaturation of Tg by boiling. |
| 2503 | 17223970 | Moreover, TNF-alpha, IFN-gamma, IL-5 and IL-10 responses were markedly inhibited by partial denaturation of Tg by boiling. |
| 2504 | 17223970 | Moreover, TNF-alpha, IFN-gamma, IL-5 and IL-10 responses were markedly inhibited by partial denaturation of Tg by boiling. |
| 2505 | 17223970 | Moreover, TNF-alpha, IFN-gamma, IL-5 and IL-10 responses were markedly inhibited by partial denaturation of Tg by boiling. |
| 2506 | 17223970 | Moreover, TNF-alpha, IFN-gamma, IL-5 and IL-10 responses were markedly inhibited by partial denaturation of Tg by boiling. |
| 2507 | 17223146 | The titre of IgG and IgG1/IgG2 isotype to SPML vaccine in serum, the proliferation of lymphocytes, SPML-specific interferon-gamma (IFN-gamma) and IL-6, TNF-alpha, IL-4 production of PBMCs in vitro and IFN-gamma, IL-6, TNF-alpha, IL-4, IL-10 in piglets serum were examined to identify the immune responses of the piglets. |
| 2508 | 17220311 | Here, we analyze the phenotypic and functional outcomes of MBP-treated dendritic cells (DCs) and show that MBP induces DC activation and production of proinflammatory cytokines (interleukin-1beta [IL-1beta], IL-6, IL-8, tumor necrosis factor alpha, and IL-12p70) within 24 h and strongly increases Ikappabeta phosphorylation in treated cells. |
| 2509 | 17220311 | Consistent with this hypothesis, MBP activated the TLR4-expressing cell line 293-hTLR4A but not control cultures to secrete IL-8. |
| 2510 | 17217432 | Levels of IL-12p40, TNFalpha, TGFbeta, IFNgamma and IL-10 mRNA were assessed by laser capture microdissection followed by quantitative real-time PCR in the pulmonary granulomas of unimmunized and BCG-vaccinated guinea pigs infected by aerosol with virulent Mycobacterium tuberculosis. |
| 2511 | 17217432 | The cytokine profile of granulomas from vaccinated guinea pigs shifted from type 1 cytokine mRNA (IFNgamma and IL-12p40) at 3 weeks to a predominantly anti-inflammatory environment (TGFbeta mRNA) at 6 weeks. |
| 2512 | 17202676 | Furthermore, the activated lymphocytes (CD8+) were capable of infiltrating into the tumor site, and much more apoptotic cells along with activation of caspase-3 were observed in the tumors from vaccinated-mice. |
| 2513 | 17202676 | Also, high expression levels of human IFN-gamma, TNF-alpha, granzyme B and perforin were detected in the tumors from vaccinated-mice. |
| 2514 | 17202359 | Using flow cytometry to assess TLR-induced cytokine production, we observed a substantial, highly significant defect in TLR1/2-induced TNF-alpha (p = 0.0003) and IL-6 (p < 0.0001) production, in older adults compared with young controls. |
| 2515 | 17202359 | Using flow cytometry to assess TLR-induced cytokine production, we observed a substantial, highly significant defect in TLR1/2-induced TNF-alpha (p = 0.0003) and IL-6 (p < 0.0001) production, in older adults compared with young controls. |
| 2516 | 17202359 | Production of IL-6 (p < 0.0001) and TNF-alpha (p = 0.003) after stimulation by N-palmitoyl-S-[2,3-bis(palmitoyloxy)-(2R,S)-propyl]-Cys-[S]-Ser1-[S]-Lys(4) trihydrochloride was strongly associated with TLR1 surface expression. |
| 2517 | 17202359 | Production of IL-6 (p < 0.0001) and TNF-alpha (p = 0.003) after stimulation by N-palmitoyl-S-[2,3-bis(palmitoyloxy)-(2R,S)-propyl]-Cys-[S]-Ser1-[S]-Lys(4) trihydrochloride was strongly associated with TLR1 surface expression. |
| 2518 | 17202335 | EDA also stimulated the production by DC of proinflammatory cytokines such as IL-12 or TNF-alpha and induced their maturation in vitro and in vivo. |
| 2519 | 17201660 | The ability of porcine reproductive and respiratory syndrome virus (PRRSV) to suppress T cell expression of CD25 (alpha chain of interleukin [IL]-2 receptor), interferon-gamma (IFN-gamma), and tumor necrosis factor-alpha (TNF-alpha) was determined by flow cytometry in naive porcine T cells in response to mitogen (concanavalin A) and cytokine inducers (phorbol 12-myristate 13-acetate plus ionomycin [PMA/I]). |
| 2520 | 17201660 | Joseph, MO), demonstrated significantly reduced CD25 expression (%CD25(+)) and IFN-gamma expression (%IFN-gamma (+)) compared with T cells incubated with uninoculated monocyte cultures. |
| 2521 | 17198083 | DC pulsed with P. carinii did not demonstrate increased expression of the cell surface markers MHC II, CD40, CD54, CD80 (B7.1), and CD86 (B7.2). |
| 2522 | 17198083 | The release of interleukin (IL)-4 was increased, but there was no increase in the release of interleukin (IL)-12p40, IL-10, tumor necrosis factor-alpha, IL-6, and nitrite compared with naive DC. |
| 2523 | 17198083 | In vivo administration of DC pulsed with P. carinii induced a P. carinii-specific response, generating CD4+ cells that proliferated and released IL-4, but not interferon-gamma, in response to P. carinii-pulsed DC in vitro. |
| 2524 | 17192314 | However, gamma interferon (IFN-gamma) enzyme-linked immunospot and IFN-gamma/tumor necrosis factor alpha intracellular-cytokine-staining assays detected cross-reactive immune responses against the Gag escape variant. |
| 2525 | 17191384 | CD28 and CD27 costimulation of CD8+ T cells: a story of survival. |
| 2526 | 17191384 | Although the requirement of CD28 and CD27 costimulation has been clearly demonstrated during primary CD8+ T cell responses and this costimulation acts by providing proliferation and survival cues to naive CD8+ T cells, a number of questions also arise from these studies. |
| 2527 | 17191384 | Is the requirement for CD28 and CD27 costimulation restricted to the initiation of the immune response in the lymph nodes, where presumably the initial contact between naive CD8+ T cell and DC occurs? |
| 2528 | 17191384 | If DC are required for optimal secondary responses (100), is CD28 costimulation the missing signal or is it other members of the B7:CD28 family or TNF family? |
| 2529 | 17183611 | There is growing evidence that engagement of OX40 (CD134), a member of the TNF receptor superfamily, can directly stimulate antigen-specific CD8+ T cells. |
| 2530 | 17183611 | It has been shown that CD8+ T cells express OX40 following activation, but the response of antigen-specific CD8+ T cells to OX40 stimulation has not been fully characterized. |
| 2531 | 17183611 | We utilized an antigen-specific transgenic CD8+ T cell model (OT-I) to determine if OX40 engagement can boost the generation of antigen-specific CD8+ T cell memory. |
| 2532 | 17183611 | Our results demonstrate that enhanced OX40 costimulation, via an agonist anti-OX40 antibody, increases CD25 and phospho-Akt expression on the antigen-specific CD8+ T cells and significantly increases the generation of long-lived antigen-specific CD8+ memory T cells. |
| 2533 | 17183611 | The increased numbers of memory CD8+ T cells generated via anti-OX40 treatment still required the presence of CD4+ T cells for their long-term maintenance in vivo. |
| 2534 | 17183611 | These data show that OX40 engagement in vivo increases the number of antigen-specific CD8+ memory T cells surviving after antigen challenge and has implications for the development of more potent vaccines against pathogens and cancer. |
| 2535 | 17182676 | Changes in paracrine interleukin-2 requirement, CCR7 expression, frequency, and cytokine secretion of human immunodeficiency virus-specific CD4+ T cells are a consequence of antigen load. |
| 2536 | 17182676 | Virus-specific CD4+ T-cell responses are thought to be required for the induction and maintenance of many effective CD8+ T-cell and B-cell immune responses in experimental animals and humans. |
| 2537 | 17182676 | A 10-color, 12-parameter flow cytometric panel was utilized to examine the frequency, memory phenotype (CD27, CCR7, and CD45RA), and cytokine production (interleukin-2 [IL-2], gamma interferon, and tumor necrosis factor alpha) of CD4+ T cells specific for HIV antigens as well as for adenovirus, Epstein-Barr virus (EBV), influenza H1N1 virus, influenza H3N2 virus, cytomegalovirus, varicella-zoster virus (VZV), and tetanus toxoid in normal controls, long-term nonprogressors (LTNP), and HIV-infected patients with progressive disease on or off therapy. |
| 2538 | 17182676 | HIV-specific CD4+ T cells from patients off antiretroviral therapy demonstrated a shift towards a CCR7(-) CD45RA(-) phenotype and a reduced percentage of IL-2-producing cells. |
| 2539 | 17182676 | The alterations in cytokine production during HIV viremia were found to be intrinsic to the HIV-specific CD4+ T cells and caused a requirement for IL-2 supplied exogenously for proliferation to occur. |
| 2540 | 17182155 | In these clinical trials we observed that CVD 909 immunization elicits a wide array of CMI, including cytotoxic T cells (CTL), IFN-gamma, TNF-alpha and IL-10 (but not IL-2, IL-4 or IL-5) production, and proliferation to S. |
| 2541 | 17179660 | Protective immunity against Bordetella pertussis by a recombinant DNA vaccine and the effect of coinjection with a granulocyte-macrophage colony stimulating factor gene. |
| 2542 | 17179660 | Protective immunity against Bordetella pertussis by a recombinant DNA vaccine and the effect of coinjection with a granulocyte-macrophage colony stimulating factor gene. |
| 2543 | 17179660 | Compared to those injected with pVAX1, the mice injected with pVAX1/ppf significantly elicited more antigen specific antibody anti-PTS1, anti-PRN, anti-FHA and cytokine IL-10, IFN-gamma. |
| 2544 | 17179660 | Compared to those injected with pVAX1, the mice injected with pVAX1/ppf significantly elicited more antigen specific antibody anti-PTS1, anti-PRN, anti-FHA and cytokine IL-10, IFN-gamma. |
| 2545 | 17179660 | When pGM-CSF was coinjected with pVAX1/ppf, the mice showed significantly increases of the three antibodies and cytokine IL-10, IL-4, IFN-gamma and TNF-alpha compared to those injected with pVAX1 only. |
| 2546 | 17179660 | When pGM-CSF was coinjected with pVAX1/ppf, the mice showed significantly increases of the three antibodies and cytokine IL-10, IL-4, IFN-gamma and TNF-alpha compared to those injected with pVAX1 only. |
| 2547 | 17179660 | The mice in group pVAX1/ppf & pGM-CSF, in particular; induced much more anti-PTS1, IL-4 and TNF-alpha than those in group pVAX1/ppf. |
| 2548 | 17179660 | The mice in group pVAX1/ppf & pGM-CSF, in particular; induced much more anti-PTS1, IL-4 and TNF-alpha than those in group pVAX1/ppf. |
| 2549 | 17178564 | In this paper we describe development of antigen-specific tolerizing DNA vaccines to treat collagen-induced arthritis (CIA) in mice, and use of protein microarrays to monitor response to therapy and to identify potential additional autoimmune targets for next generation vaccines. |
| 2550 | 17178564 | We demonstrate that tolerizing DNA vaccines encoding type II collagen (CII) reduced the incidence and severity of CIA. |
| 2551 | 17178564 | Analysis of cytokines produced by collagen-reactive T cells derived from mice receiving tolerizing DNA encoding CII, as compared to control vaccines, revealed reduced production of the pro-inflammatory cytokines IFN-gamma and TNF-alpha. |
| 2552 | 17178178 | Further, quantification of the gene expression induced by the stimulation with P-8 in asymptomatically infected dogs showed an up-regulation of IFN-gamma and TNF-alpha, which were three to 4-fold higher than that induced by soluble Leishmania antigen (SLA). |
| 2553 | 17178178 | While no measurable induction of IL-10 was observed, low levels of IL-4 mRNA were observed in response to both P-8 and SLA antigens. |
| 2554 | 17158960 | We used polychromatic flow cytometry to evaluate the production of the cytokines interferon (IFN)-gamma, tumor necrosis factor (TNF)-alpha, and interleukin (IL)-2, the chemokine macrophage inflammatory protein (MIP)-1beta, and surface mobilization of the degranulation marker CD107a by CD4+ T cells in response to stimulation with cytomegalovirus (CMV)-specific major histocompatibility complex class II peptide epitopes. |
| 2555 | 17158960 | We used polychromatic flow cytometry to evaluate the production of the cytokines interferon (IFN)-gamma, tumor necrosis factor (TNF)-alpha, and interleukin (IL)-2, the chemokine macrophage inflammatory protein (MIP)-1beta, and surface mobilization of the degranulation marker CD107a by CD4+ T cells in response to stimulation with cytomegalovirus (CMV)-specific major histocompatibility complex class II peptide epitopes. |
| 2556 | 17158960 | Surface expression of CD45RO, CD27, and CD57 on responding cells was used to classify CD4+ T cell maturation. |
| 2557 | 17158960 | Surface expression of CD45RO, CD27, and CD57 on responding cells was used to classify CD4+ T cell maturation. |
| 2558 | 17158960 | Salient features of this profile were: (a) the simultaneous production of MIP-1beta, TNF-alpha, and IFN-gamma in the absence of IL-2; and (b) direct cytolytic activity associated with surface mobilization of CD107a and intracellular expression of perforin and granzymes. |
| 2559 | 17158960 | Salient features of this profile were: (a) the simultaneous production of MIP-1beta, TNF-alpha, and IFN-gamma in the absence of IL-2; and (b) direct cytolytic activity associated with surface mobilization of CD107a and intracellular expression of perforin and granzymes. |
| 2560 | 17158960 | Thus, mature CMV-specific CD4+ T cells exhibit distinct functional properties reminiscent of antiviral CD8+ T lymphocytes. |
| 2561 | 17158960 | Thus, mature CMV-specific CD4+ T cells exhibit distinct functional properties reminiscent of antiviral CD8+ T lymphocytes. |
| 2562 | 17142751 | We have shown that the CpG-C ISS-ODN C274 stimulates macaque blood dendritic cells (DCs) and B cells and augments SIV-specific IFN-gamma responses in vitro. |
| 2563 | 17142751 | This was particularly apparent at the level of CD80 (less so CD86) expression by CD123(+) plasmacytoid DCs and was further boosted in the presence of additional C274 in vitro. |
| 2564 | 17142751 | This was more pronounced when cells were exposed to additional stimuli in vitro, producing IFN-alpha, IL-3, IL-6, IL-12, TNF-alpha, CCL2, CCL3, CCL5, and CXCL8. |
| 2565 | 17142751 | Elevated IFN-alpha, CCL2, and CCL5 were also detected in the plasma after C274 injection. |
| 2566 | 17142738 | Dendritic cell targeting of survivin protein in a xenogeneic form elicits strong CD4+ T cell immunity to mouse survivin. |
| 2567 | 17142738 | To determine whether strong CD4+ T cell immunity could be induced to a nonmutated self protein that is important for tumorigenesis, we selectively targeted the xenogeneic form of survivin, a survival protein overexpressed in tumors, to maturing dendritic cells in lymphoid tissues. |
| 2568 | 17142738 | Dendritic cell targeting via the DEC205 receptor in the presence of anti-CD40 and poly(I:C) as maturation stimuli, induced strong human and mouse survivin-specific CD4+ T cell responses, as determined by IFN-gamma, TNF-alpha, and IL-2 production, as well as the development of lytic MHC class II-restricted T cells and memory. |
| 2569 | 17142738 | Immunity was enhanced further by depletion of CD25+foxp3+ cells before vaccination. anti-DEC205-human survivin was superior in inducing CD4+ T cell responses relative to other approaches involving survivin plasmid DNA or survivin peptides with adjuvants. |
| 2570 | 17142738 | However, we were unable to induce CD8+ T cell immunity to survivin by two doses of DEC205-targeted survivin or the other strategies. |
| 2571 | 17142738 | Therefore, significant CD4+ T cell immunity to a self protein that is overexpressed in most human cancers can be induced by DEC205 targeting of the Ag in its xenogeneic form to maturing DCs. |
| 2572 | 17118497 | Specifically, the co-culture with activated Vgamma9Vdelta2 T cells with BCG-infected DC resulted in a significant increase of the expression of CD80, CD86, CD40 and CD25 molecules on DC. |
| 2573 | 17118497 | Moreover, DC were able to produce increased levels of TNF-alpha and synthesize ex novo IL-15 without altering the IL-10/IL-12 immunoregulatory pathway. |
| 2574 | 17114471 | Ag-specific IL-17 and IFN-gamma production was significantly lower in Pw-immunized TLR4-defective mice. |
| 2575 | 17114471 | Stimulation of dendritic cells (DC) with Pw promoted IL-23, IL-12, IL-1beta, and TNF-alpha production, which was impaired in DC from TLR4-defective mice. |
| 2576 | 17114471 | B. pertussis LPS, which is present in high concentrations in Pw, induced IL-23 production by DC, which enhanced IL-17 secretion by T cells, but the induction of Th-17 cells was also dependent on IL-1. |
| 2577 | 17110001 | Both the immunisation routes were equally effective in inducing bacterial clearance from the lung, upregulated the recruitment of white cells and lead to an increase in the concentration of TNF-alpha, IL-1beta and specific antibody in the bronchoalveolar lavage. |
| 2578 | 17108267 | In vitro production of cytokines, such as TNF-alpha and gamma interferon (IFN-gamma), by antigen-stimulated splenocytes from mice intravenously infected with C. albicans cells was also diminished in old mice. |
| 2579 | 17106649 | Flow cytometric analyses showed that TGF-beta2 does not suppress the upregulation of MHC (major histocompatibility complex) class II molecules and the T cell stimulatory capacity of human DC that were stimulated with a strong cytokine cocktail containing tumor necrosis factor alpha (TNF-alpha), IL-1beta, IL-6 and prostaglandin E2 (PGE2). |
| 2580 | 17106649 | Flow cytometric analyses showed that TGF-beta2 does not suppress the upregulation of MHC (major histocompatibility complex) class II molecules and the T cell stimulatory capacity of human DC that were stimulated with a strong cytokine cocktail containing tumor necrosis factor alpha (TNF-alpha), IL-1beta, IL-6 and prostaglandin E2 (PGE2). |
| 2581 | 17106649 | Although both mature and immature DC expressed comparable amounts of the TGF-beta receptor type II, Smad2 phosphorylation and subsequent upregulation of Smad7 was inhibited in mature DC, but not immature DC. |
| 2582 | 17106649 | Although both mature and immature DC expressed comparable amounts of the TGF-beta receptor type II, Smad2 phosphorylation and subsequent upregulation of Smad7 was inhibited in mature DC, but not immature DC. |
| 2583 | 17106649 | However, further analysis revealed that mature DC alone are not sufficient to mediate full T cell activation in the presence of TGF-beta2, unless IL-12 is added to the DC/T-cell coculture. |
| 2584 | 17106649 | However, further analysis revealed that mature DC alone are not sufficient to mediate full T cell activation in the presence of TGF-beta2, unless IL-12 is added to the DC/T-cell coculture. |
| 2585 | 17106649 | Finally, we demonstrate that MHC class II expression and IL-12 secretion by DC are not disturbed by TGF-beta2 after DC stimulation with a modified maturation cocktail containing the Toll-like receptor (TLR)-ligands Poly I:C or R848, TNF-alpha, IL-1beta and INF-gamma. |
| 2586 | 17106649 | Finally, we demonstrate that MHC class II expression and IL-12 secretion by DC are not disturbed by TGF-beta2 after DC stimulation with a modified maturation cocktail containing the Toll-like receptor (TLR)-ligands Poly I:C or R848, TNF-alpha, IL-1beta and INF-gamma. |
| 2587 | 17092567 | Lack of IFN-alpha/betaR signaling also blocked production of IFN-gamma and TNF-alpha in response to TLR9 activation. |
| 2588 | 17090392 | Intranasal vaccination with dmSEC induced the production of SEC-specific antibodies such as IgG1, IgG2b and IgA. dmSEC-vaccinated mice elicited significantly higher titers of interleukin-4 (IL-4) and IL-10, and lower levels of interferon-gamma (IFN-gamma) after challenge with S. aureus compared with the control group. |
| 2589 | 17090392 | Furthermore, the sera from dmSEC-immunized mice significantly inhibited IFN-gamma and tumor necrosis factor-alpha production in vitro. |
| 2590 | 17082660 | HIV-1-specific CD8+ T cells from all four uninfected immunized and 21 infected subjects secreted IFN-gamma and TNF-alpha. |
| 2591 | 17081660 | The GEM particles induced the production of the proinflammatory cytokine tumour necrosis factor-alpha (TNF-alpha) by macrophages as well as the maturation of dendritic cells. |
| 2592 | 17081660 | The pneumococcal proteins IgA1 protease (IgA1p), putative proteinase maturation protein A (PpmA) and streptococcal lipoprotein A (SlrA) were anchored in trans to the surface of the GEM particles after recombinant production of the antigens in L. lactis as hybrids with a lactococcal cell wall binding domain, named Protein Anchor domain (PA). |
| 2593 | 17079650 | Thimerosal, in a concentration-dependent manner, inhibited the secretion of LPS-induced proinflammatory cytokines TNF-alpha, IL-6, and IL-12p70 from human monocyte-derived DC. |
| 2594 | 17079650 | Thimerosal, in a concentration-dependent manner, inhibited the secretion of LPS-induced proinflammatory cytokines TNF-alpha, IL-6, and IL-12p70 from human monocyte-derived DC. |
| 2595 | 17079650 | These thimerosal-exposed DC induced increased TH2 (IL-5 and IL-13) and decreased TH1 (IFN-gamma) cytokine secretion from the T cells in the absence of additional thimerosal added to the coculture. |
| 2596 | 17079650 | These thimerosal-exposed DC induced increased TH2 (IL-5 and IL-13) and decreased TH1 (IFN-gamma) cytokine secretion from the T cells in the absence of additional thimerosal added to the coculture. |
| 2597 | 17079650 | Thimerosal exposure of DC led to the depletion of intracellular glutathione (GSH), and addition of exogenous GSH to DC abolished the TH2-promoting effect of thimerosal-treated DC, restoring secretion of TNF-alpha, IL-6, and IL-12p70 by DC and IFN-gamma secretion by T cells. |
| 2598 | 17079650 | Thimerosal exposure of DC led to the depletion of intracellular glutathione (GSH), and addition of exogenous GSH to DC abolished the TH2-promoting effect of thimerosal-treated DC, restoring secretion of TNF-alpha, IL-6, and IL-12p70 by DC and IFN-gamma secretion by T cells. |
| 2599 | 17077176 | Injection of IL-12- and IL-18-encoding plasmids ameliorates the autoimmune pathology of MRL/Mp-Tnfrsf6lpr mice: synergistic effect on autoimmune symptoms. |
| 2600 | 17077176 | Injection of IL-12- and IL-18-encoding plasmids ameliorates the autoimmune pathology of MRL/Mp-Tnfrsf6lpr mice: synergistic effect on autoimmune symptoms. |
| 2601 | 17077176 | IL-12 and IL-18 are mediators involved in the onset and progression of the autoimmune disease developing in MRL/Mp-Tnfrsf6(lpr) (lpr) mice, which display symptoms similar to the human systemic lupus erythematosus (SLE). |
| 2602 | 17077176 | IL-12 and IL-18 are mediators involved in the onset and progression of the autoimmune disease developing in MRL/Mp-Tnfrsf6(lpr) (lpr) mice, which display symptoms similar to the human systemic lupus erythematosus (SLE). |
| 2603 | 17077176 | The pathology is characterized by progressive lymphadenopathy and auto-antibody-mediated multiple organ failure, e.g. glomerulonephritis, or pneumonitis and a concomitant increase in serum levels for IFNgamma and tumor necrosis factor-alpha (TNFalpha). |
| 2604 | 17077176 | The pathology is characterized by progressive lymphadenopathy and auto-antibody-mediated multiple organ failure, e.g. glomerulonephritis, or pneumonitis and a concomitant increase in serum levels for IFNgamma and tumor necrosis factor-alpha (TNFalpha). |
| 2605 | 17077176 | In this study, we intramuscularly injected lpr mice with plasmids encoding IL-12 and IL-18, either alone or in combination, in order to affect the development of the autoimmune disease. |
| 2606 | 17077176 | In this study, we intramuscularly injected lpr mice with plasmids encoding IL-12 and IL-18, either alone or in combination, in order to affect the development of the autoimmune disease. |
| 2607 | 17077176 | Five biweekly injections of the combined plasmids starting at 4-5 weeks of age diminished serum levels of TNFalpha and reduced the ability of lymphocytes from treated mice to produce IFNgamma in vitro. |
| 2608 | 17077176 | Five biweekly injections of the combined plasmids starting at 4-5 weeks of age diminished serum levels of TNFalpha and reduced the ability of lymphocytes from treated mice to produce IFNgamma in vitro. |
| 2609 | 17077176 | We conclude that IL-12 and IL-18 synergistically affect the pathogenesis of the T(h)1-dependent autoimmune syndrome of lpr mice and that approaches that target both IL-12 and IL-18 may be a therapeutic option in the treatment of autoimmune SLE. |
| 2610 | 17077176 | We conclude that IL-12 and IL-18 synergistically affect the pathogenesis of the T(h)1-dependent autoimmune syndrome of lpr mice and that approaches that target both IL-12 and IL-18 may be a therapeutic option in the treatment of autoimmune SLE. |
| 2611 | 17063123 | When primed with toll-like receptor agonists or bacterial extract but not proinflammatory cytokines, hyperthermia specifically enhanced secretion of interleukin (IL)-12p70 by DC, without altering the secretion of IL-10, tumor necrosis factor alpha or IL-1beta. |
| 2612 | 17060980 | Mouse models (mild disease and persistent infection with E. muris and fatal monocytotropic ehrlichiosis with a Japanese tick isolate) revealed that CD4 and CD8 T type 1 lymphocyte responses, IFN-gamma, TNF-alpha, and antibodies play roles in protective immunity, while a weak CD4 T-helper response, overproduction of TNF-alpha, and very high IL-10 are associated with toxic shock-like mortality. |
| 2613 | 17054071 | Degranulation/multiple cytokine ICC assays also indicated that a significantly higher proportion of pp65-specific than IE1-specific CTLs secreted both interferon- gamma and tumor necrosis factor- alpha and possessed greater cytotoxic potential. |
| 2614 | 17052820 | Virus replication in response to challenge was blunted in PVM strain 15 vaccinated mice, as was local production of secretory mediators IFNgamma, TNF-alpha, MIP-1 alpha, and MIP-2. |
| 2615 | 17049678 | Tape-stripping induces expression of TLR-9 and tumor necrosis factor (TNF)-alpha in the skin, and CpG-ODN treatment through the tape-stripped skin enhances the migration of antigen presenting cells (APCs) to the draining lymph nodes. |
| 2616 | 17049678 | Tape-stripping induces expression of TLR-9 and tumor necrosis factor (TNF)-alpha in the skin, and CpG-ODN treatment through the tape-stripped skin enhances the migration of antigen presenting cells (APCs) to the draining lymph nodes. |
| 2617 | 17049678 | On the other hand, TLR-9 mRNA and TNF-alpha mRNA were not observed in the skin when CpG-ODN was injected intradermally in a volume of 10 microL, or in a Th1-type immune response. |
| 2618 | 17049678 | On the other hand, TLR-9 mRNA and TNF-alpha mRNA were not observed in the skin when CpG-ODN was injected intradermally in a volume of 10 microL, or in a Th1-type immune response. |
| 2619 | 17048271 | BM-derived macrophages and DC displayed enhanced expression of costimulatory molecules (CD40 and CD86) and increased production of pro-inflammatory cytokines (TNF-alpha, IL-6 and IL-12p40) and nitric oxide after infection. |
| 2620 | 17047396 | The restimulated splenocytes demonstrated increased cytotoxic response, lymphocytic proliferation and elevated levels of Th type I cytokines (IL-2, IL-12, IFN-gamma and TNF-alpha). |
| 2621 | 17030496 | To address the role of reactive oxygen species (ROS) and nitric oxide (NO) in AM apoptosis, sub-clinical Streptococcus pneumoniae infection was established in gp91(phox-/-) and inducible NO synthase deficient (iNOS(-/-)) mice. |
| 2622 | 17030496 | Both AM apoptosis and the number of macrophages containing apoptotic bodies are reduced in iNOS(-/-) as compared to control or gp91(phox-/-) mice. iNOS(-/-) mice recruit neutrophils and generate TNF-alpha to compensate for impaired AM competence but ROS deficiency has no apparent effect on AM function in this model. |
| 2623 | 17028215 | Induction of long-term lipopolysaccharide tolerance by an agonistic monoclonal antibody to the toll-like receptor 4/MD-2 complex. |
| 2624 | 17028215 | Induction of long-term lipopolysaccharide tolerance by an agonistic monoclonal antibody to the toll-like receptor 4/MD-2 complex. |
| 2625 | 17028215 | Induction of long-term lipopolysaccharide tolerance by an agonistic monoclonal antibody to the toll-like receptor 4/MD-2 complex. |
| 2626 | 17028215 | We have established an agonistic monoclonal antibody, UT12, that induces stimulatory signals comparable to those induced by lipopolysaccharide (LPS) through Toll-like receptor 4 and MD-2. |
| 2627 | 17028215 | We have established an agonistic monoclonal antibody, UT12, that induces stimulatory signals comparable to those induced by lipopolysaccharide (LPS) through Toll-like receptor 4 and MD-2. |
| 2628 | 17028215 | We have established an agonistic monoclonal antibody, UT12, that induces stimulatory signals comparable to those induced by lipopolysaccharide (LPS) through Toll-like receptor 4 and MD-2. |
| 2629 | 17028215 | UT12 activated nuclear factor kappaB and induced the production of proinflammatory cytokines such as tumor necrosis factor alpha (TNF-alpha) and interleukin-6 (IL-6) in peritoneal exudative cells. |
| 2630 | 17028215 | UT12 activated nuclear factor kappaB and induced the production of proinflammatory cytokines such as tumor necrosis factor alpha (TNF-alpha) and interleukin-6 (IL-6) in peritoneal exudative cells. |
| 2631 | 17028215 | UT12 activated nuclear factor kappaB and induced the production of proinflammatory cytokines such as tumor necrosis factor alpha (TNF-alpha) and interleukin-6 (IL-6) in peritoneal exudative cells. |
| 2632 | 17028215 | In addition, mice injected with UT12 rapidly fell into endotoxin shock concomitant with the augmentation of serum TNF-alpha and IL-6 levels, followed by death within 12 h. |
| 2633 | 17028215 | In addition, mice injected with UT12 rapidly fell into endotoxin shock concomitant with the augmentation of serum TNF-alpha and IL-6 levels, followed by death within 12 h. |
| 2634 | 17028215 | In addition, mice injected with UT12 rapidly fell into endotoxin shock concomitant with the augmentation of serum TNF-alpha and IL-6 levels, followed by death within 12 h. |
| 2635 | 17028215 | On the other hand, when the mice were pretreated with a sublethal dose of UT12, the mice survived the subsequent lethal LPS challenges, with significant suppression of serum TNF-alpha and IL-6, indicating that UT12 induced tolerance against LPS. |
| 2636 | 17028215 | On the other hand, when the mice were pretreated with a sublethal dose of UT12, the mice survived the subsequent lethal LPS challenges, with significant suppression of serum TNF-alpha and IL-6, indicating that UT12 induced tolerance against LPS. |
| 2637 | 17028215 | On the other hand, when the mice were pretreated with a sublethal dose of UT12, the mice survived the subsequent lethal LPS challenges, with significant suppression of serum TNF-alpha and IL-6, indicating that UT12 induced tolerance against LPS. |
| 2638 | 17028215 | These results illuminate a novel potential therapeutic strategy for endotoxin shock by the use of monoclonal antibodies against the Toll-like receptor 4/MD-2 complex. |
| 2639 | 17028215 | These results illuminate a novel potential therapeutic strategy for endotoxin shock by the use of monoclonal antibodies against the Toll-like receptor 4/MD-2 complex. |
| 2640 | 17028215 | These results illuminate a novel potential therapeutic strategy for endotoxin shock by the use of monoclonal antibodies against the Toll-like receptor 4/MD-2 complex. |
| 2641 | 17010367 | Optimal blood volume, number of lymphocytes, sensitivity and reproducibility of intracellular staining for IFN-gamma were determined both in non-tolerant/wild type mice as well as in tolerant CEA transgenic mice upon restimulation of PBMCs with CEA peptides. |
| 2642 | 17010367 | Groups of vaccinated mice were then sacrificed and PBMCs and splenocytes from individual animals were compared for intracytoplasmic detection of IFN-gamma and TNF-alpha. |
| 2643 | 17009044 | The kinetics of the carbohydrate-specific IgG response correlated with a temporary release of cytokines such as IFNgamma, IL-2, IL-1beta, TNFalpha and GM-CSF which was measurable in the immune serum by xMAP Multiplex technology. |
| 2644 | 16991124 | Induction of protective immunity to RM-1 prostate cancer cells with ALVAC-IL-2/IL-12/TNF-alpha combination therapy. |
| 2645 | 16991124 | Induction of protective immunity to RM-1 prostate cancer cells with ALVAC-IL-2/IL-12/TNF-alpha combination therapy. |
| 2646 | 16991124 | ALVAC recombinant canarypox viruses encoding interleukin-2, interleukin-12 and tumor necrosis factor-alpha were used to create therapeutic vaccines in 2 different ways. |
| 2647 | 16991124 | ALVAC recombinant canarypox viruses encoding interleukin-2, interleukin-12 and tumor necrosis factor-alpha were used to create therapeutic vaccines in 2 different ways. |
| 2648 | 16991124 | Tumor-free survival induced by the separate injection vaccine required natural killer (NK) cells, CD4(+), and CD8(+) T cells. |
| 2649 | 16991124 | Tumor-free survival induced by the separate injection vaccine required natural killer (NK) cells, CD4(+), and CD8(+) T cells. |
| 2650 | 16991124 | Secondary clearance of tumors also required NK and CD8(+) T cells, but not CD4(+) T cells. |
| 2651 | 16991124 | Secondary clearance of tumors also required NK and CD8(+) T cells, but not CD4(+) T cells. |
| 2652 | 16988256 | Because it is known that SOCS are induced by IL-10 and that B. burgdorferi and its lipoproteins most likely interact via TLR2 or the heterodimers TLR2/1 and/or TLR2/6, we hypothesized that SOCS are induced by IL-10 and B. burgdorferi and its lipoproteins in macrophages and that SOCS may mediate the inhibition by IL-10 of concomitantly elicited cytokines. |
| 2653 | 16988256 | We report here that mouse J774 macrophages incubated with IL-10 and added B. burgdorferi spirochetes (freeze-thawed, live, or sonicated) or lipidated outer surface protein A (L-OspA) augmented their SOCS1/SOCS3 mRNA and protein expression, with SOCS3 being more abundant. |
| 2654 | 16988256 | Pam(3)Cys, a synthetic lipopeptide, also induced SOCS1/SOCS3 expression under these conditions, but unlipidated OspA was ineffective. |
| 2655 | 16988256 | Neither endogenous IL-10 nor the translation inhibitor cycloheximide blocked SOCS1/SOCS3 induction by B. burgdorferi and its lipoproteins, indicating that the expression of other genes is not required. |
| 2656 | 16988256 | This temporally correlated with the IL-10-mediated inhibition of the inflammatory cytokines IL-1beta, IL-6, IL-12p40, IL-18, and tumor necrosis factor alpha. |
| 2657 | 16988256 | Our data are evidence to suggest that expression of SOCS is part of the mechanism of IL-10-mediated inhibition of inflammatory cytokines elicited by B. burgdorferi and its lipoproteins. |
| 2658 | 16987066 | Our data indicate that 80% of the tumors expressed low levels of CD4 mRNA, with all of them expressing higher CD8 mRNA levels. |
| 2659 | 16987066 | Most tumors expressed interleukin (IL)-4 and IL-10 mRNAs and, most importantly, all of them expressed transforming growth factor (TGF)-beta1 and interferon gamma mRNA. |
| 2660 | 16987066 | None of the tumors studied expressed IL-12, IL-6, or tumor necrosis factor (TNF) mRNA. |
| 2661 | 16982903 | Moreover, effector and/or memory phenotype CD8 T cells were responsible, because adoptive transfer of purified CD44(high) CD8 T cells to naive mice induced fatal responses following a primary low-dose infection. |
| 2662 | 16982903 | Moreover, effector and/or memory phenotype CD8 T cells were responsible, because adoptive transfer of purified CD44(high) CD8 T cells to naive mice induced fatal responses following a primary low-dose infection. |
| 2663 | 16982903 | The fatal responses were perforin- and Fas ligand-independent, and were associated with high serum concentrations of TNF-alpha and CCL2, and low levels of IL-10. |
| 2664 | 16982903 | The fatal responses were perforin- and Fas ligand-independent, and were associated with high serum concentrations of TNF-alpha and CCL2, and low levels of IL-10. |
| 2665 | 16982903 | Accordingly, blockade of either TNF-alpha or CCL2 ameliorated fatal recall responses, and in vitro coculture of memory CD8 T cells and Ixodes ovatus ehrlichia-infected peritoneal exudate cells resulted in substantial increases in TNF-alpha and CCL2. |
| 2666 | 16982903 | Accordingly, blockade of either TNF-alpha or CCL2 ameliorated fatal recall responses, and in vitro coculture of memory CD8 T cells and Ixodes ovatus ehrlichia-infected peritoneal exudate cells resulted in substantial increases in TNF-alpha and CCL2. |
| 2667 | 16973582 | Longitudinally, HIV-specific T cells in this individual were able to secrete IFN-gamma and tumor necrosis factor alpha, as well as proliferate and degranulate in response to their cognate antigenic peptides up to 5 years postinfection. |
| 2668 | 16971810 | Dendritic cells loaded with killed allogeneic melanoma cells can induce objective clinical responses and MART-1 specific CD8+ T-cell immunity. |
| 2669 | 16971810 | DCs were generated by culturing monocytes with granulocyte macrophage-colony stimulating factor (granulocyte macrophage-colony stimulating factor) and interleukin (IL-4) and activated by additional culture with tumor necrosis factor and CD40 ligand. |
| 2670 | 16971810 | Three out of 13 analyzed patients showed T-cell immunity to melanoma antigen recognized by autologous T cells (MART-1) tissue differentiation antigen. |
| 2671 | 16971810 | Two of 3 patients showed improved immune function after vaccinations demonstrated by improved secretion of interferon (IFN)-gamma or T-cell proliferation in response to MART-1 derived peptides. |
| 2672 | 16971810 | In one of these patients, vaccination led to elicitation of CD8 T-cell immunity specific to a novel peptide-derived from MART-1 antigen, suggesting that cross-priming/presentation of melanoma antigens by DC vaccine had occurred. |
| 2673 | 16971487 | Here, we describe an approach to enhance immunogenicity that involves the activation of NF-kappaB by the transgenic expression of an intracellular signaling molecule, NF-kappaB-inducing kinase (NIK). |
| 2674 | 16971487 | In vitro, NIK increases dendritic cell antigen presentation in allogeneic and antigen-specific T cell proliferation assays by potently activating NF-kappaB and consequently up-regulating the expression of cytokines (TNF-alpha, IL-6, IL-12, IL-15, and IL-18), chemokines [IL-8, RANTES (regulated on activation, normal T cell expressed and secreted), macrophage inflammatory protein-1alpha, monocyte chemoattractant protein-1, and monocyte chemoattractant protein-3], MHC antigen-presenting molecules (class I and II), and costimulatory molecules (CD80 and CD86). |
| 2675 | 16971487 | In vivo, NIK enhances immune responses against a vector-encoded antigen and shifts them toward a T helper 1 immune response with increased IgG2a levels, T cell proliferation, IFN-gamma production, and cytotoxic T lymphocyte responses more potently than complete Freund's adjuvant, a very efficacious T helper 1-inducing adjuvant. |
| 2676 | 16971487 | These findings define NIK, and possibly other inducers of NF-kappaB activation, as a potent adjuvant strategy that offers great potential for genetic vaccine development. |
| 2677 | 16970676 | Furthermore, CpG ODN enhanced the production of TNF-alpha and Th1-mediated cytokines, including IFN-gamma and IL-2 compared with JE vaccine alone. |
| 2678 | 16968412 | Transwell assays indicated that the maximal PEC cytotoxicity required both direct cell-cell contact and soluble factors such as interferon (IFN)-gamma and tumour necrosis factor (TNF)-alpha. |
| 2679 | 16968412 | Transwell assays indicated that the maximal PEC cytotoxicity required both direct cell-cell contact and soluble factors such as interferon (IFN)-gamma and tumour necrosis factor (TNF)-alpha. |
| 2680 | 16968412 | Transwell assays indicated that the maximal PEC cytotoxicity required both direct cell-cell contact and soluble factors such as interferon (IFN)-gamma and tumour necrosis factor (TNF)-alpha. |
| 2681 | 16968412 | Neutralizing endogenous cytokines interleukin (IL)-12, IL-18, IFN-gamma or TNF-alpha reduced PEC cytotoxicity by 38%, 22%, 15% and 94%, respectively. |
| 2682 | 16968412 | Neutralizing endogenous cytokines interleukin (IL)-12, IL-18, IFN-gamma or TNF-alpha reduced PEC cytotoxicity by 38%, 22%, 15% and 94%, respectively. |
| 2683 | 16968412 | Neutralizing endogenous cytokines interleukin (IL)-12, IL-18, IFN-gamma or TNF-alpha reduced PEC cytotoxicity by 38%, 22%, 15% and 94%, respectively. |
| 2684 | 16968412 | Compared with control BCG for PEC stimulation, rBCGs expressing IL-2 or IL-18 showed enhanced MBT-2 cell killing by PECs. |
| 2685 | 16968412 | Compared with control BCG for PEC stimulation, rBCGs expressing IL-2 or IL-18 showed enhanced MBT-2 cell killing by PECs. |
| 2686 | 16968412 | Compared with control BCG for PEC stimulation, rBCGs expressing IL-2 or IL-18 showed enhanced MBT-2 cell killing by PECs. |
| 2687 | 16968412 | Increased cytokine production (IFN-gamma, TNF-alpha and IL-6) was also observed in rBCG-stimulated PEC cultures. |
| 2688 | 16968412 | Increased cytokine production (IFN-gamma, TNF-alpha and IL-6) was also observed in rBCG-stimulated PEC cultures. |
| 2689 | 16968412 | Increased cytokine production (IFN-gamma, TNF-alpha and IL-6) was also observed in rBCG-stimulated PEC cultures. |
| 2690 | 16966494 | This report demonstrates that the B box domain induces phenotypic maturation of murine bone marrow-derived dendritic cells (BM-DCs) as evidenced by increased CD86, CD40 and MHC-II expression. |
| 2691 | 16966494 | This report demonstrates that the B box domain induces phenotypic maturation of murine bone marrow-derived dendritic cells (BM-DCs) as evidenced by increased CD86, CD40 and MHC-II expression. |
| 2692 | 16966494 | The B box domain enhanced secretion of pro-inflammatory cytokines and chemokines: IL-1beta, IL-2, IL-5, IL-8, IL-12 and tumor necrosis factor (TNF)-alpha, but not IL-6 and IL-10. |
| 2693 | 16966494 | The B box domain enhanced secretion of pro-inflammatory cytokines and chemokines: IL-1beta, IL-2, IL-5, IL-8, IL-12 and tumor necrosis factor (TNF)-alpha, but not IL-6 and IL-10. |
| 2694 | 16966494 | Furthermore, four peptides whose sequences correspond to different regions of HMGB1 induced production of IL-1beta, IL-2 and IL-12 (p70), but not IL-10 and IL-6 in mouse BM-DCs. |
| 2695 | 16966494 | Furthermore, four peptides whose sequences correspond to different regions of HMGB1 induced production of IL-1beta, IL-2 and IL-12 (p70), but not IL-10 and IL-6 in mouse BM-DCs. |
| 2696 | 16966494 | Interestingly, these peptides differed in their capacity to induce TNF-alpha, IL-5, IL-18 and IL-8. |
| 2697 | 16966494 | Interestingly, these peptides differed in their capacity to induce TNF-alpha, IL-5, IL-18 and IL-8. |
| 2698 | 16960116 | Treatment of human monocytes with S. gordonii but not latex beads induced a clear up-regulation of CD83, CD40, CD80, and CD54 and the down-regulation of CD14. |
| 2699 | 16960116 | Furthermore, bacterial treatment stimulated an increased expression of Toll-like receptor 5 (TLR5), TLR6, and TLR7, production of the proinflammatory cytokines tumor necrosis factor alpha and interleukin 1 beta, and reduction of the phagocytic activity. |
| 2700 | 16960110 | L. casei strain Shirota stimulated PBMNC to secrete interleukin-12 (IL-12), gamma interferon (IFN-gamma), tumor necrosis factor alpha (TNF-alpha), and IL-10. |
| 2701 | 16960110 | L. casei strain Shirota stimulated PBMNC to secrete interleukin-12 (IL-12), gamma interferon (IFN-gamma), tumor necrosis factor alpha (TNF-alpha), and IL-10. |
| 2702 | 16960110 | L. casei strain Shirota was phagocytosed by monocytes and directly stimulated them to secrete IL-12, TNF-alpha, and IL-10. |
| 2703 | 16960110 | L. casei strain Shirota was phagocytosed by monocytes and directly stimulated them to secrete IL-12, TNF-alpha, and IL-10. |
| 2704 | 16960110 | Purified T cells, but not NK cells, produced IFN-gamma effectively when stimulated with L. casei strain Shirota in the presence of monocytes, indicating that monocytes triggered by L. casei strain Shirota help T cells to produce IFN-gamma through secreting IL-12. |
| 2705 | 16960110 | Purified T cells, but not NK cells, produced IFN-gamma effectively when stimulated with L. casei strain Shirota in the presence of monocytes, indicating that monocytes triggered by L. casei strain Shirota help T cells to produce IFN-gamma through secreting IL-12. |
| 2706 | 16949577 | Schistosoma mansoni infection was established using irradiated cercariae in Cercopithecus aethiops aethiops (Grivet monkey) to describe immune responses of the serum cytokines, IL-4, IL-10, IL-12, IFN- gamma, and TNF-alpha. |
| 2707 | 16949577 | In primary infection, IL-4 was significantly raised (p=0.03) in the immunized monkeys, and there was an insignificant increase (p>0.05) in IL-10. |
| 2708 | 16949577 | However, ova excretion did not influence the cytokines, except in the controls where both IL-4 and IL-10 were significantly increased (p<0.05). |
| 2709 | 16943292 | We have recently shown that survival in plasmid DNA-primed/recombinant adenovirus-boosted rhesus monkeys that are challenged with the simian immunodeficiency virus SIVmac251 is associated with the preservation postchallenge of central memory CD4(+) T lymphocytes and robust gamma interferon (IFN-gamma)-producing SIV-specific CD8(+) and CD4(+) T-lymphocyte responses. |
| 2710 | 16943292 | We show that the preservation of the SIV-specific central memory CD8(+) T-lymphocyte population and a linked SIV-specific CD4(+) T-lymphocyte response are associated with prolonged survival in vaccinated monkeys following challenge. |
| 2711 | 16943292 | Furthermore, we demonstrate that SIV-specific IFN-gamma-, tumor necrosis factor alpha-, and interleukin-2-producing T lymphocytes are all comparably associated with protection against disease progression. |
| 2712 | 16940500 | Upon intravaginal challenge of these orally immunized mice with recombinant vaccinia virus (rVV) expressing HIV gag, gamma interferon- and tumor necrosis factor alpha-secreting Gag-specific CD8(+) T cells were dramatically increased in the spleen and MALTs. |
| 2713 | 16938461 | The genes investigated were those that code for interleukin (IL)-1alpha, IL-1beta, IL-1R, IL-1RA, IL-4RA, IL-2, IL-4, IL-6, IL-10, IL-12, interferon-gamma (IFN-gamma), transforming growth factor-beta (TGF-beta), and tumor necrosis factor-alpha (TNF-alpha). |
| 2714 | 16938461 | Analyses of the data identified TGF-beta codon 25 GG (92.85% vs. 64.44%, p=0.04, OR=7.17), IL-4 -1098 GG (16.6% vs. 0.0%, p=0.05, OR=18.33), IL-10 -1082 GG (28.5% vs. 6.8%, p=0.05, OR=5.47), and IL-10 -1082 GCC/GCC (28.57% vs. 4.5%, p=0.025, OR=8.4) polymorphisms as risk factors for progression of bladder cancer. |
| 2715 | 16931603 | Molecular adjuvants can be considered in the following groups: TNF superfamily molecules such as CD40 ligand; agonists for TLRs; agonists for NAIP, CIITA, HET-E, TP-1-leucine-rich repeat pathway receptors, such as nucleotide-binding and oligomerization domain (NOD)1, NOD2, and cryopyrin; chemokines; ILs; CSFs; IFNs; alarmins; and purinergic P2X7 receptor agonists. |
| 2716 | 16931603 | Complementing these positively acting agents are strategies to reduce the immunosuppressive effects of CD4+CD25+ regulatory T cells and negatively acting factors such as TGF-beta, IL-10, suppressor of cytokine signaling 1, and programmed cell death-1 using neutralizing antibodies, antisense, and small interfering RNA. |
| 2717 | 16926099 | Relative to elongation factor-1A, expression levels of genes encoding the proinflammatory cytokines interleukin-1beta-1 (IL-1beta), tumour necrosis factor-alpha-1 (TNFalpha) and interleukin-8 (IL-8) in pools of kidney and liver were examined 6- and 24-h after injection. |
| 2718 | 16920494 | The role of TLRs during infection with Mycobacterium bovis Bacillus Calmette-Guérin (BCG) has been evaluated for TLR2 and TLR4 only. |
| 2719 | 16920494 | The role of TLRs during infection with Mycobacterium bovis Bacillus Calmette-Guérin (BCG) has been evaluated for TLR2 and TLR4 only. |
| 2720 | 16920494 | To identify the set of TLRs involved in the recognition of BCG, we infected bone marrow-derived macrophages and bone marrow-derived dendritic cells (Flt3-ligand generated DCs) from TLR2, TLR3, TLR4, TLR7, TLR9, MyD88 knockout, TLR2/4 and TLR2/4/9 multiple knockout mice. |
| 2721 | 16920494 | To identify the set of TLRs involved in the recognition of BCG, we infected bone marrow-derived macrophages and bone marrow-derived dendritic cells (Flt3-ligand generated DCs) from TLR2, TLR3, TLR4, TLR7, TLR9, MyD88 knockout, TLR2/4 and TLR2/4/9 multiple knockout mice. |
| 2722 | 16920494 | The degree of activation and stimulation was determined by TNFalpha, IL-6 and IL-12p40 ELISA. |
| 2723 | 16920494 | The degree of activation and stimulation was determined by TNFalpha, IL-6 and IL-12p40 ELISA. |
| 2724 | 16920494 | Both macrophages and DCs produce markedly decreased amounts of TNFalpha and IL-6 in the absence of TLR2 whereas no significant reduction could be observed for TLR3, 4, 7, 9 single TLR-knockouts. |
| 2725 | 16920494 | Both macrophages and DCs produce markedly decreased amounts of TNFalpha and IL-6 in the absence of TLR2 whereas no significant reduction could be observed for TLR3, 4, 7, 9 single TLR-knockouts. |
| 2726 | 16920494 | Similarly, up-regulation of CD86 is abolished only in TLR2/4/9-deficient DCs supporting a role of TLR9 in the recognition of M. bovis BCG by murine dendritic cells. |
| 2727 | 16920494 | Similarly, up-regulation of CD86 is abolished only in TLR2/4/9-deficient DCs supporting a role of TLR9 in the recognition of M. bovis BCG by murine dendritic cells. |
| 2728 | 16916959 | The peptides were also found to stimulate the release of tumor necrosis factor alpha and interleukin-12 cytokines in the J774A.1 cell line and primary bone marrow-derived macrophages, indicating that they may have immunomodulatory potential. |
| 2729 | 16914349 | However, the use of pCI/IL-12 as adjuvant to pCI/Sm14 immunization failed to enhance protection against challenge infection. |
| 2730 | 16914349 | Protection induced by pCI/Sm14 immunization correlates with specific IgG antibody production against Sm14, Th1 type of immune response with high levels of interferon (IFN)-gamma and low levels of IL-4 in splenocyte culture supernatants and in bronchoalveolar lavage after challenge infection. |
| 2731 | 16914349 | IL-12 co-administration with pCI/Sm14 induced a significant production of nitric oxide in splenocyte culture supernatants and also lymphocyte suppression, with reduced percentage of T cells producing IFN-gamma and tumor necrosis factor-alpha. |
| 2732 | 16907922 | Among the cytokines studied, interleukin (IL)-10 and IL-12 were not detected at all, whereas low levels of interferon (IFN)-gamma after 96 h (0.4 IU/ml) and tumour necrosis factor (TNF)-alpha after 48 (135 pg/ml) and 96 h (47 pg/ml) of culture were detected in the supernatants of whole blood infected with M. tuberculosis. |
| 2733 | 16907922 | Among the cytokines studied, interleukin (IL)-10 and IL-12 were not detected at all, whereas low levels of interferon (IFN)-gamma after 96 h (0.4 IU/ml) and tumour necrosis factor (TNF)-alpha after 48 (135 pg/ml) and 96 h (47 pg/ml) of culture were detected in the supernatants of whole blood infected with M. tuberculosis. |
| 2734 | 16907922 | However, the addition of monoclonal antibodies specific to TNF-alpha and IFN-gamma to the blood cultures did not alter mycobacterial growth indicating the role of other mechanisms/factors in restricting the growth of M. tuberculosis in whole blood cultures. |
| 2735 | 16907922 | However, the addition of monoclonal antibodies specific to TNF-alpha and IFN-gamma to the blood cultures did not alter mycobacterial growth indicating the role of other mechanisms/factors in restricting the growth of M. tuberculosis in whole blood cultures. |
| 2736 | 16907905 | These family strains have developed mechanisms that modulate/suppress immune responses by the host, such as inhibition of apoptosis of infected macrophages, diminished production of interleukin (IL)-2, interferon (IFN)-gamma, tumour necrosis factor (TNF)-alpha and elevated levels of IL-10 and IL-18. |
| 2737 | 16893994 | Regarding cellular immunity, significant levels of gamma interferon (IFN-gamma) (1,100 +/- 157 pg/ml) and tumor necrosis factor alpha (650 +/- 42 pg/ml) but not interleukin-4 were detected in splenocyte culture supernatants of pCI-Ag85B-vaccinated mice following stimulation with recombinant Ag85B. |
| 2738 | 16893994 | Further, the main source of IFN-gamma is CD8(+) T cells, as demonstrated by intracellular cytokine staining. |
| 2739 | 16889876 | Important features for their efficacy include high migratory responsiveness to lymph node-chemokines and most likely their ability to produce bioactive IL-12 p70 upon subsequent contact with CD40 ligand-expressing T-cells. |
| 2740 | 16889876 | The current standard DC-maturation cocktail for clinical trials is inflammatory cytokines (TNF-alpha, IL-1beta and IL-6) combined with prostaglandin E(2) (PGE(2)), inducing phenotypically mature MoDCs with high migratory responsiveness to CCR7 ligands. |
| 2741 | 16889876 | This cocktail does not, however, induce or prime for production of IL-12 p70. |
| 2742 | 16889876 | Addition of IFN-gamma to PGE(2)-containing maturation cocktails has been shown to prime for substantial production of IL-12 p70 by subsequent CD40 ligation, but the impact of IFN-gamma on phenotypic maturation and migratory responsiveness induced by PGE(2)-containing inflammatory stimuli still remains elusive. |
| 2743 | 16889876 | Here, we demonstrate that addition of IFN-gamma to the standard maturation cocktail decreased CCR7 mRNA and down-regulated CCR7 expression on MoDCs in a dose-dependent manner. |
| 2744 | 16889876 | Moreover, addition of IFN-gamma was found to suppress MoDC-migration towards the CCR7-ligands CCL19 and CCL21. |
| 2745 | 16887158 | Relative to S. aureus-infected udder quarters receiving saline, quarters infused with LPS demonstrated a heightened inflammatory response as demonstrated by the induction of TNF-alpha and higher milk somatic cell counts and albumin levels. |
| 2746 | 16885908 | Similar effects using different cytokines such as GM-CSF, TNF-alpha, and IL-4 can be observed in acute myeloid leukemia and myelodysplastic syndromes. |
| 2747 | 16878499 | The maximum increase in IL-6, IL-10, TNF-alpha, IFN-gamma in the blood was observed in 4 hours after administration of immunomodulators (p < 0.001). |
| 2748 | 16872726 | The adjuvant RLJ-NE-299A up-regulated remarkably the expression of Th1 cytokines IL-2, IL-12, IFN-gamma, TNF alpha and Th2 cytokine IL-4 in lymph node cell cultures after 2 weeks of primary immunization with HBsAg. |
| 2749 | 16870312 | This activation induces the production of tumor necrosis factor alpha (TNF-alpha), an up-regulation of the surface molecules CD83, CD80, CD86, HLA-DR and HLA-I and increases the T cell stimulatory capacity of DCs. |
| 2750 | 16862213 | In fact, a legumain-based DNA vaccine served as a tool to prove this point, as it induced a robust CD8+ T cell response against TAMs, which dramatically reduced their density in tumor tissues and resulted in a marked decrease in proangiogenic factors released by TAMs such as TGF-beta, TNF-alpha, MMP-9, and VEGF. |
| 2751 | 16857732 | Critical role for serum opsonins and complement receptors CR3 (CD11b/CD18) and CR4 (CD11c/CD18) in phagocytosis of Francisella tularensis by human dendritic cells (DC): uptake of Francisella leads to activation of immature DC and intracellular survival of the bacteria. |
| 2752 | 16857732 | We demonstrate that complement factor C3-derived opsonins and the major complement receptors expressed by DC, the integrins CR3 (CD11b/CD18) and CR4 (CD11c/CD18), play a critical role in this adhesion-mediated phagocytosis. |
| 2753 | 16857732 | LVS induced proinflammatory cytokine production and up-regulation of costimulatory surface proteins (CD40, CD86, and MHC Class II) on DC but resisted killing. |
| 2754 | 16857732 | Serum-treated LVS rapidly induced (within 6 h) a number of cytokines including IL-10, a potent suppressor of macrophage functions and down-regulator of Th1-like responses and the Th1 response inducer IL-12. |
| 2755 | 16857732 | These results suggest that the simultaneous production of an activating (IL-12, IL-1beta, and TNF-alpha) and a suppressing (IL-10) cytokine profile could contribute to the immunopathogenesis of tularemia. |
| 2756 | 16849509 | Remarkably, newborn blood plasma confers substantially reduced BLP-induced monocyte synthesis of TNF-alpha, while preserving IL-6 synthesis, reflecting the presence in neonatal blood plasma of a soluble, low molecular mass inhibitory factor (<10 kDa) that we identify as adenosine, an endogenous purine metabolite with immunomodulatory properties. |
| 2757 | 16849509 | Remarkably, newborn blood plasma confers substantially reduced BLP-induced monocyte synthesis of TNF-alpha, while preserving IL-6 synthesis, reflecting the presence in neonatal blood plasma of a soluble, low molecular mass inhibitory factor (<10 kDa) that we identify as adenosine, an endogenous purine metabolite with immunomodulatory properties. |
| 2758 | 16849509 | Selective inhibition of neonatal TNF-alpha production is due to the distinct neonatal adenosine system, including relatively high adenosine concentrations in neonatal blood plasma and heightened sensitivity of neonatal mononuclear cells to adenosine A3 receptor-mediated accumulation of cAMP, a second messenger that inhibits TLR-mediated TNF-alpha synthesis but preserves IL-6 production. |
| 2759 | 16849509 | Selective inhibition of neonatal TNF-alpha production is due to the distinct neonatal adenosine system, including relatively high adenosine concentrations in neonatal blood plasma and heightened sensitivity of neonatal mononuclear cells to adenosine A3 receptor-mediated accumulation of cAMP, a second messenger that inhibits TLR-mediated TNF-alpha synthesis but preserves IL-6 production. |
| 2760 | 16842269 | Cellular immune responses toward a Th1 subset mediated by IFN-gamma and TNF-alpha predominate in asymptomatic dogs exhibiting apparent resistance to visceral leishmaniasis. |
| 2761 | 16842269 | On the other hand, while the role of Th2 cytokines, such as IL-4 and IL-10, in symptomatic animals is still controversial, there is increasing evidence for a correlation of these cytokines with progressive disease. |
| 2762 | 16831212 | PBMC were tested for secretion of tumor necrosis factor-alpha (TNF-alpha), interferon-gamma (IFN-gamma), interleukin-5 (IL-5) and IL-10 in response to complex (whole cells, culture filtrate and cell walls), single secreted (Ag85B, ESAT6, MPT64, PstS and MPT70) and single cytosolic (DnaK, GroES and GroEL) antigens of Mycobacterium tuberculosis. |
| 2763 | 16831212 | PBMC were tested for secretion of tumor necrosis factor-alpha (TNF-alpha), interferon-gamma (IFN-gamma), interleukin-5 (IL-5) and IL-10 in response to complex (whole cells, culture filtrate and cell walls), single secreted (Ag85B, ESAT6, MPT64, PstS and MPT70) and single cytosolic (DnaK, GroES and GroEL) antigens of Mycobacterium tuberculosis. |
| 2764 | 16831212 | PBMC were tested for secretion of tumor necrosis factor-alpha (TNF-alpha), interferon-gamma (IFN-gamma), interleukin-5 (IL-5) and IL-10 in response to complex (whole cells, culture filtrate and cell walls), single secreted (Ag85B, ESAT6, MPT64, PstS and MPT70) and single cytosolic (DnaK, GroES and GroEL) antigens of Mycobacterium tuberculosis. |
| 2765 | 16831212 | PBMC were tested for secretion of tumor necrosis factor-alpha (TNF-alpha), interferon-gamma (IFN-gamma), interleukin-5 (IL-5) and IL-10 in response to complex (whole cells, culture filtrate and cell walls), single secreted (Ag85B, ESAT6, MPT64, PstS and MPT70) and single cytosolic (DnaK, GroES and GroEL) antigens of Mycobacterium tuberculosis. |
| 2766 | 16831212 | In the absence of antigens, detectable concentrations of TNF-alpha, IFN-gamma and IL-10 were secreted by PBMC of both donor groups, but the concentrations of only IL-10 were significantly higher (P=0.015) in TB patients than in healthy subjects. |
| 2767 | 16831212 | In the absence of antigens, detectable concentrations of TNF-alpha, IFN-gamma and IL-10 were secreted by PBMC of both donor groups, but the concentrations of only IL-10 were significantly higher (P=0.015) in TB patients than in healthy subjects. |
| 2768 | 16831212 | In the absence of antigens, detectable concentrations of TNF-alpha, IFN-gamma and IL-10 were secreted by PBMC of both donor groups, but the concentrations of only IL-10 were significantly higher (P=0.015) in TB patients than in healthy subjects. |
| 2769 | 16831212 | In the absence of antigens, detectable concentrations of TNF-alpha, IFN-gamma and IL-10 were secreted by PBMC of both donor groups, but the concentrations of only IL-10 were significantly higher (P=0.015) in TB patients than in healthy subjects. |
| 2770 | 16831212 | In the presence of complex antigens, PBMC secreted IFN-gamma and TNF-alpha in response to all three preparations, whereas IL-10 was secreted in response to whole cells and cell walls only. |
| 2771 | 16831212 | In the presence of complex antigens, PBMC secreted IFN-gamma and TNF-alpha in response to all three preparations, whereas IL-10 was secreted in response to whole cells and cell walls only. |
| 2772 | 16831212 | In the presence of complex antigens, PBMC secreted IFN-gamma and TNF-alpha in response to all three preparations, whereas IL-10 was secreted in response to whole cells and cell walls only. |
| 2773 | 16831212 | In the presence of complex antigens, PBMC secreted IFN-gamma and TNF-alpha in response to all three preparations, whereas IL-10 was secreted in response to whole cells and cell walls only. |
| 2774 | 16831212 | Except for GroEL and DnaK, single antigens did not induce TNF-alpha and IL-10 secretion from PBMC in either donor group. |
| 2775 | 16831212 | Except for GroEL and DnaK, single antigens did not induce TNF-alpha and IL-10 secretion from PBMC in either donor group. |
| 2776 | 16831212 | Except for GroEL and DnaK, single antigens did not induce TNF-alpha and IL-10 secretion from PBMC in either donor group. |
| 2777 | 16831212 | Except for GroEL and DnaK, single antigens did not induce TNF-alpha and IL-10 secretion from PBMC in either donor group. |
| 2778 | 16831212 | The secretion of IFN-gamma, but not IL-10, in the presence of Ag85B, ESAT6 and MPT64 supports their potential as subunit vaccine candidates against TB. |
| 2779 | 16831212 | The secretion of IFN-gamma, but not IL-10, in the presence of Ag85B, ESAT6 and MPT64 supports their potential as subunit vaccine candidates against TB. |
| 2780 | 16831212 | The secretion of IFN-gamma, but not IL-10, in the presence of Ag85B, ESAT6 and MPT64 supports their potential as subunit vaccine candidates against TB. |
| 2781 | 16831212 | The secretion of IFN-gamma, but not IL-10, in the presence of Ag85B, ESAT6 and MPT64 supports their potential as subunit vaccine candidates against TB. |
| 2782 | 16830156 | However, previous investigations have suggested that G-CSF-mobilized peripheral blood monocytes produce reduced levels of proinflammatory cytokines such as interleukin (IL)-12 and tumor necrosis factor (TNF)-alpha. |
| 2783 | 16830156 | In this study, we assessed the functional abilities of DCs generated from G-CSF-mobilized monocytes obtained from 13 patients with CEA-positive advanced solid cancers. |
| 2784 | 16830156 | Although G-CSF-mobilized monocytes (G/Mo) less effectively produced Th-1-type cytokines than control monocytes (C/Mo), DCs generated from G/Mo restored the same level of IL-12 production as that seen in DCs generated from C/Mo. |
| 2785 | 16829620 | In mice, Anaplasma phagocytophilum control is independent of phagocyte oxidase (phox), inducible NO synthase (NOS2), tumor necrosis factor (TNF), and MyD88 Toll-like receptor signaling. |
| 2786 | 16829620 | In mice, Anaplasma phagocytophilum control is independent of phagocyte oxidase (phox), inducible NO synthase (NOS2), tumor necrosis factor (TNF), and MyD88 Toll-like receptor signaling. |
| 2787 | 16829620 | We show that despite evasion of these host responses, phox, NOS2, TNF, and MyD88 are activated and contribute to inflammation and hepatic injury more than A. phagocytophilum itself. |
| 2788 | 16829620 | We show that despite evasion of these host responses, phox, NOS2, TNF, and MyD88 are activated and contribute to inflammation and hepatic injury more than A. phagocytophilum itself. |
| 2789 | 16823912 | DC were incubated with PL resulting in up-regulation of MHC-II, CD40, CD80, and CD86 expression and production of TNFalpha and IL12(p70). |
| 2790 | 16823912 | PL-OVA presented OVA-specific peptides to CD4+ and CD8+ OVA-specific T-cell hybridomas. |
| 2791 | 16823912 | PL exerts an immunomodulatory effect on DC and is a general system to deliver antigens for presentation to CD4+ and CD8+ T-cells possibly implicated in the induction CD8+ cytotoxic T lymphocytes (CTLs) responses. |
| 2792 | 16815070 | Furthermore, during infection, splenocytes and purified T cells lost their ability to proliferate in response to concanavalin A stimulation more rapidly in the Mtb+27kDa-infected mice, which was accompanied by high IFN-gamma and NO production, but low TNF-alpha secretion levels. |
| 2793 | 16790792 | In order to quantify in vivo the mRNAs of cytokines which play important roles in leptospirosis, we have developed quantitative real-time PCR assays for interleukin-2 (IL-2), IL-4, IL-10, IL-12p40, tumor necrosis factor alpha (TNF-alpha), gamma interferon (IFN-gamma), transforming growth factor beta, and two housekeeping genes (encoding beta-actin and hypoxanthine phosphoribosyltransferase). |
| 2794 | 16790792 | In order to quantify in vivo the mRNAs of cytokines which play important roles in leptospirosis, we have developed quantitative real-time PCR assays for interleukin-2 (IL-2), IL-4, IL-10, IL-12p40, tumor necrosis factor alpha (TNF-alpha), gamma interferon (IFN-gamma), transforming growth factor beta, and two housekeeping genes (encoding beta-actin and hypoxanthine phosphoribosyltransferase). |
| 2795 | 16790792 | In this kinetic study, there was pronounced expression of Th1 cytokine mRNA (TNF-alpha, IFN-gamma, and IL-12), with transcripts being detected as early as 1 h postinfection. |
| 2796 | 16790792 | In this kinetic study, there was pronounced expression of Th1 cytokine mRNA (TNF-alpha, IFN-gamma, and IL-12), with transcripts being detected as early as 1 h postinfection. |
| 2797 | 16790792 | Expression of anti-inflammatory cytokines, such as IL-4 and IL-10, was prominent in delayed samples from 1 to 4 days postinfection in response to infection with Leptospira interrogans. |
| 2798 | 16790792 | Expression of anti-inflammatory cytokines, such as IL-4 and IL-10, was prominent in delayed samples from 1 to 4 days postinfection in response to infection with Leptospira interrogans. |
| 2799 | 16779722 | The J8R(11-19)-specific CTL line and CTL clone exerted physiologically relevant functions as they recognized VV-infected lymphoblastoid JY cells or autologous B lymphoblastoid cell lines, and the cytolytic activity was accompanied by the production of interferon- gamma , tumor necrosis factor- alpha , and interleukin-2. |
| 2800 | 16777275 | The increase of TLR3, IFNalphabeta, Mx, IFNgamma and TNFalpha expression at 72h post-infection in the kidney of VHSV-infected fish contrasted with the results obtained with the avirulent virus, which did not induce an increment of this expression in infected fish. |
| 2801 | 16776575 | In vivo analysis of adenovirus-specific cytotoxic T lymphocyte response in mice deficient in CD28, fas ligand, and perforin. |
| 2802 | 16776575 | In vivo analysis of adenovirus-specific cytotoxic T lymphocyte response in mice deficient in CD28, fas ligand, and perforin. |
| 2803 | 16776575 | In this study, we used a novel MHC class I tetramer and an in vivo CTL assay to examine the role of CD28, perforin, Fas ligand (FasL), and TNF-alpha in the generation and function of Ad-specific CTLs in vivo. |
| 2804 | 16776575 | In this study, we used a novel MHC class I tetramer and an in vivo CTL assay to examine the role of CD28, perforin, Fas ligand (FasL), and TNF-alpha in the generation and function of Ad-specific CTLs in vivo. |
| 2805 | 16776575 | During the primary response, there was a significant defect in both the generation and in vivo effector function of Ad-specific CTLs in CD28-/- mice, but not in CD4+ T cell-depleted mice or CD4-/- mice. |
| 2806 | 16776575 | During the primary response, there was a significant defect in both the generation and in vivo effector function of Ad-specific CTLs in CD28-/- mice, but not in CD4+ T cell-depleted mice or CD4-/- mice. |
| 2807 | 16776575 | In the absence of perforin, production of FasL, but not TNF-alpha, by the CTLs results in lower level Ad-specific killing of target cells. |
| 2808 | 16776575 | In the absence of perforin, production of FasL, but not TNF-alpha, by the CTLs results in lower level Ad-specific killing of target cells. |
| 2809 | 16771860 | Here we report for the first time that CD45-/- bone marrow dendritic cells (BMDC) are more activated than CD45+/+ cells and that tumour necrosis factor (TNF) and interleukin-6 (IL-6) production by BMDC and splenic dendritic cells (sDC), is increased following stimulation via Toll-like receptor (TLR)3 and TLR9. |
| 2810 | 16771860 | Here we report for the first time that CD45-/- bone marrow dendritic cells (BMDC) are more activated than CD45+/+ cells and that tumour necrosis factor (TNF) and interleukin-6 (IL-6) production by BMDC and splenic dendritic cells (sDC), is increased following stimulation via Toll-like receptor (TLR)3 and TLR9. |
| 2811 | 16771860 | Nuclear factor-kappaB activation, an important downstream consequence of TLR3 and TLR9 signalling, is also increased in CD45-/- BMDC. |
| 2812 | 16771860 | Nuclear factor-kappaB activation, an important downstream consequence of TLR3 and TLR9 signalling, is also increased in CD45-/- BMDC. |
| 2813 | 16771860 | BMDC of CD45-/- mice also produce more TNF and IL-6 following stimulation with the cytokines TNF and interferon-alpha. |
| 2814 | 16771860 | BMDC of CD45-/- mice also produce more TNF and IL-6 following stimulation with the cytokines TNF and interferon-alpha. |
| 2815 | 16765491 | Also, treatment of murine peritoneal macrophages with the 34 kDa protein showed dose dependent increase in the production of tumor necrosis factor-alpha and interleukin-12. |
| 2816 | 16757067 | Specific IgG and cell mediated immune responses (cellular proliferation) including release of tumor necrosis factor-alpha (TNF-alpha), interferon-gamma (IFN-gamma), transforming growth factor-beta (TGF-beta) and nitric oxide (NO) from host's cells stimulated with BmAFII or lipopolysaccharide (LPS)/concanavalin A (Con A) in vitro were determined. |
| 2817 | 16757067 | Specific IgG and cell mediated immune responses (cellular proliferation) including release of tumor necrosis factor-alpha (TNF-alpha), interferon-gamma (IFN-gamma), transforming growth factor-beta (TGF-beta) and nitric oxide (NO) from host's cells stimulated with BmAFII or lipopolysaccharide (LPS)/concanavalin A (Con A) in vitro were determined. |
| 2818 | 16757067 | Immunization alone resulted in downregulation of responses of cellular proliferation, IFN-gamma, TNF-alpha and NO production (P<0.01) but increased TGF-beta release (P<0.001) whereas the converse was seen after L3 inoculation in these animals. |
| 2819 | 16757067 | Immunization alone resulted in downregulation of responses of cellular proliferation, IFN-gamma, TNF-alpha and NO production (P<0.01) but increased TGF-beta release (P<0.001) whereas the converse was seen after L3 inoculation in these animals. |
| 2820 | 16756175 | The generation of TNF-alpha, IL-6, IL-12, and IFN-gamma was investigated in the lung homogenates in the early periods after intranasal infection of mice with A/Leningrad/134/57 (H2N2) wild-type virus and cold-adapted attenuated vaccine viruses: A/Leningrad/134/17157 (H2N2) and A/Leningrad/134/47/57 (H2N2). |
| 2821 | 16756175 | The generation of TNF-alpha, IL-6, IL-12, and IFN-gamma was investigated in the lung homogenates in the early periods after intranasal infection of mice with A/Leningrad/134/57 (H2N2) wild-type virus and cold-adapted attenuated vaccine viruses: A/Leningrad/134/17157 (H2N2) and A/Leningrad/134/47/57 (H2N2). |
| 2822 | 16756175 | The generation of TNF-alpha, IL-6, IL-12, and IFN-gamma was investigated in the lung homogenates in the early periods after intranasal infection of mice with A/Leningrad/134/57 (H2N2) wild-type virus and cold-adapted attenuated vaccine viruses: A/Leningrad/134/17157 (H2N2) and A/Leningrad/134/47/57 (H2N2). |
| 2823 | 16756175 | Wild-type virus induced substantially higher levels of proinflammatory cytokines: TNF-alpha, IL-6, IL-12, and IFN-gamma. |
| 2824 | 16756175 | Wild-type virus induced substantially higher levels of proinflammatory cytokines: TNF-alpha, IL-6, IL-12, and IFN-gamma. |
| 2825 | 16756175 | Wild-type virus induced substantially higher levels of proinflammatory cytokines: TNF-alpha, IL-6, IL-12, and IFN-gamma. |
| 2826 | 16756175 | The A/Leningrad/134/47/57 virus was marked by a noticeable production of IL-6 and IFN-gamma in the murine lung, but it was less than with wild-type virus infection. |
| 2827 | 16756175 | The A/Leningrad/134/47/57 virus was marked by a noticeable production of IL-6 and IFN-gamma in the murine lung, but it was less than with wild-type virus infection. |
| 2828 | 16756175 | The A/Leningrad/134/47/57 virus was marked by a noticeable production of IL-6 and IFN-gamma in the murine lung, but it was less than with wild-type virus infection. |
| 2829 | 16756175 | At the same time, the more attenuated strain A/Leningrad/134/47/57 induced TNF-alpha and IFN-gamma in the quantities similar to those in the control animals. |
| 2830 | 16756175 | At the same time, the more attenuated strain A/Leningrad/134/47/57 induced TNF-alpha and IFN-gamma in the quantities similar to those in the control animals. |
| 2831 | 16756175 | At the same time, the more attenuated strain A/Leningrad/134/47/57 induced TNF-alpha and IFN-gamma in the quantities similar to those in the control animals. |
| 2832 | 16750567 | Besides TLRs, mRNA for MyD88 and TRAF6, and nuclear translocation of NF-kappaB were enhanced that indicate their involvement in tandem in the activity of porin. |
| 2833 | 16750567 | Besides TLRs, mRNA for MyD88 and TRAF6, and nuclear translocation of NF-kappaB were enhanced that indicate their involvement in tandem in the activity of porin. |
| 2834 | 16750567 | The protein selectively up-regulated CD80 on the activated MPhi together with MHC class II molecule and CD40, and had no effect on CD86 expression. |
| 2835 | 16750567 | The protein selectively up-regulated CD80 on the activated MPhi together with MHC class II molecule and CD40, and had no effect on CD86 expression. |
| 2836 | 16750567 | The porin-induced profile of MIP-1alpha, MIP-1beta and RANTES showed strong bias for chemokines correlated with M1 polarization. |
| 2837 | 16750567 | The porin-induced profile of MIP-1alpha, MIP-1beta and RANTES showed strong bias for chemokines correlated with M1 polarization. |
| 2838 | 16750567 | Intracellular expression and release of TNF-alpha and IL-12 in presence of porin was found to be TLR2 and NF-kappaB dependent. |
| 2839 | 16750567 | Intracellular expression and release of TNF-alpha and IL-12 in presence of porin was found to be TLR2 and NF-kappaB dependent. |
| 2840 | 16750567 | Induction of TNF-alpha and IL-12 along with the chemokine profile suggests type I polarization of the MPhi that would influence Th1-type response. |
| 2841 | 16750567 | Induction of TNF-alpha and IL-12 along with the chemokine profile suggests type I polarization of the MPhi that would influence Th1-type response. |
| 2842 | 16725233 | We have studied the effect of pIL8+ co-administration on the expression of two pro-inflammatory cytokines, such as IL-1beta and tumour necrosis factor alpha (TNF-alpha); cytokines that have mainly an inhibitory role, IL-11 and transforming growth factor beta (TGF-beta); and a Th1 type cytokine, IL-18. |
| 2843 | 16714568 | Gamma interferon, tumor necrosis factor alpha, and nitric oxide synthase 2, key elements of cellular immunity, perform critical protective functions during humoral defense against lethal pulmonary Yersinia pestis infection. |
| 2844 | 16714568 | Gamma interferon, tumor necrosis factor alpha, and nitric oxide synthase 2, key elements of cellular immunity, perform critical protective functions during humoral defense against lethal pulmonary Yersinia pestis infection. |
| 2845 | 16714568 | Gamma interferon, tumor necrosis factor alpha, and nitric oxide synthase 2, key elements of cellular immunity, perform critical protective functions during humoral defense against lethal pulmonary Yersinia pestis infection. |
| 2846 | 16714568 | Gamma interferon, tumor necrosis factor alpha, and nitric oxide synthase 2, key elements of cellular immunity, perform critical protective functions during humoral defense against lethal pulmonary Yersinia pestis infection. |
| 2847 | 16714568 | Here, we demonstrate that protection by either protocol relies upon both gamma interferon (IFN-gamma) and tumor necrosis factor alpha (TNF-alpha) cytokines classically associated with type 1 cellular immunity. |
| 2848 | 16714568 | Here, we demonstrate that protection by either protocol relies upon both gamma interferon (IFN-gamma) and tumor necrosis factor alpha (TNF-alpha) cytokines classically associated with type 1 cellular immunity. |
| 2849 | 16714568 | Here, we demonstrate that protection by either protocol relies upon both gamma interferon (IFN-gamma) and tumor necrosis factor alpha (TNF-alpha) cytokines classically associated with type 1 cellular immunity. |
| 2850 | 16714568 | Here, we demonstrate that protection by either protocol relies upon both gamma interferon (IFN-gamma) and tumor necrosis factor alpha (TNF-alpha) cytokines classically associated with type 1 cellular immunity. |
| 2851 | 16714568 | In both protocols, abrogating IFN-gamma or TNF-alpha activity significantly decreases survival and increases the bacterial burden in pulmonary, splenic, and hepatic tissues. |
| 2852 | 16714568 | In both protocols, abrogating IFN-gamma or TNF-alpha activity significantly decreases survival and increases the bacterial burden in pulmonary, splenic, and hepatic tissues. |
| 2853 | 16714568 | In both protocols, abrogating IFN-gamma or TNF-alpha activity significantly decreases survival and increases the bacterial burden in pulmonary, splenic, and hepatic tissues. |
| 2854 | 16714568 | In both protocols, abrogating IFN-gamma or TNF-alpha activity significantly decreases survival and increases the bacterial burden in pulmonary, splenic, and hepatic tissues. |
| 2855 | 16714568 | We conclude that IFN-gamma, TNF-alpha, and NOS2, key elements of cellular immunity, perform critical protective functions during humoral defense against lethal pulmonary Y. pestis challenge. |
| 2856 | 16714568 | We conclude that IFN-gamma, TNF-alpha, and NOS2, key elements of cellular immunity, perform critical protective functions during humoral defense against lethal pulmonary Y. pestis challenge. |
| 2857 | 16714568 | We conclude that IFN-gamma, TNF-alpha, and NOS2, key elements of cellular immunity, perform critical protective functions during humoral defense against lethal pulmonary Y. pestis challenge. |
| 2858 | 16714568 | We conclude that IFN-gamma, TNF-alpha, and NOS2, key elements of cellular immunity, perform critical protective functions during humoral defense against lethal pulmonary Y. pestis challenge. |
| 2859 | 16714223 | The production of TNF-alpha in supernatants of in vitro stimulated lymphocytes and specific IgA, IgM and IgG antibodies in serum and saliva was determined by ELISA. |
| 2860 | 16714223 | Although no significant changes in the levels of basic lymphocyte subsets were detected, the early/late (CD57+/CD57-) CD8 T effectors ratio was increased at the end of the studied period, as were the percentage of PHA-responding (CD69+) T cells and PB phagocytizing cells. |
| 2861 | 16707559 | A decrease in LPS-induced tumor necrosis factor alpha (TNF-alpha), increased PHA-induced interleukin-10 (IL-10) release, and similar PHA-induced interferon-gamma production were observed in elderly subjects compared with young volunteers. |
| 2862 | 16707559 | A decrease in LPS-induced tumor necrosis factor alpha (TNF-alpha), increased PHA-induced interleukin-10 (IL-10) release, and similar PHA-induced interferon-gamma production were observed in elderly subjects compared with young volunteers. |
| 2863 | 16707559 | Lower antibody titer to influenza A virus was observed in elderly individuals, and the seroconversion factor was found to be correlated inversely with IL-10 production and correlated directly with TNF-alpha production and to a lesser extent, with the plasma level of DHEA. |
| 2864 | 16707559 | Lower antibody titer to influenza A virus was observed in elderly individuals, and the seroconversion factor was found to be correlated inversely with IL-10 production and correlated directly with TNF-alpha production and to a lesser extent, with the plasma level of DHEA. |
| 2865 | 16704888 | The adjuvant effects of the toll-like receptor 3 ligand polyinosinic-cytidylic acid poly (I:C) on antigen-specific CD8+ T cell responses are partially dependent on NK cells with the induction of a beneficial cytokine milieu. |
| 2866 | 16704888 | The adjuvant effects of the toll-like receptor 3 ligand polyinosinic-cytidylic acid poly (I:C) on antigen-specific CD8+ T cell responses are partially dependent on NK cells with the induction of a beneficial cytokine milieu. |
| 2867 | 16704888 | The adjuvant effects of the toll-like receptor 3 ligand polyinosinic-cytidylic acid poly (I:C) on antigen-specific CD8+ T cell responses are partially dependent on NK cells with the induction of a beneficial cytokine milieu. |
| 2868 | 16704888 | The adjuvant effects of the toll-like receptor 3 ligand polyinosinic-cytidylic acid poly (I:C) on antigen-specific CD8+ T cell responses are partially dependent on NK cells with the induction of a beneficial cytokine milieu. |
| 2869 | 16704888 | Poly (I:C), a TLR3 ligand, has shown promise as a vaccine adjuvant to CD8(+) T cell responses. |
| 2870 | 16704888 | Poly (I:C), a TLR3 ligand, has shown promise as a vaccine adjuvant to CD8(+) T cell responses. |
| 2871 | 16704888 | Poly (I:C), a TLR3 ligand, has shown promise as a vaccine adjuvant to CD8(+) T cell responses. |
| 2872 | 16704888 | Poly (I:C), a TLR3 ligand, has shown promise as a vaccine adjuvant to CD8(+) T cell responses. |
| 2873 | 16704888 | Poly (I:C) treatment was associated with a rapid induction of inflammatory cytokines in the serum, including IL-6, IL-10, MCP-1, TNF-alpha, IFN-alpha, and IFN-gamma, and selective increases in the numbers of NK (NK1.1(+)CD11b(+)) cells and Mvarphi (NK1.1(-)CD11b(+)), but not NK T (CD3(+)NK1.1(+)) cells. |
| 2874 | 16704888 | Poly (I:C) treatment was associated with a rapid induction of inflammatory cytokines in the serum, including IL-6, IL-10, MCP-1, TNF-alpha, IFN-alpha, and IFN-gamma, and selective increases in the numbers of NK (NK1.1(+)CD11b(+)) cells and Mvarphi (NK1.1(-)CD11b(+)), but not NK T (CD3(+)NK1.1(+)) cells. |
| 2875 | 16704888 | Poly (I:C) treatment was associated with a rapid induction of inflammatory cytokines in the serum, including IL-6, IL-10, MCP-1, TNF-alpha, IFN-alpha, and IFN-gamma, and selective increases in the numbers of NK (NK1.1(+)CD11b(+)) cells and Mvarphi (NK1.1(-)CD11b(+)), but not NK T (CD3(+)NK1.1(+)) cells. |
| 2876 | 16704888 | Poly (I:C) treatment was associated with a rapid induction of inflammatory cytokines in the serum, including IL-6, IL-10, MCP-1, TNF-alpha, IFN-alpha, and IFN-gamma, and selective increases in the numbers of NK (NK1.1(+)CD11b(+)) cells and Mvarphi (NK1.1(-)CD11b(+)), but not NK T (CD3(+)NK1.1(+)) cells. |
| 2877 | 16704888 | Poly (I:C) treatment in TNF-alpha, type I IFNR, IFN-gamma, IL-6, IL-12Rbeta2, or IL-15 gene-deficient mice revealed a reciprocal interaction and interdependence in the induction of these cytokines, where the absence of one cytokine impacted on the production of others. |
| 2878 | 16704888 | Poly (I:C) treatment in TNF-alpha, type I IFNR, IFN-gamma, IL-6, IL-12Rbeta2, or IL-15 gene-deficient mice revealed a reciprocal interaction and interdependence in the induction of these cytokines, where the absence of one cytokine impacted on the production of others. |
| 2879 | 16704888 | Poly (I:C) treatment in TNF-alpha, type I IFNR, IFN-gamma, IL-6, IL-12Rbeta2, or IL-15 gene-deficient mice revealed a reciprocal interaction and interdependence in the induction of these cytokines, where the absence of one cytokine impacted on the production of others. |
| 2880 | 16704888 | Poly (I:C) treatment in TNF-alpha, type I IFNR, IFN-gamma, IL-6, IL-12Rbeta2, or IL-15 gene-deficient mice revealed a reciprocal interaction and interdependence in the induction of these cytokines, where the absence of one cytokine impacted on the production of others. |
| 2881 | 16704888 | Further, the adjuvant effects of poly (I:C) were dependent on the endogenous levels of type I IFNs, TNF-alpha, IFN-gamma, IL-12, and IL-15. |
| 2882 | 16704888 | Further, the adjuvant effects of poly (I:C) were dependent on the endogenous levels of type I IFNs, TNF-alpha, IFN-gamma, IL-12, and IL-15. |
| 2883 | 16704888 | Further, the adjuvant effects of poly (I:C) were dependent on the endogenous levels of type I IFNs, TNF-alpha, IFN-gamma, IL-12, and IL-15. |
| 2884 | 16704888 | Further, the adjuvant effects of poly (I:C) were dependent on the endogenous levels of type I IFNs, TNF-alpha, IFN-gamma, IL-12, and IL-15. |
| 2885 | 16704888 | IFN-alpha and IFN-beta, but not TNF-alpha or IL-6, were able to mimic the adjuvant effects of poly (I:C). |
| 2886 | 16704888 | IFN-alpha and IFN-beta, but not TNF-alpha or IL-6, were able to mimic the adjuvant effects of poly (I:C). |
| 2887 | 16704888 | IFN-alpha and IFN-beta, but not TNF-alpha or IL-6, were able to mimic the adjuvant effects of poly (I:C). |
| 2888 | 16704888 | IFN-alpha and IFN-beta, but not TNF-alpha or IL-6, were able to mimic the adjuvant effects of poly (I:C). |
| 2889 | 16699040 | Human cytomegalovirus attenuates interleukin-1beta and tumor necrosis factor alpha proinflammatory signaling by inhibition of NF-kappaB activation. |
| 2890 | 16699040 | Human cytomegalovirus attenuates interleukin-1beta and tumor necrosis factor alpha proinflammatory signaling by inhibition of NF-kappaB activation. |
| 2891 | 16699040 | Human cytomegalovirus attenuates interleukin-1beta and tumor necrosis factor alpha proinflammatory signaling by inhibition of NF-kappaB activation. |
| 2892 | 16699040 | Human cytomegalovirus attenuates interleukin-1beta and tumor necrosis factor alpha proinflammatory signaling by inhibition of NF-kappaB activation. |
| 2893 | 16699040 | Human cytomegalovirus attenuates interleukin-1beta and tumor necrosis factor alpha proinflammatory signaling by inhibition of NF-kappaB activation. |
| 2894 | 16699040 | Human cytomegalovirus attenuates interleukin-1beta and tumor necrosis factor alpha proinflammatory signaling by inhibition of NF-kappaB activation. |
| 2895 | 16699040 | Viral infection is associated with a vigorous inflammatory response characterized by cellular infiltration and release of the proinflammatory cytokines interleukin-1 (IL-1) and tumor necrosis factor alpha (TNF-alpha). |
| 2896 | 16699040 | Viral infection is associated with a vigorous inflammatory response characterized by cellular infiltration and release of the proinflammatory cytokines interleukin-1 (IL-1) and tumor necrosis factor alpha (TNF-alpha). |
| 2897 | 16699040 | Viral infection is associated with a vigorous inflammatory response characterized by cellular infiltration and release of the proinflammatory cytokines interleukin-1 (IL-1) and tumor necrosis factor alpha (TNF-alpha). |
| 2898 | 16699040 | Viral infection is associated with a vigorous inflammatory response characterized by cellular infiltration and release of the proinflammatory cytokines interleukin-1 (IL-1) and tumor necrosis factor alpha (TNF-alpha). |
| 2899 | 16699040 | Viral infection is associated with a vigorous inflammatory response characterized by cellular infiltration and release of the proinflammatory cytokines interleukin-1 (IL-1) and tumor necrosis factor alpha (TNF-alpha). |
| 2900 | 16699040 | Viral infection is associated with a vigorous inflammatory response characterized by cellular infiltration and release of the proinflammatory cytokines interleukin-1 (IL-1) and tumor necrosis factor alpha (TNF-alpha). |
| 2901 | 16699040 | In the present study, we identified a novel function of human cytomegalovirus (HCMV) that results in inhibition of IL-1 and TNF-alpha signaling pathways. |
| 2902 | 16699040 | In the present study, we identified a novel function of human cytomegalovirus (HCMV) that results in inhibition of IL-1 and TNF-alpha signaling pathways. |
| 2903 | 16699040 | In the present study, we identified a novel function of human cytomegalovirus (HCMV) that results in inhibition of IL-1 and TNF-alpha signaling pathways. |
| 2904 | 16699040 | In the present study, we identified a novel function of human cytomegalovirus (HCMV) that results in inhibition of IL-1 and TNF-alpha signaling pathways. |
| 2905 | 16699040 | In the present study, we identified a novel function of human cytomegalovirus (HCMV) that results in inhibition of IL-1 and TNF-alpha signaling pathways. |
| 2906 | 16699040 | In the present study, we identified a novel function of human cytomegalovirus (HCMV) that results in inhibition of IL-1 and TNF-alpha signaling pathways. |
| 2907 | 16699040 | IL-1 and TNF-alpha signaling pathways converge at a point upstream of NF-kappaB activation and involve phosphorylation and degradation of the NF-kappaB inhibitory molecule IkappaBalpha. |
| 2908 | 16699040 | IL-1 and TNF-alpha signaling pathways converge at a point upstream of NF-kappaB activation and involve phosphorylation and degradation of the NF-kappaB inhibitory molecule IkappaBalpha. |
| 2909 | 16699040 | IL-1 and TNF-alpha signaling pathways converge at a point upstream of NF-kappaB activation and involve phosphorylation and degradation of the NF-kappaB inhibitory molecule IkappaBalpha. |
| 2910 | 16699040 | IL-1 and TNF-alpha signaling pathways converge at a point upstream of NF-kappaB activation and involve phosphorylation and degradation of the NF-kappaB inhibitory molecule IkappaBalpha. |
| 2911 | 16699040 | IL-1 and TNF-alpha signaling pathways converge at a point upstream of NF-kappaB activation and involve phosphorylation and degradation of the NF-kappaB inhibitory molecule IkappaBalpha. |
| 2912 | 16699040 | IL-1 and TNF-alpha signaling pathways converge at a point upstream of NF-kappaB activation and involve phosphorylation and degradation of the NF-kappaB inhibitory molecule IkappaBalpha. |
| 2913 | 16699040 | The HCMV inhibition of IL-1 and TNF-alpha pathways corresponded to a suppression of NF-kappaB activation. |
| 2914 | 16699040 | The HCMV inhibition of IL-1 and TNF-alpha pathways corresponded to a suppression of NF-kappaB activation. |
| 2915 | 16699040 | The HCMV inhibition of IL-1 and TNF-alpha pathways corresponded to a suppression of NF-kappaB activation. |
| 2916 | 16699040 | The HCMV inhibition of IL-1 and TNF-alpha pathways corresponded to a suppression of NF-kappaB activation. |
| 2917 | 16699040 | The HCMV inhibition of IL-1 and TNF-alpha pathways corresponded to a suppression of NF-kappaB activation. |
| 2918 | 16699040 | The HCMV inhibition of IL-1 and TNF-alpha pathways corresponded to a suppression of NF-kappaB activation. |
| 2919 | 16699040 | Analysis of IkappaBalpha phosphorylation and degradation suggested that HCMV induced two independent blocks in NF-kappaB activation, which occurred upstream from the point of convergence of the IL-1 and TNF-alpha pathways. |
| 2920 | 16699040 | Analysis of IkappaBalpha phosphorylation and degradation suggested that HCMV induced two independent blocks in NF-kappaB activation, which occurred upstream from the point of convergence of the IL-1 and TNF-alpha pathways. |
| 2921 | 16699040 | Analysis of IkappaBalpha phosphorylation and degradation suggested that HCMV induced two independent blocks in NF-kappaB activation, which occurred upstream from the point of convergence of the IL-1 and TNF-alpha pathways. |
| 2922 | 16699040 | Analysis of IkappaBalpha phosphorylation and degradation suggested that HCMV induced two independent blocks in NF-kappaB activation, which occurred upstream from the point of convergence of the IL-1 and TNF-alpha pathways. |
| 2923 | 16699040 | Analysis of IkappaBalpha phosphorylation and degradation suggested that HCMV induced two independent blocks in NF-kappaB activation, which occurred upstream from the point of convergence of the IL-1 and TNF-alpha pathways. |
| 2924 | 16699040 | Analysis of IkappaBalpha phosphorylation and degradation suggested that HCMV induced two independent blocks in NF-kappaB activation, which occurred upstream from the point of convergence of the IL-1 and TNF-alpha pathways. |
| 2925 | 16698670 | Tumor necrosis factor-a (TNF-a), interleukin-6 (IL-6), interleukin-1 beta (IL-1beta) and interleukin-1 receptor antagonist (IL-1ra) were used to assess the inflammatory status; and circulating immunoglobulins (IgM, IgA, IgG and IgG subclasses) and specific IgG titer to tetanus were used to assess humoral immunity. |
| 2926 | 16698670 | Tumor necrosis factor-a (TNF-a), interleukin-6 (IL-6), interleukin-1 beta (IL-1beta) and interleukin-1 receptor antagonist (IL-1ra) were used to assess the inflammatory status; and circulating immunoglobulins (IgM, IgA, IgG and IgG subclasses) and specific IgG titer to tetanus were used to assess humoral immunity. |
| 2927 | 16698670 | No significant differences were found in TNF-a, IL-1beta and IL-1ra between the groups. |
| 2928 | 16698670 | No significant differences were found in TNF-a, IL-1beta and IL-1ra between the groups. |
| 2929 | 16697684 | BLS-KETc1 also increased the levels of transcription of TNF-alpha, IL-2 and IFNgamma in Peyer's patches, and in spleen, only increased TNF-alpha was observed. |
| 2930 | 16691317 | To analyze the immune responses caused by PEPCK, the effects of PEPCK on the induction of CD4(+) T cells and cytokines such as IFN-gamma, IL-12 and TNF-alpha were evaluated in mice. |
| 2931 | 16691317 | To analyze the immune responses caused by PEPCK, the effects of PEPCK on the induction of CD4(+) T cells and cytokines such as IFN-gamma, IL-12 and TNF-alpha were evaluated in mice. |
| 2932 | 16691317 | It was found that the number of CD4(+) T cells was increased in the PEPCK immunized mice although the change of the number of CD8(+) T cells was not significant. |
| 2933 | 16691317 | It was found that the number of CD4(+) T cells was increased in the PEPCK immunized mice although the change of the number of CD8(+) T cells was not significant. |
| 2934 | 16691317 | The cytokines IFN-gamma, IL-12 and TNF-alpha were increased significantly in the mice immunized with PEPCK than those of incomplete adjuvant. |
| 2935 | 16691317 | The cytokines IFN-gamma, IL-12 and TNF-alpha were increased significantly in the mice immunized with PEPCK than those of incomplete adjuvant. |
| 2936 | 16682480 | Before treatment, S. mansoni infection intensity was positively correlated with 24-h boosts in plasma interleukin-5 (IL-5) and IL-6 levels, which were in turn negatively correlated with the posttreatment fall in eosinophil numbers. |
| 2937 | 16682480 | Before treatment, S. mansoni infection intensity was positively correlated with 24-h boosts in plasma interleukin-5 (IL-5) and IL-6 levels, which were in turn negatively correlated with the posttreatment fall in eosinophil numbers. |
| 2938 | 16682480 | Significant correlations were observed between pretreatment infection intensities and plasma IL-10 and eotaxin levels. |
| 2939 | 16682480 | Significant correlations were observed between pretreatment infection intensities and plasma IL-10 and eotaxin levels. |
| 2940 | 16682480 | Treatment induced significant fluctuations in plasma IL-5, IL-6, IL-10, tumor necrosis factor alpha (TNF-alpha), and eotaxin levels. |
| 2941 | 16682480 | Treatment induced significant fluctuations in plasma IL-5, IL-6, IL-10, tumor necrosis factor alpha (TNF-alpha), and eotaxin levels. |
| 2942 | 16682480 | Optimal relative release of ECP and EPX in vitro was detected in S. mansoni soluble egg antigen-stimulated cultures during transient eosinopenia. |
| 2943 | 16682480 | Optimal relative release of ECP and EPX in vitro was detected in S. mansoni soluble egg antigen-stimulated cultures during transient eosinopenia. |
| 2944 | 16682480 | Our data suggest that blood eosinophils are activated during S. mansoni infection and that treatment induces a burst in released antigens, causing increased production of IL-5, IL-6, IL-10, and eotaxin; a drop in TNF-alpha levels; and a transient sequestration of eosinophils, which leaves fewer degranulated eosinophils in the circulation 24 h posttreatment, followed by the development of eosinophilia 3 weeks later. |
| 2945 | 16682480 | Our data suggest that blood eosinophils are activated during S. mansoni infection and that treatment induces a burst in released antigens, causing increased production of IL-5, IL-6, IL-10, and eotaxin; a drop in TNF-alpha levels; and a transient sequestration of eosinophils, which leaves fewer degranulated eosinophils in the circulation 24 h posttreatment, followed by the development of eosinophilia 3 weeks later. |
| 2946 | 16682479 | Preincubation with TNF-alpha promoted CR3 expression on BMPMN, and this level of expression was also enhanced by WKYMVm. |
| 2947 | 16681827 | Following vaccination, T lymphocyte survival improved and cells recovered their ability to produce the Th1-associated cytokines TNF and IFN-gamma in response to anti-CD3 stimulation in vitro. |
| 2948 | 16641451 | Herein, we show that SAG induces extracellular signal-regulated kinase 1 (ERK-1) and ERK-2 phosphorylation through phosphoinositide 3-kinase (PI3K), protein kinase C, and Ras activation and p38 mitogen-activated protein kinase (MAPK) phosphorylation through PI3K and Akt activation. |
| 2949 | 16641451 | ERK-1 and ERK-2 activation results in an increase in the production of reactive oxygen species (ROS) 3 to 6 h after SAG treatment, while p38 MAPK activation and subsequent tumor necrosis factor alpha release result in the production of nitric oxide (NO) 24 h after SAG treatment. |
| 2950 | 16634802 | The effect of M. bovis infection, 4 months post-challenge, was to suppress the expression of anti-inflammatory cytokines interleukin (IL)-4 and IL-10 as well as the pro-inflammatory cytokines tumour necrosis factor (TNF) and IL-6. |
| 2951 | 16634802 | The effect of M. bovis infection, 4 months post-challenge, was to suppress the expression of anti-inflammatory cytokines interleukin (IL)-4 and IL-10 as well as the pro-inflammatory cytokines tumour necrosis factor (TNF) and IL-6. |
| 2952 | 16634802 | Expression of interferon (IFN)-gamma and IL-12 was maintained. |
| 2953 | 16634802 | Expression of interferon (IFN)-gamma and IL-12 was maintained. |
| 2954 | 16634802 | In particular, no decrease in expression of IL-4 or IL-6 was observed following challenge of vaccinated animals and decreased IFN-gamma was detected. |
| 2955 | 16634802 | In particular, no decrease in expression of IL-4 or IL-6 was observed following challenge of vaccinated animals and decreased IFN-gamma was detected. |
| 2956 | 16634802 | Also, vaccinated animals had higher levels of IL-4 and IL-10 transcripts compared to unvaccinated animals following challenge. |
| 2957 | 16634802 | Also, vaccinated animals had higher levels of IL-4 and IL-10 transcripts compared to unvaccinated animals following challenge. |
| 2958 | 16634802 | These changes in cytokine expression levels led to a significant shift in the IFN-gamma/IL-4 or IFN-gamma/IL-10 ratio within the lymph node following challenge. |
| 2959 | 16634802 | These changes in cytokine expression levels led to a significant shift in the IFN-gamma/IL-4 or IFN-gamma/IL-10 ratio within the lymph node following challenge. |
| 2960 | 16634802 | An inverse correlation between the level of pathology and bacterial load within the lymph node and the expression of IL-4, IL-10 and TNF was also observed. |
| 2961 | 16634802 | An inverse correlation between the level of pathology and bacterial load within the lymph node and the expression of IL-4, IL-10 and TNF was also observed. |
| 2962 | 16632108 | While no variations were seen in serum IL12 or TNFalpha levels, a high IFNgamma secretion was detected from Day 8, concomitant to IFNalpha, followed by IL10. |
| 2963 | 16632108 | While no variations were seen in serum IL12 or TNFalpha levels, a high IFNgamma secretion was detected from Day 8, concomitant to IFNalpha, followed by IL10. |
| 2964 | 16632108 | Specific Th1 and CD8 responses were detected on Day 28, with high IFNgamma/TNFalpha ratios. |
| 2965 | 16632108 | Specific Th1 and CD8 responses were detected on Day 28, with high IFNgamma/TNFalpha ratios. |
| 2966 | 16630025 | Interferon-alpha (IFN-alpha) alone was a poor inducer of MoDC maturation, but in association with tumour necrosis factor-alpha (TNF-alpha), or TLR ligands such as lipopolysaccharide and polyinosinic-polycytidylic acid I:C, an up-regulation of major histocompatibility complex II and CD80/86 expression was noted, along with reduced endocytic activity. |
| 2967 | 16630025 | Interferon-alpha (IFN-alpha) alone was a poor inducer of MoDC maturation, but in association with tumour necrosis factor-alpha (TNF-alpha), or TLR ligands such as lipopolysaccharide and polyinosinic-polycytidylic acid I:C, an up-regulation of major histocompatibility complex II and CD80/86 expression was noted, along with reduced endocytic activity. |
| 2968 | 16630025 | Indeed, MoDC did not respond to transmissible gastroenteritis virus (TGEV), whereas NIPC produced high levels of IFN-alpha and TNF-alpha after TGEV stimulation. |
| 2969 | 16630025 | Indeed, MoDC did not respond to transmissible gastroenteritis virus (TGEV), whereas NIPC produced high levels of IFN-alpha and TNF-alpha after TGEV stimulation. |
| 2970 | 16622195 | Splenocytes from infected C3H/HeJ mice produced almost no interleukin-1beta (IL-1beta) and tumor necrosis factor alpha (TNF-alpha) upon ex vivo restimulation with B. pertussis compared to A/J mice and also showed a delayed gamma interferon (IFN-gamma) production. |
| 2971 | 16622195 | Splenocytes from infected C3H/HeJ mice produced almost no interleukin-1beta (IL-1beta) and tumor necrosis factor alpha (TNF-alpha) upon ex vivo restimulation with B. pertussis compared to A/J mice and also showed a delayed gamma interferon (IFN-gamma) production. |
| 2972 | 16622195 | Functional Tlr4 is essential for an efficient IL-1-beta, TNF-alpha, and IFN-gamma response; efficient clearance of bacteria from the lung; and reduced lung pathology. |
| 2973 | 16622195 | Functional Tlr4 is essential for an efficient IL-1-beta, TNF-alpha, and IFN-gamma response; efficient clearance of bacteria from the lung; and reduced lung pathology. |
| 2974 | 16621986 | Upon specific vaccination, however, systemic IL-23 greatly increased the relative and absolute numbers of vaccine-induced CD8(+) T cells and enhanced their effector function at the tumor site. |
| 2975 | 16621986 | Although IL-23 specifically increased IFN-gamma production by tumor-specific T cells, IFN-gamma itself was not a primary mediator of the vaccine adjuvant effect. |
| 2976 | 16621986 | The IL-23-induced antitumor effect and accompanying reversible weight loss were both partially mediated by TNF-alpha. |
| 2977 | 16621986 | Under these conditions, it was also clear that enhanced effector function of vaccine-induced CD8(+) T cells, rather than increased T cell number, is a primary mechanism underlying the antitumor effect of IL-23. |
| 2978 | 16621986 | Collectively, these results suggest that IL-23 is a potent vaccine adjuvant for the induction of therapeutic, tumor-specific CD8(+) T cell responses. |
| 2979 | 16621198 | Particle-mediated DNA vaccination of mice with a DNA plasmid-encoding ICP27 resulted in the induction of ICP27-specific IFN-gamma and TNF-alpha production in Balb/c mice, but little protection to intranasal challenge with wild type HSV-2. |
| 2980 | 16621198 | Particle-mediated DNA vaccination of mice with a DNA plasmid-encoding ICP27 resulted in the induction of ICP27-specific IFN-gamma and TNF-alpha production in Balb/c mice, but little protection to intranasal challenge with wild type HSV-2. |
| 2981 | 16621198 | The ICP27+LT-mediated protection was correlated with a large increase in ICP27-specific IFN-gamma and TNF-alpha production but cytokine-specific monoclonal antibody treatment at the time of challenge showed that protection was mediated predominantly by IFN-gamma. |
| 2982 | 16621198 | The ICP27+LT-mediated protection was correlated with a large increase in ICP27-specific IFN-gamma and TNF-alpha production but cytokine-specific monoclonal antibody treatment at the time of challenge showed that protection was mediated predominantly by IFN-gamma. |
| 2983 | 16621198 | Furthermore, depletion of T cell subsets prior to infectious challenge demonstrated that removal of either CD8+ or CD4+ T cells impaired protection with CD8+ T cells appearing to play a direct effector role. |
| 2984 | 16621198 | Furthermore, depletion of T cell subsets prior to infectious challenge demonstrated that removal of either CD8+ or CD4+ T cells impaired protection with CD8+ T cells appearing to play a direct effector role. |
| 2985 | 16621176 | Naïve splenocytes produced high levels of TNF-alpha and IL-10 after incubation with LPS+ sonicate, while cells incubated with LPS- sonicate did not. |
| 2986 | 16621176 | Naïve splenocytes produced high levels of TNF-alpha and IL-10 after incubation with LPS+ sonicate, while cells incubated with LPS- sonicate did not. |
| 2987 | 16621176 | Mice immunized with LPS+ sonicate developed a prominent innate response characterized by increased TNF-alpha and IL-10, as well as a strong antigen specific Th1 response including, IFN-gamma, IL-2 and high IgG2a serum titers. |
| 2988 | 16621176 | Mice immunized with LPS+ sonicate developed a prominent innate response characterized by increased TNF-alpha and IL-10, as well as a strong antigen specific Th1 response including, IFN-gamma, IL-2 and high IgG2a serum titers. |
| 2989 | 16621176 | Mice that received LPS- sonicate were strongly Th2 biased in their immune response, with significantly more IL-4 than IFN-gamma and serum IgG1 titers higher than IgG2a. |
| 2990 | 16621176 | Mice that received LPS- sonicate were strongly Th2 biased in their immune response, with significantly more IL-4 than IFN-gamma and serum IgG1 titers higher than IgG2a. |
| 2991 | 16603612 | Both molecules are strong inflammatory agents and have a glycerol backbone with two lipid chains at the sn-1 and sn-2 positions. |
| 2992 | 16603612 | PAF is normally inactivated by PAF-acetylhydrolase (PAF-AH), a phospholipase A2 (PLA2), which removes a short acyl group at the sn-2 position. |
| 2993 | 16603612 | To investigate whether PAF-AH can similarly degrade LTA, we studied the effects of porcine PLA2, bee venom PLA2, and recombinant human PAF-AH on pneumococcal LTA (PnLTA) and staphylococcal LTA (StLTA). |
| 2994 | 16603612 | Following PAF-AH treatment, PnLTA and StLTA were not able to stimulate mouse RAW 264.7 cells to produce tumor necrosis factor alpha but could stimulate CHO cells expressing human TLR2. |
| 2995 | 16586371 | Both CD4+ and CD8+ T cells can mediate vaccine-induced protection against Coccidioides immitis infection in mice. |
| 2996 | 16586371 | Both CD4+ and CD8+ T cells can mediate vaccine-induced protection against Coccidioides immitis infection in mice. |
| 2997 | 16586371 | Vaccine-induced immunity required alpha beta T lymphocytes. beta -2 microglobulin knockout (KO) mice were protected by immunization, and we transferred protection using CD4+ T cells from immunized mice. |
| 2998 | 16586371 | Vaccine-induced immunity required alpha beta T lymphocytes. beta -2 microglobulin knockout (KO) mice were protected by immunization, and we transferred protection using CD4+ T cells from immunized mice. |
| 2999 | 16586371 | However, vaccination also protected CD4+ KO mice, which suggests that CD8+ T cells played a role in vaccine-induced immunity, even though they were not required. |
| 3000 | 16586371 | However, vaccination also protected CD4+ KO mice, which suggests that CD8+ T cells played a role in vaccine-induced immunity, even though they were not required. |
| 3001 | 16586371 | We adaptively transferred protection using spleen cells from immunized CD4+ KO mice to nonimmune B6 mice, but CD8+ -depleted spleen cells did not protect against infection. |
| 3002 | 16586371 | We adaptively transferred protection using spleen cells from immunized CD4+ KO mice to nonimmune B6 mice, but CD8+ -depleted spleen cells did not protect against infection. |
| 3003 | 16586371 | Recipients of spleen cells from immunized CD4+ KO mice had 6 times more tumor necrosis factor (TNF)- alpha mRNA in their lungs than did mice that received nonimmune spleen cells, and TNF receptor-1 KO mice were not fully protected by immunization. |
| 3004 | 16586371 | Recipients of spleen cells from immunized CD4+ KO mice had 6 times more tumor necrosis factor (TNF)- alpha mRNA in their lungs than did mice that received nonimmune spleen cells, and TNF receptor-1 KO mice were not fully protected by immunization. |
| 3005 | 16586371 | These results show that both CD4+ and CD8+ T cells can protect against coccidioidomycosis and that TNF- alpha is a necessary component of the acquired immune response. |
| 3006 | 16586371 | These results show that both CD4+ and CD8+ T cells can protect against coccidioidomycosis and that TNF- alpha is a necessary component of the acquired immune response. |
| 3007 | 16585589 | During the chronic stage of the infection, the bacterial load in the lungs of immune mice remained at a level 10 times lower than control mice, and this was associated with reduced numbers of CD4P(+P) and CD8P(+P) T cells, and the lower expression of protective (IL-12, IFN-gamma), inflammatory (TNF-alpha), immunoregulatory (GM-CSF), and immunosuppressive (IL-10) cytokines. |
| 3008 | 16584815 | Contrary to the parental strain, the auxotrofic mutant did not induce IL-1beta, IL-18, TNF-alpha, and IFN-gamma in the ileum and plasma 24h after the infection, did not cause pathological changes in ileal epithelium and mesenteric lymph nodes or immunoreactivity of gp91 phox and peroxynitrite and was not immunostained for GroEL stress protein. |
| 3009 | 16574669 | Induction of kappaB-driven transcriptional activity by 2.5 mug ml(-1) F. tularensis LPS isolated by phenol-water and ether-water extraction, was observed in cells transfected with Toll-like receptor (TLR) 4 and MD-2, although CD14 was required for optimal induction. |
| 3010 | 16574669 | Conversely, TLR2, TLR2/TLR1 or TLR2/TLR6 transfected cells did not show kappaB-driven transcriptional activity in the presence of F. tularensis LPS. |
| 3011 | 16574669 | Concentrations of 5-10 mug ml(-1) F. tularensis LPS elicited a similar pattern of mRNA and protein induction than 0.1 mug ml(-1) E. coli LPS, including the expression of CXC chemokines (IL-8, Gro and IFN-gamma-inducible protein-10); CC chemokines (monocyte chemoattractant protein-1 and -2, macrophage-derived chemoattractant, macrophage inflammatory protein-1alpha and -1beta and RANTES (regulated upon activation, normal T cell expressed and secreted) and pro-inflammatory cytokines (IL-6 and tumor necrosis factor alpha). |
| 3012 | 16556474 | Mutant Escherichia coli enterotoxin as a mucosal adjuvant induces specific Th1 responses of CD4+ and CD8+ T cells to nasal killed-bacillus calmette-guerin in mice. |
| 3013 | 16556474 | Mutant Escherichia coli enterotoxin as a mucosal adjuvant induces specific Th1 responses of CD4+ and CD8+ T cells to nasal killed-bacillus calmette-guerin in mice. |
| 3014 | 16556474 | Spleen cells, particularly CD4+ T cells among them produced IL-2, IFNgamma and TNFalpha in response to the killed-BCG or purified protein derivatives. |
| 3015 | 16556474 | Spleen cells, particularly CD4+ T cells among them produced IL-2, IFNgamma and TNFalpha in response to the killed-BCG or purified protein derivatives. |
| 3016 | 16556474 | CD8+ T cells including cytotoxic T lymphocytes produced IFNgamma and TNFalpha. |
| 3017 | 16556474 | CD8+ T cells including cytotoxic T lymphocytes produced IFNgamma and TNFalpha. |
| 3018 | 16556474 | CD4+ and CD8+ T cells produce cytokines effective for tuberculosis. |
| 3019 | 16556474 | CD4+ and CD8+ T cells produce cytokines effective for tuberculosis. |
| 3020 | 16548886 | In this study we analyse the interaction of the MP from Candida albicans (MP65) with dendritic cells (DC) and demonstrate that MP65 stimulates DC and induces the release of TNF-alpha, IL-6 and the activation of IL-12 gene, with maximal value 6 h post treatment. |
| 3021 | 16548886 | The latter effect is partly mediated by toll-like receptor 2 (TLR2) and TLR4, and the MyD88-dependent pathway is involved in the process. |
| 3022 | 16545418 | We show here that NS1 protein from human H5N1 influenza isolate A/HK/156/97 reduces both systemic and pulmonary pro-inflammatory cytokines in an in vivo mouse model and protects against bone marrow lymphocyte depletion, an effect which has been shown to be mediated by TNFalpha. |
| 3023 | 16531819 | The CD34(+) human acute myeloid leukemia-derived cell line MUTZ-3 is dependent on hematopoietic growth factors for its proliferation and is able to differentiate into dendritic cells (DCs) in response to the combination of granulocyte-macrophage colony-stimulating factor, interleukin-4, and tumor necrosis factor-alpha. |
| 3024 | 16528969 | Development of immunity in vaccinated mice was associated with the generation of leukemia specific cytotoxic T lymphocytes (CTLs) and secretion of cytokines TNF-alpha and IFN-gamma. |
| 3025 | 16528969 | Cured mice were in molecular remission since Bcr/Abl oncogene could not be amplified from the DNA isolated from the marrow, spleen, or liver of cured mice. |
| 3026 | 16522814 | We found that while SIV-specific T-cell responses are detectable in the majority of animals, their magnitude and breadth are, in fact, lower than what has been described in HIV-infected humans, both in terms of cytokine production (ie, IFN-gamma, TNF-alpha, and IL-2) and degranulation (ie, CD107a expression). |
| 3027 | 16522779 | Lactic acid bacteria inducing a weak interleukin-12 and tumor necrosis factor alpha response in human dendritic cells inhibit strongly stimulating lactic acid bacteria but act synergistically with gram-negative bacteria. |
| 3028 | 16522779 | Lactic acid bacteria inducing a weak interleukin-12 and tumor necrosis factor alpha response in human dendritic cells inhibit strongly stimulating lactic acid bacteria but act synergistically with gram-negative bacteria. |
| 3029 | 16522779 | Lactic acid bacteria inducing a weak interleukin-12 and tumor necrosis factor alpha response in human dendritic cells inhibit strongly stimulating lactic acid bacteria but act synergistically with gram-negative bacteria. |
| 3030 | 16522779 | Lactic acid bacteria inducing a weak interleukin-12 and tumor necrosis factor alpha response in human dendritic cells inhibit strongly stimulating lactic acid bacteria but act synergistically with gram-negative bacteria. |
| 3031 | 16522779 | Lactic acid bacteria inducing a weak interleukin-12 and tumor necrosis factor alpha response in human dendritic cells inhibit strongly stimulating lactic acid bacteria but act synergistically with gram-negative bacteria. |
| 3032 | 16522779 | While strains of LAB varied greatly in their capacity to induce interleukin-12 (IL-12) and tumor necrosis factor alpha (TNF-alpha), G- strains were consistently weak IL-12 and TNF-alpha inducers. |
| 3033 | 16522779 | While strains of LAB varied greatly in their capacity to induce interleukin-12 (IL-12) and tumor necrosis factor alpha (TNF-alpha), G- strains were consistently weak IL-12 and TNF-alpha inducers. |
| 3034 | 16522779 | While strains of LAB varied greatly in their capacity to induce interleukin-12 (IL-12) and tumor necrosis factor alpha (TNF-alpha), G- strains were consistently weak IL-12 and TNF-alpha inducers. |
| 3035 | 16522779 | While strains of LAB varied greatly in their capacity to induce interleukin-12 (IL-12) and tumor necrosis factor alpha (TNF-alpha), G- strains were consistently weak IL-12 and TNF-alpha inducers. |
| 3036 | 16522779 | While strains of LAB varied greatly in their capacity to induce interleukin-12 (IL-12) and tumor necrosis factor alpha (TNF-alpha), G- strains were consistently weak IL-12 and TNF-alpha inducers. |
| 3037 | 16522779 | Interestingly, we found that when weakly IL-12- and TNF-alpha-inducing LAB and strong IL-12- and TNF-alpha-inducing LAB were mixed, the weakly IL-12- and TNF-alpha-inducing LAB efficiently inhibited otherwise strong IL-12- and TNF-alpha-inducing LAB, yet when weakly IL-12- and TNF-alpha-inducing LAB were mixed with G- bacteria, they synergistically induced IL-12 and TNF-alpha. |
| 3038 | 16522779 | Interestingly, we found that when weakly IL-12- and TNF-alpha-inducing LAB and strong IL-12- and TNF-alpha-inducing LAB were mixed, the weakly IL-12- and TNF-alpha-inducing LAB efficiently inhibited otherwise strong IL-12- and TNF-alpha-inducing LAB, yet when weakly IL-12- and TNF-alpha-inducing LAB were mixed with G- bacteria, they synergistically induced IL-12 and TNF-alpha. |
| 3039 | 16522779 | Interestingly, we found that when weakly IL-12- and TNF-alpha-inducing LAB and strong IL-12- and TNF-alpha-inducing LAB were mixed, the weakly IL-12- and TNF-alpha-inducing LAB efficiently inhibited otherwise strong IL-12- and TNF-alpha-inducing LAB, yet when weakly IL-12- and TNF-alpha-inducing LAB were mixed with G- bacteria, they synergistically induced IL-12 and TNF-alpha. |
| 3040 | 16522779 | Interestingly, we found that when weakly IL-12- and TNF-alpha-inducing LAB and strong IL-12- and TNF-alpha-inducing LAB were mixed, the weakly IL-12- and TNF-alpha-inducing LAB efficiently inhibited otherwise strong IL-12- and TNF-alpha-inducing LAB, yet when weakly IL-12- and TNF-alpha-inducing LAB were mixed with G- bacteria, they synergistically induced IL-12 and TNF-alpha. |
| 3041 | 16522779 | Interestingly, we found that when weakly IL-12- and TNF-alpha-inducing LAB and strong IL-12- and TNF-alpha-inducing LAB were mixed, the weakly IL-12- and TNF-alpha-inducing LAB efficiently inhibited otherwise strong IL-12- and TNF-alpha-inducing LAB, yet when weakly IL-12- and TNF-alpha-inducing LAB were mixed with G- bacteria, they synergistically induced IL-12 and TNF-alpha. |
| 3042 | 16522779 | Furthermore, strong IL-12- and TNF-alpha-inducing LAB efficiently up-regulated surface markers (CD40, CD83, CD86, and HLA-DR), which were inhibited by weakly IL-12- and TNF-alpha-inducing LAB. |
| 3043 | 16522779 | Furthermore, strong IL-12- and TNF-alpha-inducing LAB efficiently up-regulated surface markers (CD40, CD83, CD86, and HLA-DR), which were inhibited by weakly IL-12- and TNF-alpha-inducing LAB. |
| 3044 | 16522779 | Furthermore, strong IL-12- and TNF-alpha-inducing LAB efficiently up-regulated surface markers (CD40, CD83, CD86, and HLA-DR), which were inhibited by weakly IL-12- and TNF-alpha-inducing LAB. |
| 3045 | 16522779 | Furthermore, strong IL-12- and TNF-alpha-inducing LAB efficiently up-regulated surface markers (CD40, CD83, CD86, and HLA-DR), which were inhibited by weakly IL-12- and TNF-alpha-inducing LAB. |
| 3046 | 16522779 | Furthermore, strong IL-12- and TNF-alpha-inducing LAB efficiently up-regulated surface markers (CD40, CD83, CD86, and HLA-DR), which were inhibited by weakly IL-12- and TNF-alpha-inducing LAB. |
| 3047 | 16522779 | All G- bacteria potently up-regulated surface markers; however, these markers were not inhibited by weakly IL-12- and TNF-alpha-inducing LAB. |
| 3048 | 16522779 | All G- bacteria potently up-regulated surface markers; however, these markers were not inhibited by weakly IL-12- and TNF-alpha-inducing LAB. |
| 3049 | 16522779 | All G- bacteria potently up-regulated surface markers; however, these markers were not inhibited by weakly IL-12- and TNF-alpha-inducing LAB. |
| 3050 | 16522779 | All G- bacteria potently up-regulated surface markers; however, these markers were not inhibited by weakly IL-12- and TNF-alpha-inducing LAB. |
| 3051 | 16522779 | All G- bacteria potently up-regulated surface markers; however, these markers were not inhibited by weakly IL-12- and TNF-alpha-inducing LAB. |
| 3052 | 16517710 | CD45(RO/+) cells produce more TNF-alpha and IFN-gamma. |
| 3053 | 16504562 | An optimal vaccine against leishmaniasis should elicit parasite specific CD4+ and cytotoxic CD8+ T cells. |
| 3054 | 16504562 | An optimal vaccine against leishmaniasis should elicit parasite specific CD4+ and cytotoxic CD8+ T cells. |
| 3055 | 16504562 | Both CD4+ and CD8+ T cells were induced by DNA-LACK/MVA-LACK immunization. |
| 3056 | 16504562 | Both CD4+ and CD8+ T cells were induced by DNA-LACK/MVA-LACK immunization. |
| 3057 | 16504562 | The levels of IFN-gamma and TNF-alpha secreting CD8+ T cells were higher in splenocytes from DNA-LACK/MVA-LACK than in DNA-LACK/VV-LACK immunized animals. |
| 3058 | 16504562 | The levels of IFN-gamma and TNF-alpha secreting CD8+ T cells were higher in splenocytes from DNA-LACK/MVA-LACK than in DNA-LACK/VV-LACK immunized animals. |
| 3059 | 16504562 | Moreover, protection against L. major was significantly higher in DNA-LACK/MVA-LACK than in DNA-LACK/VV-LACK immunized animals when boosted with the same virus dose, and correlated with high levels of IFN-gamma and TNF-alpha secreting CD8+ T cells. |
| 3060 | 16504562 | Moreover, protection against L. major was significantly higher in DNA-LACK/MVA-LACK than in DNA-LACK/VV-LACK immunized animals when boosted with the same virus dose, and correlated with high levels of IFN-gamma and TNF-alpha secreting CD8+ T cells. |
| 3061 | 16503368 | Results showed that a significant enhancement of proliferative and cytotoxic activities accompanied with increased IFN-gamma and TNF-alpha production as well as decreased IL-4 production were obtained from the mice vaccinated with 4T1-ITAC. |
| 3062 | 20483237 | In fish, prior to pufferfish (Fugu rubripes and Tetraodon nigroviridis) and zebrafish (Danio rerio) genome sequencing, only a handful of cytokines like IL-1beta, TNF-alpha, TGFbeta, some CXC (including IL-8) and CC chemokine genes were identified. |
| 3063 | 20483237 | Pro-inflammatory cytokines like TNF's, IL-6 and IL-17 family have been cloned. |
| 3064 | 20483237 | Among the T(H)1 type interleukins, IL-2, IL-15, IL-12alpha, IL-12beta, IL-18 have been cloned. |
| 3065 | 20483237 | Among IL-10 and its family members, IL-10, IL-19/20, IL-22 and IL-26 have been discovered. |
| 3066 | 20483237 | However, T(H)2 cytokines (IL-4, IL-5 and IL-13), IL-3, IL-7 and IL-9 are yet to be discovered from fish. |
| 3067 | 16499578 | T-cell interferon-gamma (IFNgamma) and macrophage tumour necrosis factor-alpha (TNFalpha) activate chemokines such as, C-C chemokine ligand-2 (CCL2) and CCL5, which play a role in granuloma formation. |
| 3068 | 16499578 | T-cell interferon-gamma (IFNgamma) and macrophage tumour necrosis factor-alpha (TNFalpha) activate chemokines such as, C-C chemokine ligand-2 (CCL2) and CCL5, which play a role in granuloma formation. |
| 3069 | 16499578 | T-cell interferon-gamma (IFNgamma) and macrophage tumour necrosis factor-alpha (TNFalpha) activate chemokines such as, C-C chemokine ligand-2 (CCL2) and CCL5, which play a role in granuloma formation. |
| 3070 | 16499578 | T-cell interferon-gamma (IFNgamma) and macrophage tumour necrosis factor-alpha (TNFalpha) activate chemokines such as, C-C chemokine ligand-2 (CCL2) and CCL5, which play a role in granuloma formation. |
| 3071 | 16499578 | Circulating serum CCL2 was raised while CCL5 was lowered in leprosy, as compared with TB patients and healthy controls. |
| 3072 | 16499578 | Circulating serum CCL2 was raised while CCL5 was lowered in leprosy, as compared with TB patients and healthy controls. |
| 3073 | 16499578 | Circulating serum CCL2 was raised while CCL5 was lowered in leprosy, as compared with TB patients and healthy controls. |
| 3074 | 16499578 | Circulating serum CCL2 was raised while CCL5 was lowered in leprosy, as compared with TB patients and healthy controls. |
| 3075 | 16499578 | In leprosy, BCG induced greater CCL2 (P=0.01), TNFalpha (P=0.02) and somewhat greater CCL5 (P=0.08) than M. leprae, while CXCL8 induction was comparable. |
| 3076 | 16499578 | In leprosy, BCG induced greater CCL2 (P=0.01), TNFalpha (P=0.02) and somewhat greater CCL5 (P=0.08) than M. leprae, while CXCL8 induction was comparable. |
| 3077 | 16499578 | In leprosy, BCG induced greater CCL2 (P=0.01), TNFalpha (P=0.02) and somewhat greater CCL5 (P=0.08) than M. leprae, while CXCL8 induction was comparable. |
| 3078 | 16499578 | In leprosy, BCG induced greater CCL2 (P=0.01), TNFalpha (P=0.02) and somewhat greater CCL5 (P=0.08) than M. leprae, while CXCL8 induction was comparable. |
| 3079 | 16499578 | Overall levels of Mycobacterium-induced CCL2, TNFalpha and CXCL8 were two to threefold lower, and CCL5 was 10-fold lower in leprosy as compared with TB. |
| 3080 | 16499578 | Overall levels of Mycobacterium-induced CCL2, TNFalpha and CXCL8 were two to threefold lower, and CCL5 was 10-fold lower in leprosy as compared with TB. |
| 3081 | 16499578 | Overall levels of Mycobacterium-induced CCL2, TNFalpha and CXCL8 were two to threefold lower, and CCL5 was 10-fold lower in leprosy as compared with TB. |
| 3082 | 16499578 | Overall levels of Mycobacterium-induced CCL2, TNFalpha and CXCL8 were two to threefold lower, and CCL5 was 10-fold lower in leprosy as compared with TB. |
| 3083 | 16499578 | Reduced inducible CCL2 combined with a lowered TNFalpha response in lepromatous leprosy may contribute to the unrestricted growth and dissemination of mycobacteria found in the disease. |
| 3084 | 16499578 | Reduced inducible CCL2 combined with a lowered TNFalpha response in lepromatous leprosy may contribute to the unrestricted growth and dissemination of mycobacteria found in the disease. |
| 3085 | 16499578 | Reduced inducible CCL2 combined with a lowered TNFalpha response in lepromatous leprosy may contribute to the unrestricted growth and dissemination of mycobacteria found in the disease. |
| 3086 | 16499578 | Reduced inducible CCL2 combined with a lowered TNFalpha response in lepromatous leprosy may contribute to the unrestricted growth and dissemination of mycobacteria found in the disease. |
| 3087 | 16493050 | Myeloid cells had a CD4+CD11b+CD11c+CD16+CD123(low)HLA-DR- phenotype, expressed myeloperoxidase, and included a population of M-CSFR+ monocyte-lineage committed cells. |
| 3088 | 16493050 | Further culture of myeloid cells in serum-free medium with GM-CSF and IL-4 generated cells that had typical dendritic morphology; expressed high levels of MHC class I and II molecules, CD1a, CD11c, CD80, CD86, DC-SIGN, and CD40; and were capable of Ag processing, triggering naive T cells in MLR, and presenting Ags to specific T cell clones through the MHC class I pathway. |
| 3089 | 16493050 | Incubation of DCs with A23187 calcium ionophore for 48 h induced an expression of mature DC markers CD83 and fascin. |
| 3090 | 16493050 | The combination of GM-CSF with IL-4 provided the best conditions for DC differentiation. |
| 3091 | 16493050 | DCs obtained with GM-CSF and TNF-alpha coexpressed a high level of CD14, and had low stimulatory capacity in MLR. |
| 3092 | 16493038 | Using cytokine flow cytometry, we have defined four novel HLA-A*02-restricted dengue viral epitopes recognized by up to 1.5% of circulating CD8+ T cells in four donors after primary vaccination. |
| 3093 | 16493038 | Stimulation with variant peptides also altered the relative frequencies of the various subsets of cells that expressed IFN-gamma, TNF-alpha, MIP-1beta, and combinations of these cytokines. |
| 3094 | 16467342 | Evaluation of sedimentation rate, rheumatoid factor, C-reactive protein, and tumor necrosis factor for the diagnosis of infective endocarditis. |
| 3095 | 16467339 | Protection by anesthesia correlates with a delay in plasma LPS circulation, resulting in a delayed inflammatory response, particularly DNA binding activity of NF-kappaB and serum levels of tumor necrosis factor alpha, interleukin-6 (IL-6), and IL-10. |
| 3096 | 16467198 | Here, we assess the quality of the HIV-specific CD8(+) T-cell response by measuring 5 CD8(+) T-cell functions (degranulation, IFN-gamma, MIP-1beta, TNF-alpha, and IL-2) simultaneously in chronically HIV-infected individuals and elite nonprogressors. |
| 3097 | 16446013 | Our results demonstrate that two vaccines can activate DC of chronic HBV infection and healthy control by upregulation CD40 and CD86, high production of IL-12p70 and TNF-alpha. |
| 3098 | 16439533 | Multimeric soluble CD40 ligand and GITR ligand as adjuvants for human immunodeficiency virus DNA vaccines. |
| 3099 | 16439533 | Multimeric soluble CD40 ligand and GITR ligand as adjuvants for human immunodeficiency virus DNA vaccines. |
| 3100 | 16439533 | CD40 ligand (CD40L), a member of the tumor necrosis factor (TNF) superfamily (TNFSF), is one candidate adjuvant, but it has been difficult to use because it is normally expressed as a trimeric membrane molecule. |
| 3101 | 16439533 | CD40 ligand (CD40L), a member of the tumor necrosis factor (TNF) superfamily (TNFSF), is one candidate adjuvant, but it has been difficult to use because it is normally expressed as a trimeric membrane molecule. |
| 3102 | 16439533 | Fusion with the body of Acrp30 was used to produce the 2-trimer form, and fusion with the body of surfactant protein D was used to produce the 4-trimer form. |
| 3103 | 16439533 | Fusion with the body of Acrp30 was used to produce the 2-trimer form, and fusion with the body of surfactant protein D was used to produce the 4-trimer form. |
| 3104 | 16439533 | These CD40L-augmented DNA vaccines elicited strong CD8(+) T-cell responses but did not elicit significant CD4(+) T-cell or antibody responses. |
| 3105 | 16439533 | These CD40L-augmented DNA vaccines elicited strong CD8(+) T-cell responses but did not elicit significant CD4(+) T-cell or antibody responses. |
| 3106 | 16439533 | To test the applicability of the multimeric fusion protein approach to other TNFSFs, a 4-trimer construct for the ligand of glucocorticoid-induced TNF family-related receptor (GITR) was also prepared. |
| 3107 | 16439533 | To test the applicability of the multimeric fusion protein approach to other TNFSFs, a 4-trimer construct for the ligand of glucocorticoid-induced TNF family-related receptor (GITR) was also prepared. |
| 3108 | 16439533 | Multimeric soluble GITR ligand (GITRL) augmented the CD8(+) T-cell, CD4(+) T-cell, and antibody responses to DNA vaccination. |
| 3109 | 16439533 | Multimeric soluble GITR ligand (GITRL) augmented the CD8(+) T-cell, CD4(+) T-cell, and antibody responses to DNA vaccination. |
| 3110 | 16439533 | In summary, multimeric CD40L and GITRL are new adjuvants for DNA vaccines. |
| 3111 | 16439533 | In summary, multimeric CD40L and GITRL are new adjuvants for DNA vaccines. |
| 3112 | 16438373 | As inducers of DC ripening, the combination of antigenic components incorporated into the vaccine "lmmunovac Bh-4", (Klebsiella pneumoniae, Proteus vulgaris, Escherichia coli, Staphylococcus aureus), as well as K. pneumoniae LPS and TNF-alpha, were used. |
| 3113 | 16428759 | Interferons, tumor necrosis factor alpha, and interleukin-6 were not essential for the adjuvant effects of flagellin. |
| 3114 | 16426015 | Peak plasma concentrations of the CCR2 ligand monocyte chemotactic protein 1 and of tumor necrosis factor alpha were reached after 4 h and 2 h, respectively. |
| 3115 | 16426002 | Tumor necrosis factor (TNF) production in PBMC supernatants was measured by an enzyme-linked immunosorbent assay after TLR ligand stimulation and was dependent on gene transcription and NF-kappaB activation. |
| 3116 | 16426002 | Finally, three patients with a mutation in the IKBKG gene, encoding the NF-kappaB essential modulator (NEMO) protein, were evaluated as disease controls and were almost uniformly below the standard deviation of healthy donors for all ligands tested. |
| 3117 | 16425132 | Ten weeks after vaccination of neonates, percutaneous Japanese BCG had induced significantly higher frequencies of BCG-specific interferon- gamma -producing CD4(+) and CD8(+) T cells in BCG-stimulated whole blood than did intradermal Danish BCG. |
| 3118 | 16425132 | Similarly, percutaneous vaccination with Japanese BCG resulted in significantly greater secretion of the T helper 1-type cytokines interferon- gamma, tumor necrosis factor- alpha , and interleukin-2; significantly lower secretion of the T helper 2-type cytokine interleukin-4; and greater CD4(+) and CD8(+) T cell proliferation. |
| 3119 | 16424939 | Peptide vaccination of mice immune to LCMV or vaccinia virus causes serious CD8 T cell-mediated, TNF-dependent immunopathology. |
| 3120 | 16424939 | Peptide vaccination of mice immune to LCMV or vaccinia virus causes serious CD8 T cell-mediated, TNF-dependent immunopathology. |
| 3121 | 16424939 | Detailed analyses of the LCMV infected mice revealed enterocyte apoptosis and implicated TNF produced by peptide-specific CD8 T cells as the major mediator of disease. |
| 3122 | 16424939 | Detailed analyses of the LCMV infected mice revealed enterocyte apoptosis and implicated TNF produced by peptide-specific CD8 T cells as the major mediator of disease. |
| 3123 | 16420604 | Both DEN2 and LAV2 increased the expression of the phenotypic markers CD80, CD86, CD40, CD1a, HLA ABC and CD83, demonstrating cellular activation. |
| 3124 | 16420604 | Stimulated dendritic cells produced tumor necrosis factor-alpha in particular, and, to a lower extent, interleukin 6. |
| 3125 | 16412062 | Secreted levels of TNF-alpha and IL-1 from AM of patients with small, squamous, and large cell undifferentiated carcinoma were decreased compared to controls. |
| 3126 | 16412062 | Secreted levels of TNF-alpha and IL-1 from AM of patients with small, squamous, and large cell undifferentiated carcinoma were decreased compared to controls. |
| 3127 | 16412062 | AM from adenocarcinoma patients showed similar levels of IL-10, IL-6, IL-1 and TNF-alpha compared to controls. |
| 3128 | 16412062 | AM from adenocarcinoma patients showed similar levels of IL-10, IL-6, IL-1 and TNF-alpha compared to controls. |
| 3129 | 16412062 | Surface expression of ICAM-1 and CD83 was decreased on AM from patients with large, squamous and small cell carcinoma compared to controls but not adenocarcinoma. |
| 3130 | 16412062 | Surface expression of ICAM-1 and CD83 was decreased on AM from patients with large, squamous and small cell carcinoma compared to controls but not adenocarcinoma. |
| 3131 | 16388878 | Intra-tracheal infection of Balb/c mice with either mce mutant induced lower but progressive production of IFN-gamma and TNF-alpha, as well as larger delayed type hypersensitivity (DTH) reactions, than their parental H37Rv strain. |
| 3132 | 16385626 | Although our results indicate that DC-SIGN is not the major receptor for VLP in DC, this interaction contributes to the activation of DC surface antigens (HLA class I) and of various cytokines/chemokines, particularly TNF-alpha, IL-6, and RANTES. |
| 3133 | 16367944 | Immunization led to significant production of interferon (IFN)-gamma and tumour necrosis factor (TNF)-alpha by antigen-stimulated lymphocytes. |
| 3134 | 16367944 | In contrast, no significant induction of interleukin (IL)-4 or IL-10 was observed. |
| 3135 | 16365602 | They strongly express CD83, CD86, and CCR7 and have potent ability to migrate to CCL21. |
| 3136 | 16365602 | In addition, they were able to activate natural killer and T helper 1 (TH1) cells and to induce peptide-antigen-specific cytotoxic T lymphocytes more significantly than monocyte-derived DCs stimulated with a conventional cytokine cocktail of tumor necrosis factor-alpha, interleukin (IL)-1beta, IL-6, and PGE2 (monocyte-conditioned medium [MCM]-mimic DCs). |
| 3137 | 16365602 | The profound ability of OPA-DCs to stimulate these effectors is attributable to their higher expression of IL-12p70, IL-23, and IL-27 than MCM-mimic DCs, which was supported by the findings that the neutralization of IL-12p70 and IL-23 reduced the TH1 priming ability of OPA-DCs. |
| 3138 | 16353546 | This type of response involves participation of alveolar macrophages and T CD4+, CD8+ and T gammadelta lymphocytes, and production of cytokines such as IL-2, IFN-gamma, IL-12, IL-18 and TNF-alpha, as well as chemokines such as RANTES, MCP-1, MIP-1alpha and IL-8 which play an important role in the migration of different cell subpopulations to the infection site for the formation of granulome. |
| 3139 | 16352562 | To understand the role of cytokines during rotavirus infection, we assessed the kinetics of tumor necrosis factor alpha (TNF-alpha) and interleukin-6 (IL-6) (proinflammatory), IL-12 (Th1 inducer), gamma interferon (IFN-gamma) (Th1), IL-4 and IL-10 (Th2), and transforming growth factor beta (Th3) cytokine responses by enzyme-linked immunosorbent assay in serum and intestinal contents of neonatal gnotobiotic pigs and IL-12, IFN-gamma, IL-4, and IL-10 cytokine-secreting cell (CSC) responses of mononuclear cells from ileum, spleen, and blood by ELISPOT. |
| 3140 | 16352562 | In serum, IL-6 was significantly elevated at postinoculation day (PID) 1 in the VirHRV group and at PID 3 in both HRV groups. |
| 3141 | 16352562 | A significantly higher percentage of pigs had IFN-gamma and IL-10 responses in serum after VirHRV infection than after AttHRV infection or in controls. |
| 3142 | 16352562 | Higher protection rates may be associated with more balanced Th1- and Th2-type responses, but induction of higher earlier IFN-gamma (Th1) and proinflammatory cytokines triggered by VirHRV may also play an important role in the higher intestinal immunoglobulin A responses and protection rates induced by VirHRV. |
| 3143 | 16314006 | Specific IgG prevents enteroinvasive Escherichia coli/Salmonella typhi-induced diarrhea and may exert an effective protection by enhancing splenic NK cell activity, elevating IL-2 level and inhibiting excessive release of TNF-alpha in mice. |
| 3144 | 16313358 | We found changes in cell-surface expression of CD11a, CD44, CD45RB, CD49d, CD54 and CD62L on Env-specific CD8(+) T cells that appeared to differentiate them from other CD8(+) T cells within 1 week to 1 month following immunization. |
| 3145 | 16313358 | However, CD62L expression did not correlate with differences in the abilities of CTLs to proliferate or produce interferon gamma (IFN-gamma) and tumour necrosis factor alpha (TNF-alpha) in vitro in response to Env peptide stimulation. |
| 3146 | 16306600 | Th-cytotoxic T-lymphocyte chimeric epitopes extended by Nepsilon-palmitoyl lysines induce herpes simplex virus type 1-specific effector CD8+ Tc1 responses and protect against ocular infection. |
| 3147 | 16306600 | As a model antigen, the HSV-1 glycoprotein B498-505 (gB498-505) CD8+ CTL epitope was synthesized in line with the Pan DR peptide (PADRE), a universal CD4+ Th epitope. |
| 3148 | 16306600 | The palmitoyl-tailed Th-CTL chimeric epitopes provoked cell surface expression of major histocompatibility complex and costimulatory molecules and production of interleukin-12 and tumor necrosis factor alpha proinflammatory cytokines by immature dendritic cells. |
| 3149 | 16305402 | A ten-fold lower dose (0.5 microg instead of 5 microg) of CpG ODN in nanoparticles was adequate to obtain levels of IFN-gamma, TNF-alpha, and IL-2 comparable to those observed following immunisations in saline. |
| 3150 | 16303787 | Maturation of human monocyte-derived dendritic cells (MoDCs) in the presence of prostaglandin E2 optimizes CD4 and CD8 T cell-mediated responses to protein antigens: role of PGE2 in chemokine and cytokine expression by MoDCs. |
| 3151 | 16303787 | Maturation of human monocyte-derived dendritic cells (MoDCs) in the presence of prostaglandin E2 optimizes CD4 and CD8 T cell-mediated responses to protein antigens: role of PGE2 in chemokine and cytokine expression by MoDCs. |
| 3152 | 16303787 | We demonstrate here that the addition of PGE2 to TNF for the maturation of MoDCs enhanced CD4 and CD8 T cell proliferative responses to neoantigen and recall antigen, and enhanced Th1-type responses. |
| 3153 | 16303787 | We demonstrate here that the addition of PGE2 to TNF for the maturation of MoDCs enhanced CD4 and CD8 T cell proliferative responses to neoantigen and recall antigen, and enhanced Th1-type responses. |
| 3154 | 16303787 | The increased stimulatory capacity of MoDCs matured with PGE2 was associated with a fully mature, migratory-type MoDC phenotype and more rapid down-regulation of the expression of inflammatory chemokines, with up-regulated expression of the constitutive chemokines TARC and MDC. |
| 3155 | 16303787 | The increased stimulatory capacity of MoDCs matured with PGE2 was associated with a fully mature, migratory-type MoDC phenotype and more rapid down-regulation of the expression of inflammatory chemokines, with up-regulated expression of the constitutive chemokines TARC and MDC. |
| 3156 | 16303787 | In addition, although MoDCs matured with TNF and PGE2 selectively produced the inhibitory IL-12p40 subunit at steady state, they were able to produce the bioactive IL-12p70 heterodimer after stimulation with CD40 ligand and/or IFN-gamma. |
| 3157 | 16303787 | In addition, although MoDCs matured with TNF and PGE2 selectively produced the inhibitory IL-12p40 subunit at steady state, they were able to produce the bioactive IL-12p70 heterodimer after stimulation with CD40 ligand and/or IFN-gamma. |
| 3158 | 16303787 | Despite increased IL-6 mRNA expression, MoDCs matured with PGE2 did not overcome the suppressive effects of CD4+ CD25+ T cells in allogeneic mixed lymphocyte reactions. |
| 3159 | 16303787 | Despite increased IL-6 mRNA expression, MoDCs matured with PGE2 did not overcome the suppressive effects of CD4+ CD25+ T cells in allogeneic mixed lymphocyte reactions. |
| 3160 | 16286158 | Vaccines containing the ginseng-fraction Rb1 induced serum-detectable amounts of IL-4 and IL-10 as early as 24h after primary injection that was confirmed in sera collected at 24 and 72 h post re-vaccination. |
| 3161 | 16286158 | Five weeks after booster, immune lymphocytes were still producing large amounts of cytokines including IFN-gamma, IL-2, IL-4, IL-10 and TNF-alpha and the antibody titres were still similar to those titres recorded 1 week post booster. |
| 3162 | 16283303 | Patients were vaccinated either by intradermal injection of PSA-peptide and GM-CSF or by intravenous administration of autologous dendritic cells pulsed with PSA-peptide at weeks 1, 4 and 10. |
| 3163 | 16283303 | The phenotype of recovered T cells demonstrated variable proportions of CD4+CD8-, CD4-CD8+ and CD4+CD8+ T cell populations. |
| 3164 | 16283303 | Cytokine analysis of PSA-peptide stimulated T cells per bead array assay exhibited specific IFN-gamma and TNF-alpha response in six of seven patients. |
| 3165 | 16283303 | Specific IL-4 response was observed in five patients, while IL-10 response was detected in one patient. |
| 3166 | 16279537 | The generation of ripe dendrite cells (DC) of marrow origin was obtained with the use of the vaccine Immunovac-BN-4, an immunomodulator of microbial origin, as well as Klebsiella pneumoniae LPS and TNF-alpha, as ripening inducers. |
| 3167 | 16279537 | The generation of ripe dendrite cells (DC) of marrow origin was obtained with the use of the vaccine Immunovac-BN-4, an immunomodulator of microbial origin, as well as Klebsiella pneumoniae LPS and TNF-alpha, as ripening inducers. |
| 3168 | 16279537 | The immunophenotype of cells altered from CD34+, CD38-, CD40-, CD80-, CD86-, MHC I-, MHC II-, F4/80- to CD34-, CD38+, CD40+, CD80+, MHC I+, MHC II+, F4/ 80(low). |
| 3169 | 16279537 | The immunophenotype of cells altered from CD34+, CD38-, CD40-, CD80-, CD86-, MHC I-, MHC II-, F4/80- to CD34-, CD38+, CD40+, CD80+, MHC I+, MHC II+, F4/ 80(low). |
| 3170 | 16279537 | In culture medium with ripe DC the levels of such cytokines as IL-1b, IL-6, IL-12, IFN-gamma, TNF-alpha significantly increased and the production of IL-4 decreased. |
| 3171 | 16279537 | In culture medium with ripe DC the levels of such cytokines as IL-1b, IL-6, IL-12, IFN-gamma, TNF-alpha significantly increased and the production of IL-4 decreased. |
| 3172 | 16279537 | The content of IL-2 and IL-10 remained unchanged. |
| 3173 | 16279537 | The content of IL-2 and IL-10 remained unchanged. |
| 3174 | 16278080 | Tumour necrosis factor alpha (TNF-alpha) was measured in the supernates of cultured cells and both TNF-alpha and interleukin-4 (IL-4) were measured in serum samples. |
| 3175 | 16275627 | Chlorophyllin attenuates IFN-gamma expression in lipopolysaccharide-stimulated murine splenic mononuclear cells via suppressing IL-12 production. |
| 3176 | 16275627 | RT-PCR analysis showed that LPS-activated IFN-gamma expression gradually declined by CHL treatment in a dose dependent manner while mRNA production of TNF-alpha, IL-2, and FasL was not changed. |
| 3177 | 16275627 | CHL also suppressed IL-12 production (p70, a heterodimer of p40 and p35) and the mRNA expression of IL-12 p40 and IL-12 receptors (both IL-12Rbeta1 and IL-12Rbeta2), which are involved in the induction of IFN-gamma expression. |
| 3178 | 16275627 | Furthermore, an electrophoretic mobility shift assay showed that CHL inhibited DNA binding activity of NF-kappaB, STAT-3, and STAT-4 to their cognate DNA recognition motifs, all of which contribute to the IL-12-induced IFN-gamma transcription. |
| 3179 | 16275627 | Exogenous addition of recombinant IL-12 abrogated the inhibitory effect of CHL on IFN-gamma and its mRNA expression in LPS-activated splenocytes. |
| 3180 | 16275627 | Collectively, these results show that CHL inhibits IFN-gamma production by LPS-stimulated splenic mononuclear cells due to down-regulation of IL-12 production. |
| 3181 | 16272329 | Such suppression was also evident upon the Salmonella-CFA/I infection of macrophages resulting in diminished TNF-alpha, IL-1, and IL-6 production and suggesting that the CFA/I fimbrial expression by Salmonella may protect against a proinflammatory disease. |
| 3182 | 16272329 | This protective effect was accompanied by a loss of encephalitogenic IFN-gamma-secreting Th cells and was replaced with an increase in IL-4, IL-10, and IL-13 secretion. |
| 3183 | 16269200 | Upon exposure to the various MS types, Mphi increased only the production of reactive oxygen intermediates (ROI), while the production of nitric oxide (NO), tumor necrosis factor alpha (TNF-alpha), and the expression of cyclooxigenase-2 (COX-2), inducible NO synthase (iNOS), the cell surface markers MHC class I and II, and CD 86 remained unaffected. |
| 3184 | 16265904 | In particular, an important role for CD8+ T cells has been uncovered, as well divergent roles for members of the tumor necrosis factor (TNF) family of molecules, including TNF and lymphotoxin alpha. |
| 3185 | 16257383 | In vivo depletion of CD4+CD25+ regulatory T cells enhances the antigen-specific primary and memory CTL response elicited by mature mRNA-electroporated dendritic cells. |
| 3186 | 16257383 | We point out that the mRNA electroporation results in a negative effect on the interleukin (IL)-12p70, IL-6, and tumor necrosis factor-alpha secretion after maturation. |
| 3187 | 16257383 | In addition, a significant improvement in CTL response is obtained both in the primary and in the memory effector phases when CD4+CD25+ regulatory T cells (Treg) are depleted in vivo prior to immunization. |
| 3188 | 16253558 | Real-time RT-PCR assays revealed that the mRNA levels for IFNgamma, TNFalpha, and IL-8 rose over the first few days of TB pleuritis and then declined over the 9 days of the study. |
| 3189 | 16253558 | Real-time RT-PCR assays revealed that the mRNA levels for IFNgamma, TNFalpha, and IL-8 rose over the first few days of TB pleuritis and then declined over the 9 days of the study. |
| 3190 | 16253558 | The intracellular survival of mycobacteria was enhanced when endogeous TNFalpha activity was neutralized with anti-rgpTNFalpha antiserum. rgp RANTES (CCL5) upregulated mRNA levels for TNFalpha, IL-1beta, MCP-1 (CCL2), and IL-8 (CXCL8) in alveolar and peritoneal macrophages. |
| 3191 | 16253558 | The intracellular survival of mycobacteria was enhanced when endogeous TNFalpha activity was neutralized with anti-rgpTNFalpha antiserum. rgp RANTES (CCL5) upregulated mRNA levels for TNFalpha, IL-1beta, MCP-1 (CCL2), and IL-8 (CXCL8) in alveolar and peritoneal macrophages. |
| 3192 | 16253122 | Tumour necrosis factor (TNF)-alpha and interleukin (IL)-6 were quantified in serum of both the test and control groups. |
| 3193 | 16253122 | Tumour necrosis factor (TNF)-alpha and interleukin (IL)-6 were quantified in serum of both the test and control groups. |
| 3194 | 16253122 | Mice that had received whole IgM effluent (1.5 mg/l of anti-LPS O6 IgM antibodies) before the challenge with LPS O6 presented 20.5 microg/l of IL-6 and 1.5 microg/l of TNF-alpha. |
| 3195 | 16253122 | Mice that had received whole IgM effluent (1.5 mg/l of anti-LPS O6 IgM antibodies) before the challenge with LPS O6 presented 20.5 microg/l of IL-6 and 1.5 microg/l of TNF-alpha. |
| 3196 | 16246469 | However, both wild type meningococcal LOS and KDO(2)-lipid A, significantly up-regulated CD80, CD83 and CD86 and released significantly higher amounts of IL-12p70, IL-6, IL-10, TNFalpha, MCP-1, IP-10 and RANTES. |
| 3197 | 16246469 | Further, DCs stimulated with wild type or KDO(2)-lipid A but not meningococcal lipid A or penta-acylated KDO(2)-lipid A stimulated naïve allogeneic CD4+ T cells to secrete enhanced levels of IFN-gamma, relative to T cells primed with immature DCs. |
| 3198 | 16246469 | In contrast to Escherichia coli LPS, IL-5 production was enhanced or maintained in CD4+ T-cells stimulated with MDDC exposed to wild-type meningococcal LOS and KDO(2)-lipid A. |
| 3199 | 16246469 | These data suggest that KDO linked to a fully acylated meningococcal lipid A is required for meningococcal endotoxin's immunostimulatory activity of human MDDC via TLR4/MD-2 and that different endotoxin structures influence Th responses mediated by MDDC. |
| 3200 | 16242986 | IL-1, LPS and butyrate but not TNF, IL-6 and IL-8, increased the Stx mediated cytotoxicity. |
| 3201 | 16242273 | Characterization of the cytokine response of bovine monocyte-derived macrophages by real-time polymerase chain reaction indicated that in vitro stimulation of these cells with rBoIL 2 resulted in a profound up-regulation of genes encoding tumor necrosis factor-alpha, IL 12p40, and interferon-gamma reflecting activation of the cells. |
| 3202 | 16239537 | The antipentasaccharide antibodies induced by the conjugate inhibited the secretion of tumor necrosis factor alpha, interleukin-6, and NO by LOS-stimulated J774A.1 cells. |
| 3203 | 16233848 | In approaches using a poorly immunogenic melanoma B16, the effects of various cytokines (IL-1beta, -2, -4, -6 and -12, IFN-beta and -gamma, GM-CSF and TNF-alpha) were assessed in combination with HCLV. |
| 3204 | 16232228 | Immunization led to significant production of interferon (IFN)-gamma and tumour necrosis factor (TNF)-alpha by antigen-stimulated lymphocytes. |
| 3205 | 16232228 | In contrast, no significant induction of interleukin (IL)-4 or IL-10 was observed. |
| 3206 | 16224278 | When T-cell responses were compared in allogeneic mixed leukocyte reaction, DCs stimulated with Ribomunyl induced higher levels of IFNgamma than DCs stimulated with the cytokine cocktail: tumor necrosis factor-alpha, IL-1beta, IL-6, and prostaglandin E2. |
| 3207 | 16224278 | In the presence of IL-10 neutralizing antibodies, DC IL-12p70 production and T-cell IFNgamma were increased in vitro. |
| 3208 | 16224278 | Similarly, DCs stimulated with Ribomunyl, IFNgamma, and anti-IL-10 induced high levels of tetanus toxoid-specific T-cell proliferation and IFNgamma secretion. |
| 3209 | 16224278 | Thus, MoDCs generated in SFM efficiently stimulate T-cell IFNgamma production after maturation in the presence of a clinical-grade TLR4 agonist and IL-10 neutralization. |
| 3210 | 16196366 | AML cells or monocytes were cultured in RPMI 1640 media supplemented with foetal bovine serum or autologous serum where possible and different combinations of cytokines GM-CSF, IL-4 and TNF-alpha. |
| 3211 | 16186817 | Recently activated, but not resting, CD4(+) T cells express CD154, providing costimulatory signals to B cells and antigen-presenting cells (APCs). |
| 3212 | 16186817 | Therefore, de novo CD154 expression after stimulation identifies antigen-specific CD4(+) T cells. |
| 3213 | 16186817 | Using this assay, we found that stimulated cells expressing tumor necrosis factor (TNF)-alpha, interleukin (IL)-2 or interferon (IFN)-gamma were predominantly CD154(+). |
| 3214 | 16186817 | For vaccine- or pathogen-specific responses, we found substantial heterogeneity in expression of CD154 and cytokines, suggesting previously unrecognized diversity in abilities of responding cells to stimulate APCs through CD40. |
| 3215 | 16186238 | Interleukin 1 alpha (IL1alpha), alpha interferon (IFN-alpha), IL6, tumour necrosis factor alpha (TNF-alpha), GROalpha and MIP-1beta mRNA were elevated soon after infection, and expression coincided with virus replication. |
| 3216 | 16186238 | A biphasic response was observed for RANTES, IFN-gamma, IL4, IL10 and IL12-p40, with increased mRNA levels early during virus replication followed by a later increase that coincided with pulmonary inflammation. |
| 3217 | 16177369 | Redirection of TT into the ON/E coincided with elevated production of interleukin 6 (IL-6) but not IL-1beta or tumor necrosis factor alpha in the nasal mucosa. |
| 3218 | 16176850 | Regulation of CD4 T cell memory by OX40 (CD134). |
| 3219 | 16176850 | Recent advances in studies of T cell memory have implicated the tumor-necrosis-factor receptor (TNFR) family member, OX40 (CD134), as a key co-stimulatory molecule involved in the regulation of CD4 memory T cells. |
| 3220 | 16164822 | On days 0, 30 and 90 a quantitative analysis was performed on lymphoproliferative responses to polyclonal mitogens, IL-2 and the specific antigen U, the production of specific serum and saliva IgA, IgM and IgG antibodies to all components of U and the concentration of pro-inflammatory cytokines. |
| 3221 | 16164822 | The highest concentrations of serum proinflammatory cytokines TNF-alpha, IL-1beta and IL-6 were registered at baseline followed by a decrease until the end of the observation period. |
| 3222 | 16163436 | Intra-articular administration of cDNA coding for soluble TNF receptors, IL-1, or IL-1Ra decreases signs of the disease in animal models. |
| 3223 | 16154304 | In this study, we investigated the effect of babassu mesocarp flour aqueous extract (BM) on C3H/HePas mice peritoneal cellular migration and macrophage activation by measuring the nitric oxide (NO), hydrogen peroxide (H(2)O(2)) and tumor necrosis factor (TNF) release, spreading activity and major histocompatibility complex (MHC) class II expression. |
| 3224 | 16154304 | In this study, we investigated the effect of babassu mesocarp flour aqueous extract (BM) on C3H/HePas mice peritoneal cellular migration and macrophage activation by measuring the nitric oxide (NO), hydrogen peroxide (H(2)O(2)) and tumor necrosis factor (TNF) release, spreading activity and major histocompatibility complex (MHC) class II expression. |
| 3225 | 16154304 | Our results demonstrate that BM injected once ip in mice at 10 and 20 mg/kg increased the cellular influx to the peritoneal cavity, the MHC class II expression and the spreading ability, and also induced the production of NO, TNF and H(2)O(2). |
| 3226 | 16154304 | Our results demonstrate that BM injected once ip in mice at 10 and 20 mg/kg increased the cellular influx to the peritoneal cavity, the MHC class II expression and the spreading ability, and also induced the production of NO, TNF and H(2)O(2). |
| 3227 | 16152624 | Identification of new NY-ESO-1 epitopes recognized by CD4+ T cells and presented by HLA-DQ B1 03011. |
| 3228 | 16152624 | Since CD4+ T cells play a critical role in generating and maintaining antigen-specific cellular and humoral immune responses, we searched for new NY-ESO-1 epitopes presented by MHC class II molecules. |
| 3229 | 16152624 | CD4+ T cells of patients with NY-ESO-1-expressing cancer were presensitized with 18-mer overlapping synthetic peptides spanning the entire sequence of NY-ESO-1. |
| 3230 | 16152624 | Two partly overlapping NY-ESO-1 epitopes p49-66 and p55-72 were identified as targets for NY-ESO-1-specific CD4+ T cells. |
| 3231 | 16152624 | Peptide-specific CD4+ T-cell clones were generated by repetitive stimulation with NY-ESO-1 p49-66 and p55-72. |
| 3232 | 16152624 | Further experiments confirmed distinct specificities for the CD4+ T-cell clones indicating that at least 2 different CD4+ T-cell epitopes are located in the region p49-72 of the NY-ESO-1 sequence. |
| 3233 | 16152624 | The specific production of IFN-gamma and TNF-alpha suggests that the NY-ESO-1-specific CD4+ T-cell clones belong to the Th1 subtype. |
| 3234 | 16129449 | A low, average frequency (0.61%) of measles virus (MV)-specific CD4 and CD8+ T cells was detected in rhesus monkeys experimentally infected with or vaccinated against MV. |
| 3235 | 16129449 | Both IFN-gamma and TNF-alpha positive T cells were visualized by flow cytometry. |
| 3236 | 20476989 | Many immune cytokines are subject to circadian variation, for example, interleukin-1, -6, -10 and -12, macrophage migration inhibitory factor, tumor necrosis factor-alpha and interferon-gamma. |
| 3237 | 16122847 | Mo-DCs pulsed with rUreA activated allogenic CD56+ NK-cells, as determined by TNF-alpha and IFN-gamma secretion, but not allogenic CD4+/CD45RA+ naïve T-cells. |
| 3238 | 16116238 | Viral vectors may address both of these issues, as they can be used to deliver intact tumor Ags to DCs, and have been shown to inhibit the suppression mediated by CD4+CD25+ regulatory T cells. |
| 3239 | 16116238 | Viral vectors may address both of these issues, as they can be used to deliver intact tumor Ags to DCs, and have been shown to inhibit the suppression mediated by CD4+CD25+ regulatory T cells. |
| 3240 | 16116238 | Viral vectors may address both of these issues, as they can be used to deliver intact tumor Ags to DCs, and have been shown to inhibit the suppression mediated by CD4+CD25+ regulatory T cells. |
| 3241 | 16116238 | VRP infection of immature DCs was superior to TNF-alpha treatment at inducing phenotypic maturation of DCs, and was comparable to LPS stimulation. |
| 3242 | 16116238 | VRP infection of immature DCs was superior to TNF-alpha treatment at inducing phenotypic maturation of DCs, and was comparable to LPS stimulation. |
| 3243 | 16116238 | VRP infection of immature DCs was superior to TNF-alpha treatment at inducing phenotypic maturation of DCs, and was comparable to LPS stimulation. |
| 3244 | 16116238 | Additionally, VRP-infected DC cultures secreted substantial amounts of the proinflammatory cytokines IL-6, TNF-alpha, and IFN-alpha. |
| 3245 | 16116238 | Additionally, VRP-infected DC cultures secreted substantial amounts of the proinflammatory cytokines IL-6, TNF-alpha, and IFN-alpha. |
| 3246 | 16116238 | Additionally, VRP-infected DC cultures secreted substantial amounts of the proinflammatory cytokines IL-6, TNF-alpha, and IFN-alpha. |
| 3247 | 16116238 | Finally, DCs transduced with a VRP encoding the influenza matrix protein (FMP) stimulated 50% greater expansion of FMP-specific CD8+ CTL when compared with TNF-alpha-matured DCs pulsed with an HLA-A*0201-restricted FMP peptide. |
| 3248 | 16116238 | Finally, DCs transduced with a VRP encoding the influenza matrix protein (FMP) stimulated 50% greater expansion of FMP-specific CD8+ CTL when compared with TNF-alpha-matured DCs pulsed with an HLA-A*0201-restricted FMP peptide. |
| 3249 | 16116238 | Finally, DCs transduced with a VRP encoding the influenza matrix protein (FMP) stimulated 50% greater expansion of FMP-specific CD8+ CTL when compared with TNF-alpha-matured DCs pulsed with an HLA-A*0201-restricted FMP peptide. |
| 3250 | 16116197 | All PPS-containing preparations induced IL-6 and TNF-alpha from wild-type, but not TLR2-/-, macrophages. |
| 3251 | 16116197 | The commercial 23-valent PPS vaccine, Pneumovax-23 also contained TLR ligands (TLR2 and TLR4), which were absolutely critical for the IgG-inducing activity of the vaccine in mice. |
| 3252 | 16115702 | The mutant increased IL-12p40, TNFalpha and nitric oxide production by IFNgamma-stimulated bone marrow macrophages but cholera toxin did not. |
| 3253 | 16115702 | The mutant increased IL-12p40, TNFalpha and nitric oxide production by IFNgamma-stimulated bone marrow macrophages but cholera toxin did not. |
| 3254 | 16115702 | These findings indicate that the mutant may induce Thl-type response to the vaccine through its IL-12 and TNFalpha induction by macrophages. |
| 3255 | 16115702 | These findings indicate that the mutant may induce Thl-type response to the vaccine through its IL-12 and TNFalpha induction by macrophages. |
| 3256 | 16113842 | Furthermore, B-CLL-DCs generated from the 2 CLL subgroups up-regulated MHC-II, CD80, CD86, CD83, CD40, and CD54 and down-regulated CD206 in response to stimulation with a cocktail of cytokines (CyC) and secreted increased levels of tumor necrosis factor alpha, interleukin (IL)-8, IL-6, IL-12 (p70), and RANTES in a manner typical of mature normal-DCs. |
| 3257 | 16113340 | Following intranasal inoculation, Vibrio cholerae KFV101 (DeltactxAB DeltahapA DeltahlyA DeltartxA) colonizes and stimulates tumor necrosis factor alpha and interleukin 1beta (IL-1beta) in mice, similar to what occurs with isogenic strain P4 (DeltactxAB), but is less virulent and stimulates reduced levels of IL-6, demonstrating a role for accessory toxins in pathogenesis. |
| 3258 | 16113315 | Dendritic cells were produced by culturing murine bone marrow progenitor cells in medium containing granulocyte-macrophage colony-stimulating factor and tumor necrosis factor alpha. |
| 3259 | 16107268 | In addition, BS significantly inhibited the production of cytokines such as interleukin (IL)-1beta, IL-2, interferon (IFN)-gamma and tumor necrosis factor (TNF)-alpha, by peripheral blood mononuclear cells (PBMNC) and soluble IL-2 receptor expression at concentrations greater than 1 microg/ml. |
| 3260 | 16098219 | Despite the significant impact of LPS composition on the adhesion and phagocytosis of N. meningitidis no differences were found in terms of cytokine levels secreted by DC for IL1-beta, IL-6, IL-8, TNF-alpha, IFN-gamma and GM-CSF. |
| 3261 | 16081844 | IFN-gamma and TNF-alpha responses to inactivated DEN Ags were detected in up to 0.54 and 1.17% of total circulating CD4+ T cells, respectively. |
| 3262 | 16081844 | IFN-gamma and TNF-alpha responses to inactivated DEN Ags were detected in up to 0.54 and 1.17% of total circulating CD4+ T cells, respectively. |
| 3263 | 16081844 | IFN-gamma and TNF-alpha responses to inactivated DEN Ags were detected in up to 0.54 and 1.17% of total circulating CD4+ T cells, respectively. |
| 3264 | 16081844 | IFN-gamma and TNF-alpha responses to inactivated DEN Ags were detected in up to 0.54 and 1.17% of total circulating CD4+ T cells, respectively. |
| 3265 | 16081844 | The ratio of TNF-alpha- to IFN-gamma-producing CD4+ T cells was higher after stimulation with Ags from heterologous DEN serotypes. |
| 3266 | 16081844 | The ratio of TNF-alpha- to IFN-gamma-producing CD4+ T cells was higher after stimulation with Ags from heterologous DEN serotypes. |
| 3267 | 16081844 | The ratio of TNF-alpha- to IFN-gamma-producing CD4+ T cells was higher after stimulation with Ags from heterologous DEN serotypes. |
| 3268 | 16081844 | The ratio of TNF-alpha- to IFN-gamma-producing CD4+ T cells was higher after stimulation with Ags from heterologous DEN serotypes. |
| 3269 | 16081844 | IFN-gamma and TNF-alpha responses to individual HLA class II-restricted peptide epitopes were detected in up to 0.05 and 0.27% of CD4+ T cells, respectively. |
| 3270 | 16081844 | IFN-gamma and TNF-alpha responses to individual HLA class II-restricted peptide epitopes were detected in up to 0.05 and 0.27% of CD4+ T cells, respectively. |
| 3271 | 16081844 | IFN-gamma and TNF-alpha responses to individual HLA class II-restricted peptide epitopes were detected in up to 0.05 and 0.27% of CD4+ T cells, respectively. |
| 3272 | 16081844 | IFN-gamma and TNF-alpha responses to individual HLA class II-restricted peptide epitopes were detected in up to 0.05 and 0.27% of CD4+ T cells, respectively. |
| 3273 | 16081844 | TNF-alpha- to IFN-gamma-positive CD4+ T cell ratios varied between peptides, but the ratio of the sum of responses was highest against heterologous serotypes. |
| 3274 | 16081844 | TNF-alpha- to IFN-gamma-positive CD4+ T cell ratios varied between peptides, but the ratio of the sum of responses was highest against heterologous serotypes. |
| 3275 | 16081844 | TNF-alpha- to IFN-gamma-positive CD4+ T cell ratios varied between peptides, but the ratio of the sum of responses was highest against heterologous serotypes. |
| 3276 | 16081844 | TNF-alpha- to IFN-gamma-positive CD4+ T cell ratios varied between peptides, but the ratio of the sum of responses was highest against heterologous serotypes. |
| 3277 | 16078439 | The obtained results will direct our further investigations toward obtaining mAbs for receptors for TNFalpha and IFNgamma, transfection of suppressor gene into tumor cell cultures and genes for IL-2 and TNFalpha. |
| 3278 | 16053938 | The level of IFN-gamma, IL-4 and TNF-alpha released by spleen lymphocytes stimulated with PPD was detected with ELISA. |
| 3279 | 16053938 | The level of IFN-gamma, IL-4 and TNF-alpha released by spleen lymphocytes stimulated with PPD was detected with ELISA. |
| 3280 | 16053938 | Vaccination with pcD85B induced high level of IFN-gamma and TNF-alpha. |
| 3281 | 16053938 | Vaccination with pcD85B induced high level of IFN-gamma and TNF-alpha. |
| 3282 | 16041032 | LcrV triggers the release of interleukin 10 (IL-10) by host immune cells and suppresses proinflammatory cytokines such as tumor necrosis factor alpha and gamma interferon as well as innate defense mechanisms required to combat the pathogenesis of plague. |
| 3283 | 16041023 | Recombinant Ags 85A, 85B, and 85C induced significant lymphocyte proliferation as well as the production of gamma interferon (IFN-gamma), interleukin-2 (IL-2), IL-12, and tumor necrosis factor alpha (TNF-alpha), but not IL-4, from low and medium shedders. |
| 3284 | 16041023 | The 35-kDa protein also induced significant lymphocyte proliferation as well as the production of IFN-gamma and IL-4 from low and medium shedders. |
| 3285 | 16041023 | CD4(+) T cells and CD25(+) (IL-2R) T cells were stimulated the most by 85A and 85B, while the 35-kDa protein primarily stimulated CD21(+) B cells involved in humoral immune responses. |
| 3286 | 16041007 | Mucosal type 2/3 responses (producing interleukin-4 [IL-4], IL-6 and/or transforming growth factor beta) could be necessary for optimal induction of protective secretory immunoglobulin A responses. |
| 3287 | 16041007 | On the other hand, systemic type 1 responses (including gamma interferon [IFN-gamma], tumor necrosis factor alpha, and optimal cytotoxic T-cell responses) are likely to be critical for protection against the disseminated intracellular replication that occurs after mucosal invasion. |
| 3288 | 16041007 | T. cruzi infection followed by nifurtimox treatment rescue was used to immunize CD4, CD8, beta2-microglobulin, inducible nitric oxide synthase (iNOS), IL-12, IFN-gamma, and IL-4 knockout mice. |
| 3289 | 16041007 | Despite the previously demonstrated importance of CD4(+) T cells, CD8(+) T cells, and nitric oxide for T. cruzi immunity, CD4, CD8, and iNOS knockout mice developed mucosal and systemic protective immunity. |
| 3290 | 16041007 | However, IL-12, IFN-gamma, and beta2-microglobulin-deficient mice failed to develop mucosal or systemic protection. |
| 3291 | 16037714 | Fas ligand and TNF-related apoptosis-inducing ligand induction on infiltrating lymphocytes in bladder carcinoma by bacillus Calmette-Guérin treatment. |
| 3292 | 16037410 | Dendritic cells differentiated in the presence of IFN-{beta} and IL-3 are potent inducers of an antigen-specific CD8+ T cell response. |
| 3293 | 16037410 | Classically, mature monocyte-derived DC are generated in vitro in the presence of interleukin (IL)-4, granulocyte macrophage-colony stimulating factor, and inflammatory cytokines (G4-DC). |
| 3294 | 16037410 | Recently, it has been described that DC can also be generated in the presence of IL-3 and interferon (IFN)-beta and that these DC are efficiently matured using polyriboinosinic polyribocytidylic acid (I3-DC). |
| 3295 | 16037410 | Phenotypic characterization of the DC revealed differences in the expression of the monocyte marker CD14 and the maturation marker CD83. |
| 3296 | 16037410 | Low expression of CD14 and high expression of CD83 characterized G4-DC, whereas I3-DC displayed intermediate expression of CD14 and CD83. |
| 3297 | 16037410 | Upon CD40 ligation, G4-DC produced lower amounts of IFN-alpha and pulmonary and activation-regulated chemokine, similar amounts of IL-6, macrophage-inflammatory protein (MIP)-1alpha, and MIP-1beta, and higher amounts of IL-12 p70, tumor necrosis factor alpha, and MIP-3beta than I3-DC. |
| 3298 | 16037410 | Finally, in vitro stimulations showed that fresh and frozen peptide-loaded I3-DC are more potent inducers of Melan-A-specific CD8(+) T cell responses than G4-DC. |
| 3299 | 16029505 | The results demonstrate that as monocytes passed through the column matrix, they became activated and differentiated into semi-mature DC expressing significantly increased levels of class II, CD83 and CD86 (markers associated with maturing DC) and reduced expression of the monocyte markers CD14 and CD36. |
| 3300 | 16029505 | After CD8 T cells were stimulated by DC loaded with malignant cells, they mediated increased apoptosis of residual CTCL cells and TNF-alpha secretion indicating development of enhanced cytolytic function. |
| 3301 | 16027518 | Neutralization of the biological activity of some immunosuppressive cytokines produced by RCC (IL-6 and tumor necrosis factor-alpha) with monoclonal antibodies is currently under investigation. |
| 3302 | 16025264 | There has been a recent interest in using IL-15 to enhance antitumor activity in several models because of its ability to stimulate CD8+ T cell expansion, inhibit apoptosis and promote memory T cell survival and maintenance. |
| 3303 | 16025264 | In this study, we determined whether IL-15 used as immunologic adjuvant would augment vaccine-primed CD8+ T cell immunity against C6VL and further improve the survival of tumor-bearing mice. |
| 3304 | 16025264 | We report that IL-15 given after C6VL lysate-pulsed dendritic cell vaccines stimulated local and systemic expansion of NK, NKT and CD8+ CD44hi T cells. |
| 3305 | 16025264 | T cells from mice infused with IL-15 following vaccination did not secrete increased levels of tumor-specific TNF-alpha or IFN-gamma or have enhanced C6VL-specific CTL activity compared to T cells from recipients of the vaccine alone. |
| 3306 | 16025264 | Thus, while activated- and memory-phenotype CD8+ T cells were dramatically expanded by IL-15 infusion, vaccine-primed CD8+ T cell specific for C6VL were not significantly expanded. |
| 3307 | 16025264 | This is the first account of using IL-15 as an adjuvant in a therapeutic model of active immunotherapy where there was not a preexisting pool of tumor-specific CD8+ T cells. |
| 3308 | 16025264 | Our results contrast the recent studies where IL-15 was successfully used to augment tumor-reactivity of adoptively transferred transgenic CD8+ T cells. |
| 3309 | 16025264 | This suggests that the adjuvant potential of IL-15 may be greatest in settings where it can augment the number and activity of preexisting tumor-specific CD8+ T cells. |
| 3310 | 16024732 | Furthermore, neither pretreatment with effective doses of antiserum against rat-TNF-alpha (50 microl paw(-1)) nor against IL-18 (10 microg paw(-1)) inhibited the IL-12-induced hyperalgesia. |
| 3311 | 16024732 | Likewise, antiserum against IL-12 (10 ng paw(-1)) did not alter IL-18-induced hyperalgesia. |
| 3312 | 16010587 | Th1 cells, characterized by secretion of IFN-gamma and TNF-alpha, are primarily responsible for activating and regulating the development and persistence of CTL. |
| 3313 | 16009271 | Using TNF-alpha/PGE(2)/IL-1beta/IL-6 as maturation stimulus, AIMV/sf-DCs revealed to be comparable with RPMI/HS-DCs with regard to phenotypic expression of maturation markers, survival in vitro, migratory capacity and stimulation of lymphocyte proliferation except for CD1a which was expressed on a fraction of DCs only when cultured in serumfree AIMV medium. |
| 3314 | 15985222 | To investigate whether immunization with glutathione S-transferase (GST) and mutant toxic shock syndrome toxin 1 (mTSST-1) fusion protein can protect against Staphylococcus aureus infection, we purified a non-toxic mutant GST-mTSST-1 fusion protein. |
| 3315 | 15985222 | Furthermore, the serum samples from GST-mTSST-1-immunized mice also significantly inhibited interferon-gamma and tumor necrosis factor-alpha production from murine spleen cells by TSST-1. |
| 3316 | 15984339 | We have investigated the hypothesis that active viral infection increases the susceptibility of bovine leukocytes to the M. haemolytica leukotoxin by increasing the expression of or activating the beta2 integrin CD11a/CD18 (LFA-1) on the leukocyte surface. |
| 3317 | 15984339 | In vitro exposure to proinflammatory cytokines (i.e. interleukin-1beta, tumor necrosis factor-alpha and interferon-gamma) increases LFA-1 expression on bovine leukocytes, which in turn correlates with increased binding and responsiveness to the leukotoxin. |
| 3318 | 15981208 | In cellular activation, the CD28 ligands B7-1 (CD80) and B7-2 (CD86) are thought to play nearly identical roles in T cell activation. |
| 3319 | 15981208 | We monitored the T cell response upon co-culture with HLA Class I-matched and mismatched renal carcinoma cells, respectively, that express different levels of B7-1 and B7-2, respectively. |
| 3320 | 15981208 | In a HLA Class I-mismatched co-culture, T cell proliferation, IFN-gamma and GM-CSF secretion equally depend on the levels of B7-1 and B7-2 on tumor cells. |
| 3321 | 15981208 | In contrast, in a HLA Class I-matched situation, B7-2 is more effective in the induction of IFN-gamma and GM-CSF secretion than B7-1, but both B7 molecules induce T cell proliferation equally efficient. |
| 3322 | 15981208 | B7-2 is more effective than B7-1 in inducing TNF-alpha and IL-10 secretion in both HLA Class I-matched and mismatched situations. |
| 3323 | 15981208 | The distinct patterns of cytokine induction by B7-1 and B7-2 obviously depend on the HLA Class I compatibility. |
| 3324 | 15976761 | Plasma CRP, interleukin (IL)-6, monocyte chemotactic protein 1, tumor necrosis factor alpha, IL-2 soluble receptor alpha, and serum amyloid A were measured, and differences in mean concentrations of absolute and normalized values on days 1, 3, and 7 were compared with mean baseline values. |
| 3325 | 15976761 | Plasma CRP, interleukin (IL)-6, monocyte chemotactic protein 1, tumor necrosis factor alpha, IL-2 soluble receptor alpha, and serum amyloid A were measured, and differences in mean concentrations of absolute and normalized values on days 1, 3, and 7 were compared with mean baseline values. |
| 3326 | 15976761 | The mean increases in normalized high sensitivity CRP values were significant on day 1 (P < .01) and day 3 (P = .05), whereas the mean increase in normalized serum amyloid A was significant only on day 1 (P < .05). |
| 3327 | 15976761 | The mean increases in normalized high sensitivity CRP values were significant on day 1 (P < .01) and day 3 (P = .05), whereas the mean increase in normalized serum amyloid A was significant only on day 1 (P < .05). |
| 3328 | 15976761 | No significant changes were seen in mean concentrations of IL-2 soluble receptor alpha, monocyte chemotactic protein-1, or tumor necrosis factor-alpha. |
| 3329 | 15976761 | No significant changes were seen in mean concentrations of IL-2 soluble receptor alpha, monocyte chemotactic protein-1, or tumor necrosis factor-alpha. |
| 3330 | 15972497 | Our results showed that StxB1 and mStx1, but not native Stx1 (nStx1), resulted in enhanced expression of CD86, CD40, and major histocompatibility complex (MHC) class II molecules and, to some extent, also enhanced the expression of CD80 on bone marrow-derived DCs. |
| 3331 | 15972497 | StxB1-treated DCs exhibited an increase in tumor necrosis factor alpha and interleukin-12 (IL-12) production, a stimulation of DO11.10 T-cell proliferation, and the production of both Th1 and Th2 cytokines, including gamma interferon (IFN-gamma), IL-4, IL-5, IL-6, and IL-10. |
| 3332 | 15972497 | When mice were given StxB1 subcutaneously, the levels of CD80, CD86, and CD40, as well as MHC class II expression by splenic DCs, were enhanced. |
| 3333 | 15972497 | OVA-specific CD4+ T cells isolated from mice immunized with OVA plus mStx1 or StxB1 produced IFN-gamma, IL-4, IL-5, IL-6, and IL-10, indicating that mStx1 and StxB1 elicit both Th1- and Th2-type responses. |
| 3334 | 15964669 | Here, we demonstrate that MALP-2 induces MIP1alpha and beta, MIP-2, Gro, TNFalpha, IL1alpha and IL6 in cells of cotton rats (Sigmodon hispidus) in vitro. |
| 3335 | 15958260 | By neutralizing TNF-alpha in the supernatant of PPD-pulsed splenocytes with anti-rgpTNF-alpha, we observed hyperproliferation. |
| 3336 | 15958066 | It induced lower but progressive production of interferon (IFN)-gamma, interleukin (IL)-4 and tumour necrosis factor (TNF)-alpha. |
| 3337 | 15956570 | The cytopathic effect (CPE) seen with some subgroups of avian sarcoma and leukosis virus (ASLV) is associated with viral Env activation of the death-promoting activity of TVB (a tumor necrosis factor receptor-related receptor that is most closely related to mammalian TNF-related apoptosis-inducing ligand [TRAIL] receptors) and with viral superinfection leading to unintegrated viral DNA (UVD) accumulation, which is presumed to activate a cellular DNA damage response. |
| 3338 | 15949924 | These two types of fimbriae were moderate inductors of IL-6 and interferon and almost inactive with regard to the stimulation of TNF when tested in human whole blood assay. |
| 3339 | 15949138 | Despite normal basal expression of Toll-like receptors and membrane CD14, innate immune responses of neonatal mononuclear cells to lipopolysaccharide are characterized by markedly reduced release of the pro-inflammatory Th1-polarizing cytokines TNF-alpha and interferon-gamma with relative preservation of anti-inflammatory Th2-polarizing cytokines. |
| 3340 | 15944311 | In contrast, SAG1(c) mutants produced reduced brain cyst loads early in chronic infection, but these substantially increased over time accompanying a hyperproduction of IFN-gamma, TNF-alpha, and IL-10, and severe encephalitis. |
| 3341 | 15944311 | We conclude that stage-specific expression of SRS Ags is among the key mechanisms by which optimal parasite persistency is established and maintained. |
| 3342 | 15944074 | Plasma concentrations of interleukin-6 (IL-6), interleukin-1 receptor antagonist (IL-1Ra), and tumour necrosis factor-alpha (TNF-alpha) were assessed at baseline and 3 h post-injection. |
| 3343 | 15944074 | Plasma concentrations of interleukin-6 (IL-6), interleukin-1 receptor antagonist (IL-1Ra), and tumour necrosis factor-alpha (TNF-alpha) were assessed at baseline and 3 h post-injection. |
| 3344 | 15944074 | No changes in TNF-alpha or IL-1Ra concentration were recorded in either group. |
| 3345 | 15944074 | No changes in TNF-alpha or IL-1Ra concentration were recorded in either group. |
| 3346 | 15941685 | An increased capacity of CD3+ cells to produce interferon (IFN)-gamma and tumor necrosis factor (TNF)-alpha, and of the TCRgammadelta+ subset to produce TNF-alpha was seen in adults after stimulation of peripheral blood mononuclear cells (PBMC) with a late-stage, schizont-rich, parasite preparation. |
| 3347 | 15941685 | An increased capacity of CD3+ cells to produce interferon (IFN)-gamma and tumor necrosis factor (TNF)-alpha, and of the TCRgammadelta+ subset to produce TNF-alpha was seen in adults after stimulation of peripheral blood mononuclear cells (PBMC) with a late-stage, schizont-rich, parasite preparation. |
| 3348 | 15941685 | An increased capacity of CD3+ cells to produce interferon (IFN)-gamma and tumor necrosis factor (TNF)-alpha, and of the TCRgammadelta+ subset to produce TNF-alpha was seen in adults after stimulation of peripheral blood mononuclear cells (PBMC) with a late-stage, schizont-rich, parasite preparation. |
| 3349 | 15941685 | Mitogenic stimulation with PMA and ionomycin induced much higher frequencies of IFN-gamma- and TNF-alpha-expressing CD4+, CD8+ as well as TCRgammadelta+ cells in adults, while differences for interleukin (IL)-2 expression were restricted to CD4+ and CD8+ T cells. |
| 3350 | 15941685 | Mitogenic stimulation with PMA and ionomycin induced much higher frequencies of IFN-gamma- and TNF-alpha-expressing CD4+, CD8+ as well as TCRgammadelta+ cells in adults, while differences for interleukin (IL)-2 expression were restricted to CD4+ and CD8+ T cells. |
| 3351 | 15941685 | Mitogenic stimulation with PMA and ionomycin induced much higher frequencies of IFN-gamma- and TNF-alpha-expressing CD4+, CD8+ as well as TCRgammadelta+ cells in adults, while differences for interleukin (IL)-2 expression were restricted to CD4+ and CD8+ T cells. |
| 3352 | 15941685 | Impressive increases in the capacity to produce P. falciparum-specific and non-specific IFN-gamma and TNF-alpha appear to be the main cellular correlates of naturally acquired immunity in Central Africa. |
| 3353 | 15941685 | Impressive increases in the capacity to produce P. falciparum-specific and non-specific IFN-gamma and TNF-alpha appear to be the main cellular correlates of naturally acquired immunity in Central Africa. |
| 3354 | 15941685 | Impressive increases in the capacity to produce P. falciparum-specific and non-specific IFN-gamma and TNF-alpha appear to be the main cellular correlates of naturally acquired immunity in Central Africa. |
| 3355 | 15925273 | The recognition leads to activation of intracellular pathways involving nuclear factor kappa B (NF-kappaB) and mitogen-activated protein kinases (MAPK), such as the c-Jun NH2-terminal kinase (JNK), and p38. |
| 3356 | 15925273 | We show that in vitro infection with Francisella tularensis results in activation of NF-kappaB, phosphorylation of p38 and c-Jun, and secretion of TNF-alpha in adherent mouse peritoneal cells, in the mouse macrophage-like cell line J774A.1, in the human macrophage cell line THP-1, and in human peripheral blood monocytic cells. |
| 3357 | 15922719 | Cytokines, such as IL-10, GMCSF, IFN-gamma, and TNF-alpha were also detected in the supernatants of the cultured human cells from the chimeric mice, when they were stimulated with allogeneic cells. |
| 3358 | 15908422 | Immunodepletion studies of P-4-vaccinated mice indicate that CD4+ and not CD8+ T cells are critical for protection against Leishmania pifanoi (Leishmania mexicana complex). |
| 3359 | 15908422 | Immunodepletion studies of P-4-vaccinated mice indicate that CD4+ and not CD8+ T cells are critical for protection against Leishmania pifanoi (Leishmania mexicana complex). |
| 3360 | 15908422 | Although a moderate CD8+ T-cell response is elicited by vaccination, CD4+ T cells are the dominant responding population in vitro and at the cutaneous site of infection. |
| 3361 | 15908422 | Although a moderate CD8+ T-cell response is elicited by vaccination, CD4+ T cells are the dominant responding population in vitro and at the cutaneous site of infection. |
| 3362 | 15908422 | These protective T cells produce gamma interferon (IFN-gamma), macrophage migration inhibitory factor (MIF), and tumor necrosis factor/lymphotoxin (TNF/LT), each of which significantly contributed to intracellular parasite destruction in vitro. |
| 3363 | 15908422 | These protective T cells produce gamma interferon (IFN-gamma), macrophage migration inhibitory factor (MIF), and tumor necrosis factor/lymphotoxin (TNF/LT), each of which significantly contributed to intracellular parasite destruction in vitro. |
| 3364 | 15908422 | These results indicate that a singular CD4+ T-cell response (IFN-gamma, MIF, and/or LT/TNF) can provide protection against New World cutaneous leishmaniasis. |
| 3365 | 15908422 | These results indicate that a singular CD4+ T-cell response (IFN-gamma, MIF, and/or LT/TNF) can provide protection against New World cutaneous leishmaniasis. |
| 3366 | 15905560 | Kinetoplastid membrane protein-11 DNA vaccination induces complete protection against both pentavalent antimonial-sensitive and -resistant strains of Leishmania donovani that correlates with inducible nitric oxide synthase activity and IL-4 generation: evidence for mixed Th1- and Th2-like responses in visceral leishmaniasis. |
| 3367 | 15905560 | KMP-11 DNA vaccinated hamsters were protected by a surge in IFN-gamma, TNF-alpha, and IL-12 levels along with extreme down-regulation of IL-10. |
| 3368 | 15899826 | In this study, we identified murine breast cancer cell lines that support DNA replication of E1-deleted adenovirus vectors and which can be killed by an oncolytic adenovirus expressing adenovirus E1A and tumor necrosis factor (TNF)-related apoptosis inducing ligand (TRAIL) in a replication-dependent manner (Ad.IR-E1A/TRAIL). |
| 3369 | 15899826 | In this study, we identified murine breast cancer cell lines that support DNA replication of E1-deleted adenovirus vectors and which can be killed by an oncolytic adenovirus expressing adenovirus E1A and tumor necrosis factor (TNF)-related apoptosis inducing ligand (TRAIL) in a replication-dependent manner (Ad.IR-E1A/TRAIL). |
| 3370 | 15899826 | We showed that systemic or intratumoral (i.t.) injection of adenovirus vectors into mice increases plasma levels of proinflammatory cytokines and chemokines, including TNF-alpha, INF-gamma, and MCP-1, which are potent inducers of dendritic cell maturation. |
| 3371 | 15899826 | We showed that systemic or intratumoral (i.t.) injection of adenovirus vectors into mice increases plasma levels of proinflammatory cytokines and chemokines, including TNF-alpha, INF-gamma, and MCP-1, which are potent inducers of dendritic cell maturation. |
| 3372 | 15899826 | Furthermore, we showed that in vivo expression of Flt3L from an adenovirus vector increases the number of CD11b+ and CD11c+ cells (populations that include dendritic cells) in the blood circulation. |
| 3373 | 15899826 | Furthermore, we showed that in vivo expression of Flt3L from an adenovirus vector increases the number of CD11b+ and CD11c+ cells (populations that include dendritic cells) in the blood circulation. |
| 3374 | 15899826 | Based on these findings, we tested whether Ad.IR-E1A/TRAIL induced killing of tumor cells in combination with dendritic cell mobilization by Ad.Flt3L or, for comparison, Ad.GM-CSF would have an additive antitumor effect. |
| 3375 | 15899826 | Based on these findings, we tested whether Ad.IR-E1A/TRAIL induced killing of tumor cells in combination with dendritic cell mobilization by Ad.Flt3L or, for comparison, Ad.GM-CSF would have an additive antitumor effect. |
| 3376 | 15899826 | We found that vaccination of mice with C3L5 cells that underwent viral oncolysis in combination with Flt3L or granulocyte-macrophage colony-stimulating factor (GM-CSF) expression induces a systemic antitumor immune response. |
| 3377 | 15899826 | We found that vaccination of mice with C3L5 cells that underwent viral oncolysis in combination with Flt3L or granulocyte-macrophage colony-stimulating factor (GM-CSF) expression induces a systemic antitumor immune response. |
| 3378 | 15897626 | Interferon (IFN)-gamma, tumor necrosis factor (TNF)-alpha, transforming growth factor (TGF)-beta, interleukin (IL)-1beta, IL-2, IL-10, IL-12p40, granulocyte-macrophage-colony stimulating factor (GM-CSF) and iNOS mRNA expression were detected significantly and reproducibly when these primer sets were used. |
| 3379 | 15893422 | Pathogenesis of Lyme neuroborreliosis: mitogen-activated protein kinases Erk1, Erk2, and p38 in the response of astrocytes to Borrelia burgdorferi lipoproteins. |
| 3380 | 15893422 | Pathogenesis of Lyme neuroborreliosis: mitogen-activated protein kinases Erk1, Erk2, and p38 in the response of astrocytes to Borrelia burgdorferi lipoproteins. |
| 3381 | 15893422 | Pathogenesis of Lyme neuroborreliosis: mitogen-activated protein kinases Erk1, Erk2, and p38 in the response of astrocytes to Borrelia burgdorferi lipoproteins. |
| 3382 | 15893422 | Pathogenesis of Lyme neuroborreliosis: mitogen-activated protein kinases Erk1, Erk2, and p38 in the response of astrocytes to Borrelia burgdorferi lipoproteins. |
| 3383 | 15893422 | Dysregulated production of pro-inflammatory cytokines such as IL-6 and TNF-alpha can lead to neuronal damage. |
| 3384 | 15893422 | Dysregulated production of pro-inflammatory cytokines such as IL-6 and TNF-alpha can lead to neuronal damage. |
| 3385 | 15893422 | Dysregulated production of pro-inflammatory cytokines such as IL-6 and TNF-alpha can lead to neuronal damage. |
| 3386 | 15893422 | Dysregulated production of pro-inflammatory cytokines such as IL-6 and TNF-alpha can lead to neuronal damage. |
| 3387 | 15893422 | Lipoproteins are the key inflammatory molecule type of Borrelia burgdorferi, the spirochete that causes Lyme disease, and we had previously shown that lipoprotein-induced TNF-alpha production in astrocytes caused astrocyte apoptosis, and IL-6 enhanced proliferation of these cells. |
| 3388 | 15893422 | Lipoproteins are the key inflammatory molecule type of Borrelia burgdorferi, the spirochete that causes Lyme disease, and we had previously shown that lipoprotein-induced TNF-alpha production in astrocytes caused astrocyte apoptosis, and IL-6 enhanced proliferation of these cells. |
| 3389 | 15893422 | Lipoproteins are the key inflammatory molecule type of Borrelia burgdorferi, the spirochete that causes Lyme disease, and we had previously shown that lipoprotein-induced TNF-alpha production in astrocytes caused astrocyte apoptosis, and IL-6 enhanced proliferation of these cells. |
| 3390 | 15893422 | Lipoproteins are the key inflammatory molecule type of Borrelia burgdorferi, the spirochete that causes Lyme disease, and we had previously shown that lipoprotein-induced TNF-alpha production in astrocytes caused astrocyte apoptosis, and IL-6 enhanced proliferation of these cells. |
| 3391 | 15893422 | Lipoproteins readily activated p38 and Erk1/2 MAPK, thus enlisting these pathways among the kinase pathways that spirochetes may address as they invade the central nervous system. |
| 3392 | 15893422 | Lipoproteins readily activated p38 and Erk1/2 MAPK, thus enlisting these pathways among the kinase pathways that spirochetes may address as they invade the central nervous system. |
| 3393 | 15893422 | Lipoproteins readily activated p38 and Erk1/2 MAPK, thus enlisting these pathways among the kinase pathways that spirochetes may address as they invade the central nervous system. |
| 3394 | 15893422 | Lipoproteins readily activated p38 and Erk1/2 MAPK, thus enlisting these pathways among the kinase pathways that spirochetes may address as they invade the central nervous system. |
| 3395 | 15893422 | We also investigated whether specific inhibition of p38 and Erk1/2 MAPK would inhibit TNF-alpha and IL-6 production and thus astrocyte apoptosis, and proliferation, respectively. |
| 3396 | 15893422 | We also investigated whether specific inhibition of p38 and Erk1/2 MAPK would inhibit TNF-alpha and IL-6 production and thus astrocyte apoptosis, and proliferation, respectively. |
| 3397 | 15893422 | We also investigated whether specific inhibition of p38 and Erk1/2 MAPK would inhibit TNF-alpha and IL-6 production and thus astrocyte apoptosis, and proliferation, respectively. |
| 3398 | 15893422 | We also investigated whether specific inhibition of p38 and Erk1/2 MAPK would inhibit TNF-alpha and IL-6 production and thus astrocyte apoptosis, and proliferation, respectively. |
| 3399 | 15893422 | Lipoprotein-stimulated IL-6 production was unaffected by the MAPK inhibitors. |
| 3400 | 15893422 | Lipoprotein-stimulated IL-6 production was unaffected by the MAPK inhibitors. |
| 3401 | 15893422 | Lipoprotein-stimulated IL-6 production was unaffected by the MAPK inhibitors. |
| 3402 | 15893422 | Lipoprotein-stimulated IL-6 production was unaffected by the MAPK inhibitors. |
| 3403 | 15893422 | In contrast, inhibition of both p38 and Erk1/2 significantly diminished TNF-alpha production, and totally abrogated production of this cytokine when both MAPK pathways were inhibited simultaneously. |
| 3404 | 15893422 | In contrast, inhibition of both p38 and Erk1/2 significantly diminished TNF-alpha production, and totally abrogated production of this cytokine when both MAPK pathways were inhibited simultaneously. |
| 3405 | 15893422 | In contrast, inhibition of both p38 and Erk1/2 significantly diminished TNF-alpha production, and totally abrogated production of this cytokine when both MAPK pathways were inhibited simultaneously. |
| 3406 | 15893422 | In contrast, inhibition of both p38 and Erk1/2 significantly diminished TNF-alpha production, and totally abrogated production of this cytokine when both MAPK pathways were inhibited simultaneously. |
| 3407 | 15890793 | Enhanced leukocyte infiltration may be driven by increased levels of the type 1 cytokines, IL-2 and IFN-gamma, and TNF-alpha, observed at the site of antigen reexposure in animals that had been stressed at the time of primary immunization. |
| 3408 | 15890793 | In contrast, no differences were observed in type 2 cytokines, IL-4 or IL-5. |
| 3409 | 15876450 | Cytokine production (IFN-gamma, TNF-alpha, IL-6, IL-10) by whole blood cultures, circulating cytokines and acute phase proteins were analysed before and 2 days after vaccination. |
| 3410 | 15855014 | Here, we evaluated innate and adaptive immune system cytokine responses induced by HPV-16 L1 VLP in whole blood (WB) cultures from individuals receiving the vaccine (n=20) or placebo (n=4) before and after vaccination. 11 cytokines were measured: IL-1beta, IL-2, IL-4, IL-5, IL-6, IL-8, IL-10, IL-12, IFN-gamma, TNF-alpha, and GM-CSF using multiplex bead arrays. |
| 3411 | 15845475 | Human blood monocyte-derived macrophages, purified from healthy donors, were incubated with each outer membrane constituent, and cytokine production of macrophage supernatants interleukin-1beta (IL-1beta), tumor necrosis factor alpha (TNF-alpha), IL-10, IL-12, and IL-8 was measured. |
| 3412 | 15845475 | Human blood monocyte-derived macrophages, purified from healthy donors, were incubated with each outer membrane constituent, and cytokine production of macrophage supernatants interleukin-1beta (IL-1beta), tumor necrosis factor alpha (TNF-alpha), IL-10, IL-12, and IL-8 was measured. |
| 3413 | 15845475 | Human blood monocyte-derived macrophages, purified from healthy donors, were incubated with each outer membrane constituent, and cytokine production of macrophage supernatants interleukin-1beta (IL-1beta), tumor necrosis factor alpha (TNF-alpha), IL-10, IL-12, and IL-8 was measured. |
| 3414 | 15845475 | Human blood monocyte-derived macrophages, purified from healthy donors, were incubated with each outer membrane constituent, and cytokine production of macrophage supernatants interleukin-1beta (IL-1beta), tumor necrosis factor alpha (TNF-alpha), IL-10, IL-12, and IL-8 was measured. |
| 3415 | 15845475 | OMP P6 selectively upregulated IL-10, TNF-alpha, and IL-8. |
| 3416 | 15845475 | OMP P6 selectively upregulated IL-10, TNF-alpha, and IL-8. |
| 3417 | 15845475 | OMP P6 selectively upregulated IL-10, TNF-alpha, and IL-8. |
| 3418 | 15845475 | OMP P6 selectively upregulated IL-10, TNF-alpha, and IL-8. |
| 3419 | 15845475 | While OMP P6 (0.1 mug/ml for 8 h) elicited slightly greater concentrations of IL-10, it resulted in over ninefold greater concentrations of TNF-alpha and over fourfold greater concentrations of IL-8 than did OMP P2. |
| 3420 | 15845475 | While OMP P6 (0.1 mug/ml for 8 h) elicited slightly greater concentrations of IL-10, it resulted in over ninefold greater concentrations of TNF-alpha and over fourfold greater concentrations of IL-8 than did OMP P2. |
| 3421 | 15845475 | While OMP P6 (0.1 mug/ml for 8 h) elicited slightly greater concentrations of IL-10, it resulted in over ninefold greater concentrations of TNF-alpha and over fourfold greater concentrations of IL-8 than did OMP P2. |
| 3422 | 15845475 | While OMP P6 (0.1 mug/ml for 8 h) elicited slightly greater concentrations of IL-10, it resulted in over ninefold greater concentrations of TNF-alpha and over fourfold greater concentrations of IL-8 than did OMP P2. |
| 3423 | 15845475 | OMP P6 of NTHI is a specific trigger of bacteria-induced human macrophage inflammatory events, with IL-8 and TNF-alpha as key effectors of P6-induced macrophage responses. |
| 3424 | 15845475 | OMP P6 of NTHI is a specific trigger of bacteria-induced human macrophage inflammatory events, with IL-8 and TNF-alpha as key effectors of P6-induced macrophage responses. |
| 3425 | 15845475 | OMP P6 of NTHI is a specific trigger of bacteria-induced human macrophage inflammatory events, with IL-8 and TNF-alpha as key effectors of P6-induced macrophage responses. |
| 3426 | 15845475 | OMP P6 of NTHI is a specific trigger of bacteria-induced human macrophage inflammatory events, with IL-8 and TNF-alpha as key effectors of P6-induced macrophage responses. |
| 3427 | 15843575 | Recently we reported that Cpn-infected mice generate an MHC class I-restricted CD8(+) Tc1 response against various Cpn Ags, and that CD8(+) CTL to multiple epitopes inhibit Cpn growth in vitro. |
| 3428 | 15843575 | CD8(+) T cell lines generated to minigene-encoded CTL epitopes secreted IFN-gamma and TNF-alpha and exhibited CTL activity upon recognition of Cpn-infected macrophages. |
| 3429 | 15843575 | Immunization and challenge studies with beta(2)-microglobulin(-/-) mice indicated that the reduction of lung Cpn burdens was mediated by the MHC class I-dependent CD8(+) T cells to minigene-included Cpn CTL epitopes, rather than by pan-DR epitope-specific CD4(+) T cells. |
| 3430 | 15838378 | This increase in cell number was associated with an increase in CD8 T-cell function, as defined by specific IFN-gamma and TNF-alpha production, and protection from tumor challenge. |
| 3431 | 15837365 | Compared to younger animals, older calves showed significantly less fever and lower TNFalpha levels and less virus-specific IFNgamma release. |
| 3432 | 15832296 | However, HPV16 VLP induced pDC to secrete of IFN-alpha and IL-6, both cytokines that play a role in the generation of antibody responses, as well as TNFalpha and IL-8. |
| 3433 | 15832296 | Finally, CpG-activated pDC, but not pDC exposed to HPV16 VLP, activated lymphocytes to secrete IL-10 and low levels of IFN-gamma. |
| 3434 | 15832293 | They strongly activate DC and monocytes, leading to TNF-alpha and IFN-alpha secretion. |
| 3435 | 15832293 | The detailed analysis of the activated cell types, the study of the cytokines released from PBMC cultured with protamine-RNA complexes and recently published results suggest that TLR-7 and TLR-8 may be involved in the recognition of protamine-stabilized RNA. |
| 3436 | 15827150 | Effects of nonstructural proteins NS1 and NS2 of human respiratory syncytial virus on interferon regulatory factor 3, NF-kappaB, and proinflammatory cytokines. |
| 3437 | 15827150 | It has been shown previously that HRSV nonstructural proteins 1 and 2 (NS1 and NS2) inhibit the induction of alpha/beta interferon (IFN-alpha/beta) in A549 cells and human macrophages. |
| 3438 | 15827150 | Two principal transcription factors for the early IFN-beta and -alpha1 response are interferon regulatory factor 3 (IRF-3) and nuclear factor kappaB (NF-kappaB). |
| 3439 | 15827150 | At early times postinfection, wild-type HRSV and the NS1/NS2 deletion mutants were very similar in the ability to activate IRF-3. |
| 3440 | 15827150 | However, once NS1 and NS2 were expressed significantly, they acted cooperatively to suppress activation and nuclear translocation of IRF-3. |
| 3441 | 15827150 | Since these viruses differed greatly in the induction of IFN-alpha/beta, NF-kappaB activation was evaluated in Vero cells, which lack the structural genes for IFN-alpha/beta and would preclude confounding effects of IFN-alpha/beta. |
| 3442 | 15827150 | Since recombinant HRSVs from which the NS1 or NS2 genes have been deleted are being developed as vaccine candidates, we investigated whether the changes in activation of host transcription factors and increased IFN-alpha/beta production had an effect on the epithelial production of proinflammatory factors. |
| 3443 | 15827150 | Viruses lacking NS1 and/or NS2 stimulated modestly lower production of RANTES (Regulated on Activation Normal T-cell Expressed and Secreted), interleukin 8, and tumor necrosis factor alpha compared to wild-type recombinant RSV, supporting their use as attenuated vaccine candidates. |
| 3444 | 15814697 | DcR3/TR6, a secreted protein belonging to the TNF receptor superfamily, interacts with lymphotoxin-like, exhibits inducible expression, and competes with herpes simplex virus glycoprotein D for herpes virus entrance mediator (LIGHT), Fas ligand (FasL), and TL1A, all members of the TNF superfamily. |
| 3445 | 15814697 | Solid-phase TR6 can trigger reverse signaling of LIGHT and FasL expressed on T cells, and lead to T cell costimulation. |
| 3446 | 15814697 | We demonstrated that mastocytoma P815 cells expressing surface TR6 (TR6-P815) effectively augmented the T cells response in vitro and ex vivo in terms of proliferation, as well as IL-2 and IFN-gamma secretion. |
| 3447 | 15812230 | Nonreplicating recombinant vaccinia virus expressing CD40 ligand enhances APC capacity to stimulate specific CD4+ and CD8+ T cell responses. |
| 3448 | 15812230 | Recently, we and others have demonstrated, in vitro and in vivo, that coexpression of CD80 and CD86 costimulatory molecules enhances the immunogenic capacity of a recombinant vaccinia virus (rVV) encoding different tumor-associated antigens. |
| 3449 | 15812230 | To further investigate the capacity of these vectors to provide ligands for different costimulatory pathways relevant in the generation of T cell responses, we constructed a recombinant virus (rVV) expressing CD40 ligand or CD154 (CD154rVV). |
| 3450 | 15812230 | Upon binding the CD40 receptor expressed on antigen presenting cells (APC), this molecule, physiologically expressed on activated CD4+ T cells, increases their antigen presentation and immunostimulatory capacities. |
| 3451 | 15812230 | CD154rVV infection of autologous fibroblasts, monocytes, or iDC promoted the expression of a number of cytokines, including GM-CSF, TNF-alpha, and IL-15 in iDC. |
| 3452 | 15812230 | Most importantly, IL-12 p40 gene expression and protein secretion were induced by CD154rVV but not by wild-type VV (WT VV) in either CD14+ cells or iDC, and these effects could be blocked by anti-CD40 monoclonal antibodies. |
| 3453 | 15812230 | Furthermore, phenotypic characterization of CD154rVV infected iDC revealed enhanced expression of CD83 and CD86 surface markers as compared with wild-type vaccinia virus infection. |
| 3454 | 15812230 | However, cytokine genes typically expressed by T cell receptor triggered T cells such as those encoding IL-2 and IFN-gamma, or T cell proliferation, were detectable to a significantly higher extent in CD154rVV infected cultures, as compared with WT VV. |
| 3455 | 15812230 | Activation of specific CD8+ T cells was then investigated using MART-1/Melan-A(27-35) epitope as the model of tumor-associated antigen (TAA). |
| 3456 | 15804174 | Moreover, cationic liposome stimulates the expression of CD80/CD86 on dendritic cells (DCs), but not the release of TNF-alpha from DCs, suggesting the existence of a NF-kappaB-independent immunostimulation pathway for cationic lipids such as DOTAP. |
| 3457 | 15795295 | RNase protection analyses revealed increased expression of numerous cytokines and chemokines, including interleukin-1beta (IL-1beta), IL-6, tumor necrosis factor alpha, macrophage inflammatory protein 1alpha (MIP-1alpha), MIP-1beta, MIP-2, interferon gamma-inducible protein, monocyte chemotactic protein 1, and T-cell activation gene 3 at 12 h postinfection with KyARgp2F. |
| 3458 | 15780734 | For each hamster included in the study, prion-specific serum antibodies as well as deposition of pathological prion protein (PrP(res)), glial fibrillary acidic protein (GFAP), and mRNA expression for cytokines (TNF alpha, IL-1beta, IL-10) in brain tissues were evaluated. |
| 3459 | 15780734 | For each hamster included in the study, prion-specific serum antibodies as well as deposition of pathological prion protein (PrP(res)), glial fibrillary acidic protein (GFAP), and mRNA expression for cytokines (TNF alpha, IL-1beta, IL-10) in brain tissues were evaluated. |
| 3460 | 15780734 | In immunized animals, increased survival after challenge was associated with a reduction of cerebral lesion, PrP deposition and GFAP expression; in these animals, anti-prion protein peptide antibody levels were increased, and the expression of pro-inflammatory cytokines (TNF alpha and IL-1beta) was reduced. |
| 3461 | 15780734 | In immunized animals, increased survival after challenge was associated with a reduction of cerebral lesion, PrP deposition and GFAP expression; in these animals, anti-prion protein peptide antibody levels were increased, and the expression of pro-inflammatory cytokines (TNF alpha and IL-1beta) was reduced. |
| 3462 | 15780449 | The serum levels of interferon-gamma (IFN-gamma) and interleukin-2 (IL-2) were increased, while no significant increase was observed in interleukin-4 (IL-4), interleukin-6 (IL-6), interleukin-10 (IL-10) or tumor necrosis factor-alpha (TNF-alpha). |
| 3463 | 15780438 | More importantly, analysis of the cytokine responses revealed a reduction in the IFN-gamma and TNF-alpha production in the lungs of IgA-/- compared to IgA+/+ mice. |
| 3464 | 15778401 | Prenatal blockage of lymphotoxin beta receptor and TNF receptor p55 signaling cascade resulted in the acceleration of tissue genesis for isolated lymphoid follicles in the large intestine. |
| 3465 | 15758077 | The huMDM released large amounts of CXC chemokine ligand 8 (CXCL8) and CC chemokine ligand 2 when incubated with live or killed LVS organisms, and live bacteria also elicited production of interleukin-1beta (IL-1beta). |
| 3466 | 15758077 | Furthermore, human monocytes secreted CXCL8, IL-1beta, and tumor necrosis factor alpha in response to various bacterial preparations. |
| 3467 | 15731055 | DC exposed to live EBs acquired a mature DC morphology; expressed high levels of major histocompatibility complex (MHC) class II, CD80, CD86, CD40, and ICAM-1; produced elevated amounts of interleukin-12 and tumor necrosis factor alpha; and were efficiently recognized by Chlamydia-specific CD4+ T cells. |
| 3468 | 15731055 | In contrast, UV-EB-pulsed DC expressed low levels of CD40 and CD86 but displayed high levels of MHC class II, ICAM-1, and CD80; secreted low levels of proinflammatory cytokines; and exhibited reduced recognition by Chlamydia-specific CD4+ T cells. |
| 3469 | 15725957 | Co-incubation of immature DCs with ghosts resulted in decreased expression of CD1a, CD80, and CD83 molecules, while addition of maturation mix (TNF-alpha, IL-1 beta, IL-6, and PGE2) to the cultures enhanced expression of these molecules. |
| 3470 | 15725957 | No marked changes were observed in the expression of the CD11c, CD40, and CD86 surface molecules. |
| 3471 | 15725107 | Canine cytokine mRNA expression in peripheral blood mononuclear cells collected prior to treatment and at the completion of the study was determined for IFN-gamma, IL-4, TNF and IL-10 genes using quantitative reverse transcription competitive polymerase chain reaction. |
| 3472 | 15715049 | BM mononuclear cells from 3 dogs with melanoma and from 1 healthy dog were cultured for 12 days in media supplemented with recombinant human granulocyte-macrophage colony stimulating factor, stem cell factor, tumor necrosis factor, and Flt-3 ligand. |
| 3473 | 15715049 | Phenotypic analysis of the expanded DC population demonstrated expression of CD11c/CD18 and major histocompatibility complex class II surface markers, and ultrastructural features characteristic of DCs were observed on electron microscopy. |
| 3474 | 15693140 | Dendritic cells derived from metastatic cancer patients vaccinated with allogeneic dendritic cell-autologous tumor cell hybrids express more CD86 and induce higher levels of interferon-gamma in mixed lymphocyte reactions. |
| 3475 | 15693140 | Mononuclear cells were isolated from patients' peripheral blood by density gradient centrifugation, and adherent cells were cultured in medium containing GM-CSF plus IL-4 and, after 5 days, TNF-alpha. |
| 3476 | 15693140 | After 2 more days, Mo-DCs were harvested and their CD80, CD86, and CD83 expression was assessed by flow cytometry. |
| 3477 | 15693140 | They were also used as stimulators in mixed lymphocyte reactions (MLR), where IFN-gamma production was measured by ELISA. |
| 3478 | 15693140 | Mo-DCs from unvaccinated patients expressed significantly lower levels of CD86, and tended to express lower levels of CD83 than Mo-DCs from healthy donors. |
| 3479 | 15693140 | However, Mo-DCs generated after hybrid cell vaccination presented increased expression of the same markers and induced significantly higher levels of IFN-gamma in MLR. |
| 3480 | 15683854 | Lactoferrin was initially shown to augment IL-12(p40) production from macrophages stimulated with LPS. |
| 3481 | 15683854 | A single immunization of mice with Lactoferrin as an adjunct adjuvant resulted in amplified splenocyte proliferative response to heat-killed BCG, and elevated IL-12(p40) production with increased relative ratios of IL-12/IL-10. |
| 3482 | 15683854 | Furthermore, splenocyte recall response to HK-BCG was augmented for proinflammatory mediators, TNF-alpha, IL-1beta, and IL-6, approaching responses generated to complete Freund's adjuvant (CFA) immunized controls. |
| 3483 | 15683451 | In a clinical phase I/II study, monocyte-derived DC were generated in vitro utilizing granulocyte macrophage colony-stimulating factor and rh-interleukin-4 (IL-4) and used for cancer immunotherapy. |
| 3484 | 15683451 | In a clinical phase I/II study, monocyte-derived DC were generated in vitro utilizing granulocyte macrophage colony-stimulating factor and rh-interleukin-4 (IL-4) and used for cancer immunotherapy. |
| 3485 | 15683451 | Polyriboinosinic polyribocytidylic acid (Poly I:C) + tumour necrosis factor-alpha (TNF-alpha) induced significant IL-12 p70 secretion, which was increased after addition of a decoy IL-10 receptor. |
| 3486 | 15683451 | Polyriboinosinic polyribocytidylic acid (Poly I:C) + tumour necrosis factor-alpha (TNF-alpha) induced significant IL-12 p70 secretion, which was increased after addition of a decoy IL-10 receptor. |
| 3487 | 15683451 | The lymph node homing chemokine receptor CCR-7 expression was induced by TNF-alpha + IL-1beta + IL-6 + prostaglandin E2 but was not induced by Poly I:C + TNF-alpha. |
| 3488 | 15683451 | The lymph node homing chemokine receptor CCR-7 expression was induced by TNF-alpha + IL-1beta + IL-6 + prostaglandin E2 but was not induced by Poly I:C + TNF-alpha. |
| 3489 | 15683451 | In general, DC from patients had an intermediate maturity phenotype with a significantly higher expression of CD40 and CD54 compared with healthy donors. |
| 3490 | 15683451 | In general, DC from patients had an intermediate maturity phenotype with a significantly higher expression of CD40 and CD54 compared with healthy donors. |
| 3491 | 15664925 | Invariant Valpha14 chain NKT cells promote Plasmodium berghei circumsporozoite protein-specific gamma interferon- and tumor necrosis factor alpha-producing CD8+ T cells in the liver after poxvirus vaccination of mice. |
| 3492 | 15664925 | Invariant Valpha14 chain NKT cells promote Plasmodium berghei circumsporozoite protein-specific gamma interferon- and tumor necrosis factor alpha-producing CD8+ T cells in the liver after poxvirus vaccination of mice. |
| 3493 | 15664925 | Invariant Valpha14 chain NKT cells promote Plasmodium berghei circumsporozoite protein-specific gamma interferon- and tumor necrosis factor alpha-producing CD8+ T cells in the liver after poxvirus vaccination of mice. |
| 3494 | 15664925 | Invariant Valpha14 chain NKT cells promote Plasmodium berghei circumsporozoite protein-specific gamma interferon- and tumor necrosis factor alpha-producing CD8+ T cells in the liver after poxvirus vaccination of mice. |
| 3495 | 15664925 | Most studies in mice have focused on splenic and peripheral blood T cells and identified gamma interferon (IFN-gamma)-producing CD8+ T cells as correlates of protection, which can be induced by prime-boost vaccination with recombinant poxviruses. |
| 3496 | 15664925 | Most studies in mice have focused on splenic and peripheral blood T cells and identified gamma interferon (IFN-gamma)-producing CD8+ T cells as correlates of protection, which can be induced by prime-boost vaccination with recombinant poxviruses. |
| 3497 | 15664925 | Most studies in mice have focused on splenic and peripheral blood T cells and identified gamma interferon (IFN-gamma)-producing CD8+ T cells as correlates of protection, which can be induced by prime-boost vaccination with recombinant poxviruses. |
| 3498 | 15664925 | Most studies in mice have focused on splenic and peripheral blood T cells and identified gamma interferon (IFN-gamma)-producing CD8+ T cells as correlates of protection, which can be induced by prime-boost vaccination with recombinant poxviruses. |
| 3499 | 15664925 | We show that intradermal vaccination with recombinant poxviruses activated Valpha14iNKT cells and NK cells in the livers of BALB/c mice while inducing IFN-gamma- and tumor necrosis factor alpha (TNF-alpha)-producing pre-erythrocytic stage antigen-specific CD8+ T cells. |
| 3500 | 15664925 | We show that intradermal vaccination with recombinant poxviruses activated Valpha14iNKT cells and NK cells in the livers of BALB/c mice while inducing IFN-gamma- and tumor necrosis factor alpha (TNF-alpha)-producing pre-erythrocytic stage antigen-specific CD8+ T cells. |
| 3501 | 15664925 | We show that intradermal vaccination with recombinant poxviruses activated Valpha14iNKT cells and NK cells in the livers of BALB/c mice while inducing IFN-gamma- and tumor necrosis factor alpha (TNF-alpha)-producing pre-erythrocytic stage antigen-specific CD8+ T cells. |
| 3502 | 15664925 | We show that intradermal vaccination with recombinant poxviruses activated Valpha14iNKT cells and NK cells in the livers of BALB/c mice while inducing IFN-gamma- and tumor necrosis factor alpha (TNF-alpha)-producing pre-erythrocytic stage antigen-specific CD8+ T cells. |
| 3503 | 15664925 | Greater numbers of hepatic Valpha14iNKT cells secreted interleukin-4 than IFN-gamma. |
| 3504 | 15664925 | Greater numbers of hepatic Valpha14iNKT cells secreted interleukin-4 than IFN-gamma. |
| 3505 | 15664925 | Greater numbers of hepatic Valpha14iNKT cells secreted interleukin-4 than IFN-gamma. |
| 3506 | 15664925 | Greater numbers of hepatic Valpha14iNKT cells secreted interleukin-4 than IFN-gamma. |
| 3507 | 15664925 | Vaccinated Valpha14iNKT-cell-deficient mice had lower, but still protective levels of hepatic and splenic IFN-gamma+ and TNF-alpha+ CD8+ T cells and better protection rates later after challenge with Plasmodium berghei sporozoites. |
| 3508 | 15664925 | Vaccinated Valpha14iNKT-cell-deficient mice had lower, but still protective levels of hepatic and splenic IFN-gamma+ and TNF-alpha+ CD8+ T cells and better protection rates later after challenge with Plasmodium berghei sporozoites. |
| 3509 | 15664925 | Vaccinated Valpha14iNKT-cell-deficient mice had lower, but still protective levels of hepatic and splenic IFN-gamma+ and TNF-alpha+ CD8+ T cells and better protection rates later after challenge with Plasmodium berghei sporozoites. |
| 3510 | 15664925 | Vaccinated Valpha14iNKT-cell-deficient mice had lower, but still protective levels of hepatic and splenic IFN-gamma+ and TNF-alpha+ CD8+ T cells and better protection rates later after challenge with Plasmodium berghei sporozoites. |
| 3511 | 15664925 | Furthermore, double-positive INF-gamma+/TNF-alpha+ CD8+ T cells were enriched in protected livers, suggesting that cells expressing both of these cytokines may be most relevant for protection. |
| 3512 | 15664925 | Furthermore, double-positive INF-gamma+/TNF-alpha+ CD8+ T cells were enriched in protected livers, suggesting that cells expressing both of these cytokines may be most relevant for protection. |
| 3513 | 15664925 | Furthermore, double-positive INF-gamma+/TNF-alpha+ CD8+ T cells were enriched in protected livers, suggesting that cells expressing both of these cytokines may be most relevant for protection. |
| 3514 | 15664925 | Furthermore, double-positive INF-gamma+/TNF-alpha+ CD8+ T cells were enriched in protected livers, suggesting that cells expressing both of these cytokines may be most relevant for protection. |
| 3515 | 15664921 | Maturation was evaluated by the ability of MPs to facilitate expression of costimulatory molecules such as CD40, CD86, CD83, and major histocompatibility complex classes I and II and to inhibit receptors such as CD14, CD16, and CD32. |
| 3516 | 15664921 | Activation of DCs was measured by the capacity of MPs to promote interleukin-12 and tumor necrosis factor alpha secretion. |
| 3517 | 15664921 | MP-loaded DCs are efficient stimulators of T cells and show a remarkable capacity to promote CD4 and CD8 proliferation. |
| 3518 | 15661389 | All immunized macaques but one gave a good cross-reactive antibody response to Tat but the proliferative response and levels of IL-2, IFN-gamma and TNF-alpha secretion of peripheral blood mononuclear cells (PBMCs) recalled ex vivo with active Tat protein were weak. |
| 3519 | 15657949 | Virus infection-associated bone marrow B cell depletion and impairment of humoral immunity to heterologous infection mediated by TNF-alpha/LTalpha. |
| 3520 | 15657949 | Virus infection-associated bone marrow B cell depletion and impairment of humoral immunity to heterologous infection mediated by TNF-alpha/LTalpha. |
| 3521 | 15657949 | Virus infection-associated bone marrow B cell depletion and impairment of humoral immunity to heterologous infection mediated by TNF-alpha/LTalpha. |
| 3522 | 15657949 | We previously showed that influenza virus infection of mice induces a depletion of bone marrow B lineage cells due to apoptosis of early B cells mediated by a mechanism involving TNF-alpha/LTalpha. |
| 3523 | 15657949 | We previously showed that influenza virus infection of mice induces a depletion of bone marrow B lineage cells due to apoptosis of early B cells mediated by a mechanism involving TNF-alpha/LTalpha. |
| 3524 | 15657949 | We previously showed that influenza virus infection of mice induces a depletion of bone marrow B lineage cells due to apoptosis of early B cells mediated by a mechanism involving TNF-alpha/LTalpha. |
| 3525 | 15657949 | These results show that the TNF-alpha/LTalpha production induced following infection with diverse viruses has detrimental effects on early B cells in the bone marrow, and may be among the factors that lead to the severely compromised humoral immunity observed to subsequent heterologous infections. |
| 3526 | 15657949 | These results show that the TNF-alpha/LTalpha production induced following infection with diverse viruses has detrimental effects on early B cells in the bone marrow, and may be among the factors that lead to the severely compromised humoral immunity observed to subsequent heterologous infections. |
| 3527 | 15657949 | These results show that the TNF-alpha/LTalpha production induced following infection with diverse viruses has detrimental effects on early B cells in the bone marrow, and may be among the factors that lead to the severely compromised humoral immunity observed to subsequent heterologous infections. |
| 3528 | 15652403 | The TNF-related weak inducer of apoptosis (TWEAK) is a TNF family member mediating proinflammatory effects by its receptor fibroblast growth factor-inducible-14 (Fn14). |
| 3529 | 15652403 | We studied the role of TWEAK/Fn14 in experimental autoimmune encephalomyelitis (EAE) by protein vaccination with TWEAK and Fn14 and recombinant TWEAK-DNA, respectively. |
| 3530 | 15652403 | TWEAK increased the secretion of CCL2 [monocyte chemotactic protein-1 (MCP-1)] by CNS endothelial cells and astrocytes in vitro, suggesting CCL2 as a critical mediator of TWEAKs proinflammatory effects. |
| 3531 | 15652403 | Purified IgG from TWEAK- or Fn14-vaccinated rats prevented TWEAK-induced production of CCL2 by endothelial cells. |
| 3532 | 15634888 | These T cells were fully functional in terms of their ability to produce IFN-gamma and TNF-alpha and to mediate cytolytic activity. |
| 3533 | 15629885 | Upon stimulation with LPS, in comparison with young MPhi, aged MPhi secreted reduced amounts of IL-6, tumor necrosis factor alpha, IL-1beta, and IL-12, cytokines necessary for B cells to respond to TI Ag. |
| 3534 | 15629885 | As aged MPhi have a reduced number of cells expressing Toll-like receptor 4 and CD14, the imbalance in cytokine production might be partly a result of fewer cells expressing key components of the LPS receptor complex. |
| 3535 | 15626469 | A panel of three CpG-oligodeoxynucleotides (ODN) and three eukaryotic expression vectors currently used in experimental DNA vaccines in pigs (pcDNA1, pcDNA3.1 and pCI) were screened for their immunostimulatory activity on porcine PBMC by evaluating in vitro the lymphocyte proliferative responses and cytokine profiles (IL-1alpha, IL-2, IL-4, IL-6, IL-10, IFN-gamma, TGF-beta, TNF-alpha). |
| 3536 | 15626469 | A panel of three CpG-oligodeoxynucleotides (ODN) and three eukaryotic expression vectors currently used in experimental DNA vaccines in pigs (pcDNA1, pcDNA3.1 and pCI) were screened for their immunostimulatory activity on porcine PBMC by evaluating in vitro the lymphocyte proliferative responses and cytokine profiles (IL-1alpha, IL-2, IL-4, IL-6, IL-10, IFN-gamma, TGF-beta, TNF-alpha). |
| 3537 | 15626469 | Furthermore, CpG-ODN A significantly induced IL-6 and TNF-alpha together with elevated levels of IFN-gamma and IL-2 mRNA expression even though considerable heterogeneity was observed in the response of individual pigs. |
| 3538 | 15626469 | Furthermore, CpG-ODN A significantly induced IL-6 and TNF-alpha together with elevated levels of IFN-gamma and IL-2 mRNA expression even though considerable heterogeneity was observed in the response of individual pigs. |
| 3539 | 15626469 | For pcDNA1, proliferation was absent together with significantly decreased levels of IL-6 and IFN-gamma. |
| 3540 | 15626469 | For pcDNA1, proliferation was absent together with significantly decreased levels of IL-6 and IFN-gamma. |
| 3541 | 15611232 | Type I IFN negatively regulates CD8+ T cell responses through IL-10-producing CD4+ T regulatory 1 cells. |
| 3542 | 15611232 | We used vaccine-induced, antiviral CD8(+) T cell responses in IFN-beta (IFN-beta(-/-))- or type I IFN receptor (IFNAR(-/-))-deficient mice to study immunomodulating effects of type I IFN that are not complicated by the interference of a concomitant virus infection. |
| 3543 | 15611232 | Compared with normal B6 mice, IFNAR(-/-) or IFN-beta(-/-) mice have normal numbers of CD4(+) and CD8(+) T cells, and CD25(+)FoxP3(+) T regulatory (T(R)) cells in liver and spleen. |
| 3544 | 15611232 | IFN-gamma and TNF-alpha production and clonal expansion of specific CD8(+) T cells from normal and knockout mice are similar. |
| 3545 | 15611232 | CD25(+)FoxP3(+) T(R) cells down-modulate vaccine-primed CD8(+) T cell responses in normal, IFNAR(-/-), or IFN-beta(-/-) mice to a comparable extent. |
| 3546 | 15611232 | Low IFN-alpha or IFN-beta doses (500-10(3) U/mouse) down-modulate CD8(+) T cells priming in vivo. |
| 3547 | 15611232 | IFNAR- and IFN-beta-deficient mice generate 2- to 3-fold lower numbers of IL-10-producing CD4(+) T cells after polyclonal or specific stimulation in vitro or in vivo. |
| 3548 | 15611232 | CD8(+) T cell responses are thus subjected to negative control by both CD25(+)FoxP3(+) T(R) cells and CD4(+)IL-10(+) T(R1) cells, but only development of the latter T(R) cells depends on type I IFN. |
| 3549 | 15607810 | DC1 induction depends on NK cell-produced IFN-gamma and TNF-alpha, with a possible involvement of additional factors. |
| 3550 | 15607810 | While NKG2D-dependent tumor cell recognition is sufficient to induce the cytotoxic "effector" function of NK cells, the induction of "NK cell help" requires additional signals from type-1 IFNs, products of virally-infected cells, or from IL-2. |
| 3551 | 15597328 | CpG also induces IL-12, TNF, MCP-1 and macrophage nitric oxide production. |
| 3552 | 15597328 | CD4(+) and CD8(+) T cells producing IFN-gamma increase in frequency, while those producing IL-5 decrease. |
| 3553 | 15591383 | Antigen-induced T cell subset proliferation, and secretion of interferon-gamma, nitric oxide, and tumor necrosis factor-alpha by cells from vaccinated calves were comparable to or greater than responses of vaccinated adults during the 11-wk study. |
| 3554 | 15585869 | APCs expressing the activation markers MHC class II, CD80, and CD40 increased in number in the lung. |
| 3555 | 15585869 | LTK63 treatment increased the pathogen-specific IgA response in the nasal mucosa and simultaneously decreased inflammatory cytokine production (IFN-gamma and TNF-alpha) after infection. |
| 3556 | 15585869 | The number of activated CD8(+)CD44(+) T cells and the respiratory syncytial virus- or influenza-specific CD8-proliferative responses increased, although the total inflammatory infiltrate was reduced. |
| 3557 | 15557632 | The DeltafbpA mutant induced a stronger expression of pulmonary mRNA messages in mice for tumor necrosis factor alpha, interleukin-1 beta (IL-1beta), gamma interferon, IL-6, IL-2, and inducible nitric oxide (NO) synthase, which led to its decline, while H37Rv persisted despite strong immune responses. |
| 3558 | 15553669 | Monocytes were separated from the peripheral blood collected by leukapheresis, and were cultured with GM-CSF and IL-4 for 6 days. |
| 3559 | 15553669 | Then, TNF-alpha, IL-1beta, IL-6 and PGE2 were added for maturation of DC. |
| 3560 | 15553669 | Th1/Th2 and Tc1/Tc2 balances improved in six of the nine patients after vaccination. |
| 3561 | 15553669 | In this study, it was shown that immunosuppressive factors, such as IAP and TGF-beta, and Th1 balance are useful as markers of immunomonitoring for tumor-DC fusion vaccine in patients with advanced or recurrent gastrointestinal patients. |
| 3562 | 15544517 | This article deals with the following matters: an outline of the host immune response to mycobacterial pathogens, particularly in terms of mobilization of the cytokine network in response to mycobacterial infection, and adjunctive immunotherapy using (1) recombinant immunomodulating cytokines, (especially Th-1 and Th-1-like cytokines such as IFN-gamma, IL-2, IL-12, IL-18 and GM-CSF), (2) inhibitors of immunosuppressive cytokines (TGF-beta) and some proinflammatory tissue-damaging cytokines (TNF-alpha), and (3) immunomodulatory agents such as ATP and its analogs, imidazoquinoline, diethyldithiocarbamate, poloxamer, dibenzopyran, galactosylceramide, nonsteroidal anti-inflammatory drugs, Chinese traditional medicines, levamisole, synthesized mycobacterial oligoDNA, DNA vaccine expressing mycobacterial HSP65 or IL-12, and heat-killed Mycobacterium vaccae. |
| 3563 | 15539940 | Marked heterogeneity was observed among the hybrid clones and only one clone exhibited characteristic features of DC (CD86 and I-A expression, dendritic morphology, T cell-stimulatory capacity and IL-1beta, IL-6 and TNFalpha production), suggesting that only small fractions of DC-tumor hybrids acquire and maintain the properties of parental DC. |
| 3564 | 15536145 | Recombinant CXCL10, CXCL9, CXCL11, and CXCL12 chemokines induced expression of B7-H1 on mouse and human NK cells in vitro. |
| 3565 | 15536145 | Mouse and human B7-H1+ NK cells induced proliferation of T cells and production of interferon gamma and tumor necrosis factor alpha in vitro, and in vivo blocking of B7-H1 inhibited the protective effect of vaccination. |
| 3566 | 15531030 | Incubation of immature human PBMC-derived DCs with SHIV VLPs for 48 h resulted in the significant up-regulation of CD40, CD80, CD83, CD54, CD86, HLA-A, B, C and HLA-DR, DP, DQ molecules on activated DC CD11c+ subpopulations. |
| 3567 | 15531030 | SHIV VLPs efficiently stimulated DCs to release IL-12, IFN-gamma and TNF-alpha. |
| 3568 | 15530685 | Significant increases in mRNA and protein production of T-helper 1 (Th1) cytokines (IL-2, IFNgamma), mRNA production of a cytotoxic-effector molecule (perforin), and lymphoproliferation response were observed in peripheral blood mononuclear cells (PBMC) from dual-subtype FIV-vaccinated cats after in vitro stimulation with inactivated FIV. |
| 3569 | 15530685 | In contrast, no statistically significant increase in FIV-stimulated mRNA production of Th2 cytokines (IL-4, IL-6) or other cytotoxic-effector molecules (TNFalpha, FasL) was observed in the PBMC from dual-subtype vaccinated cats. |
| 3570 | 15530685 | Moreover, no FIV-specific increases in the IFNgamma, IL-2, and perforin mRNA productions and in the IFNgamma bioactivity and lymphoproliferation responses were observed in the PBMC from cell-immunized cats. |
| 3571 | 15530685 | These observations suggest that IFNgamma induction, lymphoproliferation, and significant portion of IL-2 and perforin productions in the PBMC from dual-subtype vaccinated cats are clearly specific for viral antigens. |
| 3572 | 15530685 | Overall, dual-subtype FIV vaccine elicited strong Th1 response (IFN(, IL-2), which may contribute to the vaccine protection by enhancing the perforin-mediated cytotoxic-cell activity against FIV. |
| 3573 | 15507306 | Peripheral blood mononuclear cells (PBMC) isolated from these pigs responded to PRRSV exposure with a limited increase in their expression of the Th1 immune markers, IFNG, tumor necrosis factor-alpha and interleukin-15 (IL15), and a reduction in the quantity of mRNAs encoding the innate and inflammatory proteins, IL1B, IL8 and IFNA. |
| 3574 | 15507306 | Efforts to enhance Th1 immunity, by utilizing an expression plasmid encoding porcine IFNA (pINA) as an adjuvant, resulted in a temporary increase in the frequency of PRRSV-specific IFNG SC but only minor changes overall in the expression of Th1 associated cytokine or innate immune marker mRNA by virus-stimulated PBMC. |
| 3575 | 15507306 | Administration of pINA, however, did correlate with decreased IL1B secretion by cultured, unstimulated PBMC but had no effect on their ability to release IFNG. |
| 3576 | 15501769 | These data revealed that epitope-specific gamma interferon (IFN-gamma)-positive CD8+ T cells occur at higher frequencies in the spleen, liver, and blood than in draining or peripheral lymph nodes during the expansion phase. |
| 3577 | 15501769 | These data revealed that epitope-specific gamma interferon (IFN-gamma)-positive CD8+ T cells occur at higher frequencies in the spleen, liver, and blood than in draining or peripheral lymph nodes during the expansion phase. |
| 3578 | 15501769 | The location and function of both CD4+ and CD8+ Salmonella-specific memory T cells in mice who were given a single dose of Salmonella enterica serovar Typhimurium was also quantitated by an ex vivo restimulation with bacterial lysate to detect the total Salmonella-specific memory pool. |
| 3579 | 15501769 | The location and function of both CD4+ and CD8+ Salmonella-specific memory T cells in mice who were given a single dose of Salmonella enterica serovar Typhimurium was also quantitated by an ex vivo restimulation with bacterial lysate to detect the total Salmonella-specific memory pool. |
| 3580 | 15501769 | Mice immunized up to 6 months previously with S. enterica serovar Typhimurium had bacterium-specific CD4+ T cells that were capable of producing IFN-gamma or tumor necrosis factor alpha (TNF-alpha) at each site analyzed. |
| 3581 | 15501769 | Mice immunized up to 6 months previously with S. enterica serovar Typhimurium had bacterium-specific CD4+ T cells that were capable of producing IFN-gamma or tumor necrosis factor alpha (TNF-alpha) at each site analyzed. |
| 3582 | 15501769 | Similar findings were observed for CD8+ T cells that were capable of producing IFN-gamma, while a much lower frequency and more restricted distribution were associated with TNF-alpha-producing CD8+ T cells. |
| 3583 | 15501769 | Similar findings were observed for CD8+ T cells that were capable of producing IFN-gamma, while a much lower frequency and more restricted distribution were associated with TNF-alpha-producing CD8+ T cells. |
| 3584 | 15501769 | This study is the first to assess the frequencies, locations, and functions of both CD4+ and CD8+ memory T-cell populations in the same Salmonella-infected individuals and demonstrates the organ-specific functional compartmentalization of memory T cells after Salmonella infection. |
| 3585 | 15501769 | This study is the first to assess the frequencies, locations, and functions of both CD4+ and CD8+ memory T-cell populations in the same Salmonella-infected individuals and demonstrates the organ-specific functional compartmentalization of memory T cells after Salmonella infection. |
| 3586 | 15494483 | We used 12-color flow cytometry to characterize Ag-specific T cells elicited by vaccines or natural infection to determine lineage and differentiation status as well as the capacity to produce four cytokines (IFN-gamma, TNF-alpha, IL-2, and IL-4) and a chemokine (MIP1beta). |
| 3587 | 15494434 | Secretory phospholipase A2 (sPLA2), which hydrolyzes the sn-2 ester bond of glycerophospholipids, regulates a variety of cellular functions including migration of endothelial cells and neurite outgrowth. |
| 3588 | 15494434 | We report that human monocyte-derived DC cultures lack sPLA2 activity but respond to exogenous sPLA2. sPLA2 alone and in cooperation with TNF-alpha and interleukin 1 beta (IL-1beta) induced fatty acid release from DC membranes, which was accompanied by upregulation of surface markers and by an increase in the migratory and immunostimulatory capacity of the DCs. |
| 3589 | 15471952 | When measured in real time, peptide antigen and the cytokines, interleukin 12 (IL-12) and IL-18, independently regulate the on/off kinetics of protective (interferon gamma, tumor necrosis factor alpha) and immunomodulatory (IL-2, CD40L) cytokine production by activated T cells and memory T cells. |
| 3590 | 15471952 | The remarkable differences in effector functions elicited by innate or adaptive signals (IL-12/ IL-18 or peptide, respectively) illustrate the complex and stringent regulation of cytokine expression by CD8(+) T cells. |
| 3591 | 15456623 | The cytokine profile (interleukin [IL]-4, 5, 10 and 2, interferon [IFN-gamma], and tumor necrosis factor [TNF-alpha]) was determined before the start of treatment and at the end of follow-up (4-5 months). |
| 3592 | 15456623 | The cytokine profile (interleukin [IL]-4, 5, 10 and 2, interferon [IFN-gamma], and tumor necrosis factor [TNF-alpha]) was determined before the start of treatment and at the end of follow-up (4-5 months). |
| 3593 | 15456623 | Levels of IL-4, 5 and 10 (Th2 profile) decreased while those of IL-2, IFN-gamma, and TNF-alpha (Th1 profile) decreased. |
| 3594 | 15456623 | Levels of IL-4, 5 and 10 (Th2 profile) decreased while those of IL-2, IFN-gamma, and TNF-alpha (Th1 profile) decreased. |
| 3595 | 15385460 | Serum levels of the proinflammatory cytokines interleukin-1 beta (IL-1beta), IL-6, IL-8, IL-10, tumor necrosis factor alpha, and IL-12(p70) in Malian children with severe Plasmodium falciparum malaria and matched uncomplicated malaria or healthy controls. |
| 3596 | 15385460 | Serum levels of the proinflammatory cytokines interleukin-1 beta (IL-1beta), IL-6, IL-8, IL-10, tumor necrosis factor alpha, and IL-12(p70) in Malian children with severe Plasmodium falciparum malaria and matched uncomplicated malaria or healthy controls. |
| 3597 | 15385460 | Significantly elevated levels (given as geometric mean concentrations in picograms/milliliter) of interleukin-6 (IL-6; 485.2 versus 54.1; P = <0.001), IL-10 (1,099.3 versus 14.1; P = <0.001), tumor necrosis factor alpha (10.1 versus 7.7; P = <0.001), and IL-12(p70) (48.9 versus 31.3; P = 0.004) in serum were found in severe cases versus healthy controls. |
| 3598 | 15385460 | Significantly elevated levels (given as geometric mean concentrations in picograms/milliliter) of interleukin-6 (IL-6; 485.2 versus 54.1; P = <0.001), IL-10 (1,099.3 versus 14.1; P = <0.001), tumor necrosis factor alpha (10.1 versus 7.7; P = <0.001), and IL-12(p70) (48.9 versus 31.3; P = 0.004) in serum were found in severe cases versus healthy controls. |
| 3599 | 15385460 | Significantly elevated levels of IL-6 (485.2 versus 141.0; P = <0.001) and IL-10 (1,099.3 versus 133.9; P = <0.001) were seen in severe malaria cases versus uncomplicated malaria controls. |
| 3600 | 15385460 | Significantly elevated levels of IL-6 (485.2 versus 141.0; P = <0.001) and IL-10 (1,099.3 versus 133.9; P = <0.001) were seen in severe malaria cases versus uncomplicated malaria controls. |
| 3601 | 15385460 | Cerebral malaria was associated with significantly elevated levels of IL-6 (754.5 versus 311.4; P = <0.001) and IL-10 (1,405.6 versus 868.6; P = 0.006) compared to severe malaria cases without cerebral manifestations. |
| 3602 | 15385460 | Cerebral malaria was associated with significantly elevated levels of IL-6 (754.5 versus 311.4; P = <0.001) and IL-10 (1,405.6 versus 868.6; P = 0.006) compared to severe malaria cases without cerebral manifestations. |
| 3603 | 15385460 | Conversely, lower levels of IL-6 (199.2 versus 487.6; P = 0.03) and IL-10 (391.1 versus 1,160.9; P = 0.002) were noted in children with severe anemia compared to severe malaria cases with hemoglobin at >5 g/dl. |
| 3604 | 15385460 | Conversely, lower levels of IL-6 (199.2 versus 487.6; P = 0.03) and IL-10 (391.1 versus 1,160.9; P = 0.002) were noted in children with severe anemia compared to severe malaria cases with hemoglobin at >5 g/dl. |
| 3605 | 15373916 | When PBMC of a subset of TB patients (n = 11) were tested for secretion of protective Th1 cytokines [IFN-gamma, tumour necrosis factor (TNF)-alpha and interleukin (IL)-12] and the immunosuppressive cytokine IL-10, the complex CF and CW antigens as well as the recombinant Mtb9.8, Mtb9.9, Mtb40 and Ag85B induced the secretion of both types of cytokines. |
| 3606 | 15359643 | Peripheral blood CD14+ monocytes from multiple myeloma (MM) patients can be induced to differentiate into fully functional, mature, CD83+ dendritic cells (DCs) which are highly efficient in priming autologous T lymphocytes in response to the patient-specific tumor idiotype (Id). |
| 3607 | 15359643 | Peripheral blood CD14+ monocytes from multiple myeloma (MM) patients can be induced to differentiate into fully functional, mature, CD83+ dendritic cells (DCs) which are highly efficient in priming autologous T lymphocytes in response to the patient-specific tumor idiotype (Id). |
| 3608 | 15359643 | Cells were then cultured, according to Good Manufacturing Practice guidelines, in FCS-free medium in cell culture bags, and differentiated to DCs with GM-CSF plus IL-4 followed by TNF-alpha or, more recently, by a cocktail of IL-1beta, IL-6, TNF-alpha and prostaglandin-E2. |
| 3609 | 15359643 | Cells were then cultured, according to Good Manufacturing Practice guidelines, in FCS-free medium in cell culture bags, and differentiated to DCs with GM-CSF plus IL-4 followed by TNF-alpha or, more recently, by a cocktail of IL-1beta, IL-6, TNF-alpha and prostaglandin-E2. |
| 3610 | 15359643 | Notably, the cytokine cocktail induced a significantly higher percentage and yield (31+/-10.9 of initial CD14+ cells) of DCs than TNF-alpha alone, secretion of larger amounts of IL-12, potent stimulatory activity on allogeneic and autologous T cells. |
| 3611 | 15359643 | Notably, the cytokine cocktail induced a significantly higher percentage and yield (31+/-10.9 of initial CD14+ cells) of DCs than TNF-alpha alone, secretion of larger amounts of IL-12, potent stimulatory activity on allogeneic and autologous T cells. |
| 3612 | 15356430 | Urinary tract diseases revealed after DTP vaccination in infants and young children: cytokine irregularities and down-regulation of cytochrome P-450 enzymes induced by the vaccine may uncover latent diseases in genetically predisposed subjects. |
| 3613 | 15356430 | Urinary tract diseases revealed after DTP vaccination in infants and young children: cytokine irregularities and down-regulation of cytochrome P-450 enzymes induced by the vaccine may uncover latent diseases in genetically predisposed subjects. |
| 3614 | 15356430 | Urinary tract diseases revealed after DTP vaccination in infants and young children: cytokine irregularities and down-regulation of cytochrome P-450 enzymes induced by the vaccine may uncover latent diseases in genetically predisposed subjects. |
| 3615 | 15356430 | It is suggested that the whole-cell pertussis present in DTP vaccine, acting as an excessive stimulus in these patients, produced symptoms reminiscent of biologic responses to circulating proinflammatory monokines such as IL-1beta, TNF-alpha, and IL-6 because earlier it was reported that in vitro the whole-cell vaccine induced significantly more such cytokine production than did the acellular pertussis or diphtheria-tetanus-only vaccine. |
| 3616 | 15356430 | It is suggested that the whole-cell pertussis present in DTP vaccine, acting as an excessive stimulus in these patients, produced symptoms reminiscent of biologic responses to circulating proinflammatory monokines such as IL-1beta, TNF-alpha, and IL-6 because earlier it was reported that in vitro the whole-cell vaccine induced significantly more such cytokine production than did the acellular pertussis or diphtheria-tetanus-only vaccine. |
| 3617 | 15356430 | It is suggested that the whole-cell pertussis present in DTP vaccine, acting as an excessive stimulus in these patients, produced symptoms reminiscent of biologic responses to circulating proinflammatory monokines such as IL-1beta, TNF-alpha, and IL-6 because earlier it was reported that in vitro the whole-cell vaccine induced significantly more such cytokine production than did the acellular pertussis or diphtheria-tetanus-only vaccine. |
| 3618 | 15356430 | Analysis of the cellular immune disturbances previously reported in urinary tract infection/inflammation (increased serum and/or urinary IL-1alpha, IL-1 receptor antagonist, IL-6 and IL-8), steroid-sensitive nephrotic syndrome (increased IL-2, IFN-gamma, TNF-alpha, and decreased or increased IL-4, depending on the cells studied), and atopic dermatitis (decreased IFN-gamma and increased IL-4 production), may suggest that similar subclinical chronic cytokine-mediated abnormalities produced in the course of latent diseases revealed in our patients, combined with those caused by DTP vaccination stimulus, were responsible for the pathomechanism of these clinical entities. |
| 3619 | 15356430 | Analysis of the cellular immune disturbances previously reported in urinary tract infection/inflammation (increased serum and/or urinary IL-1alpha, IL-1 receptor antagonist, IL-6 and IL-8), steroid-sensitive nephrotic syndrome (increased IL-2, IFN-gamma, TNF-alpha, and decreased or increased IL-4, depending on the cells studied), and atopic dermatitis (decreased IFN-gamma and increased IL-4 production), may suggest that similar subclinical chronic cytokine-mediated abnormalities produced in the course of latent diseases revealed in our patients, combined with those caused by DTP vaccination stimulus, were responsible for the pathomechanism of these clinical entities. |
| 3620 | 15356430 | Analysis of the cellular immune disturbances previously reported in urinary tract infection/inflammation (increased serum and/or urinary IL-1alpha, IL-1 receptor antagonist, IL-6 and IL-8), steroid-sensitive nephrotic syndrome (increased IL-2, IFN-gamma, TNF-alpha, and decreased or increased IL-4, depending on the cells studied), and atopic dermatitis (decreased IFN-gamma and increased IL-4 production), may suggest that similar subclinical chronic cytokine-mediated abnormalities produced in the course of latent diseases revealed in our patients, combined with those caused by DTP vaccination stimulus, were responsible for the pathomechanism of these clinical entities. |
| 3621 | 15356430 | This speculation is in agreement with the reports on the long-lasting induction of cytokine release and down-regulation of hepatic cytochrome P-450 isoenzyme activities after administration of DTP vaccine to mice and may be supported by the fact that TH1 phenotype is associated with the up-regulation of intercellular adhesion molecule-1 and RANTES, whereas TH2 phenotype is associated with the up-regulation of the vascular cell adhesion molecule and P-selectin, which are key players in the migration into inflamed tissues and localization of lymphocytes and other allergic effector and inflammatory cells. |
| 3622 | 15356430 | This speculation is in agreement with the reports on the long-lasting induction of cytokine release and down-regulation of hepatic cytochrome P-450 isoenzyme activities after administration of DTP vaccine to mice and may be supported by the fact that TH1 phenotype is associated with the up-regulation of intercellular adhesion molecule-1 and RANTES, whereas TH2 phenotype is associated with the up-regulation of the vascular cell adhesion molecule and P-selectin, which are key players in the migration into inflamed tissues and localization of lymphocytes and other allergic effector and inflammatory cells. |
| 3623 | 15356430 | This speculation is in agreement with the reports on the long-lasting induction of cytokine release and down-regulation of hepatic cytochrome P-450 isoenzyme activities after administration of DTP vaccine to mice and may be supported by the fact that TH1 phenotype is associated with the up-regulation of intercellular adhesion molecule-1 and RANTES, whereas TH2 phenotype is associated with the up-regulation of the vascular cell adhesion molecule and P-selectin, which are key players in the migration into inflamed tissues and localization of lymphocytes and other allergic effector and inflammatory cells. |
| 3624 | 15356430 | Because several inflammatory cytokines down-regulate gene expression of major cytochrome P-450 and/or other enzymes with the specific effects on mRNA levels, protein expression, and enzyme activity, thus affecting the metabolism of several endogenous lipophilic substances such as steroids, lipid-soluble vitamins, prostaglandins, leukotrienes, thromboxanes, and exogenous substances, their irregularities in the body may eventually lead to the flare of latent diseases in some predisposed subjects. |
| 3625 | 15356430 | Because several inflammatory cytokines down-regulate gene expression of major cytochrome P-450 and/or other enzymes with the specific effects on mRNA levels, protein expression, and enzyme activity, thus affecting the metabolism of several endogenous lipophilic substances such as steroids, lipid-soluble vitamins, prostaglandins, leukotrienes, thromboxanes, and exogenous substances, their irregularities in the body may eventually lead to the flare of latent diseases in some predisposed subjects. |
| 3626 | 15356430 | Because several inflammatory cytokines down-regulate gene expression of major cytochrome P-450 and/or other enzymes with the specific effects on mRNA levels, protein expression, and enzyme activity, thus affecting the metabolism of several endogenous lipophilic substances such as steroids, lipid-soluble vitamins, prostaglandins, leukotrienes, thromboxanes, and exogenous substances, their irregularities in the body may eventually lead to the flare of latent diseases in some predisposed subjects. |
| 3627 | 15356430 | Also, interleukin genetic polymorphisms, especially the constellation of TNF-alpha and IL-6 genetic variants, might predispose some infants with infection to a more than usually intense inflammatory response in the kidneys after vaccination. |
| 3628 | 15356430 | Also, interleukin genetic polymorphisms, especially the constellation of TNF-alpha and IL-6 genetic variants, might predispose some infants with infection to a more than usually intense inflammatory response in the kidneys after vaccination. |
| 3629 | 15356430 | Also, interleukin genetic polymorphisms, especially the constellation of TNF-alpha and IL-6 genetic variants, might predispose some infants with infection to a more than usually intense inflammatory response in the kidneys after vaccination. |
| 3630 | 15353364 | Typical pro-inflammatory cytokines include TNFalpha, IL1 and IL6. |
| 3631 | 15353364 | Typical pro-inflammatory cytokines include TNFalpha, IL1 and IL6. |
| 3632 | 15353364 | Here we showed that administration of adenoviral antigens alone led to a predominant elevation of serum IL6 but not TNFalpha Administration of endotoxin together with adenoviral antigens led to elevation of both serum IL6 and TNFalpha. |
| 3633 | 15353364 | Here we showed that administration of adenoviral antigens alone led to a predominant elevation of serum IL6 but not TNFalpha Administration of endotoxin together with adenoviral antigens led to elevation of both serum IL6 and TNFalpha. |
| 3634 | 15342937 | Selective generation of different dendritic cell precursors from CD34+ cells by interleukin-6 and interleukin-3. |
| 3635 | 15342937 | Selective generation of different dendritic cell precursors from CD34+ cells by interleukin-6 and interleukin-3. |
| 3636 | 15342937 | Selective generation of different dendritic cell precursors from CD34+ cells by interleukin-6 and interleukin-3. |
| 3637 | 15342937 | Several cytokines, especially stem cell factor (SCF) and FLT3-ligand (FL), have been identified as essential to produce large numbers of myeloid precursors and even to increase DC yield obtained by the action of granulocyte-macrophage colony-stimulating factor (GM-CSF) and tumor necrosis factor alpha (TNF-alpha). |
| 3638 | 15342937 | Several cytokines, especially stem cell factor (SCF) and FLT3-ligand (FL), have been identified as essential to produce large numbers of myeloid precursors and even to increase DC yield obtained by the action of granulocyte-macrophage colony-stimulating factor (GM-CSF) and tumor necrosis factor alpha (TNF-alpha). |
| 3639 | 15342937 | Several cytokines, especially stem cell factor (SCF) and FLT3-ligand (FL), have been identified as essential to produce large numbers of myeloid precursors and even to increase DC yield obtained by the action of granulocyte-macrophage colony-stimulating factor (GM-CSF) and tumor necrosis factor alpha (TNF-alpha). |
| 3640 | 15342937 | We report here that in the absence of serum, SCF, FL, and thrombopoietin (TPO) plus interleukin-6 (IL-6) and SCF, FL, and TPO plus IL-3 were able to generate CD14+CD1a- and CD14- CD1a+ myeloid DC precursors from CD34+ cells, but IL-6 had an inhibitory effect on the generation of CD14- CD1a+ cells. |
| 3641 | 15342937 | We report here that in the absence of serum, SCF, FL, and thrombopoietin (TPO) plus interleukin-6 (IL-6) and SCF, FL, and TPO plus IL-3 were able to generate CD14+CD1a- and CD14- CD1a+ myeloid DC precursors from CD34+ cells, but IL-6 had an inhibitory effect on the generation of CD14- CD1a+ cells. |
| 3642 | 15342937 | We report here that in the absence of serum, SCF, FL, and thrombopoietin (TPO) plus interleukin-6 (IL-6) and SCF, FL, and TPO plus IL-3 were able to generate CD14+CD1a- and CD14- CD1a+ myeloid DC precursors from CD34+ cells, but IL-6 had an inhibitory effect on the generation of CD14- CD1a+ cells. |
| 3643 | 15342937 | Both DC precursors differentiated into mature DCs by GM-CSF, IL-4, and TNF-alpha, and DCs obtained from both types of culture exhibited equal allostimulatory capacity. |
| 3644 | 15342937 | Both DC precursors differentiated into mature DCs by GM-CSF, IL-4, and TNF-alpha, and DCs obtained from both types of culture exhibited equal allostimulatory capacity. |
| 3645 | 15342937 | Both DC precursors differentiated into mature DCs by GM-CSF, IL-4, and TNF-alpha, and DCs obtained from both types of culture exhibited equal allostimulatory capacity. |
| 3646 | 15342937 | CD1a+ DCs generated could be identified on the basis of DC-specific intracellular adhesion molecule-grabbing nonintegrin (DC-SIGN) expression, a novel C-type lectin receptor expressed on dermal DCs but not on Langerhans cells. |
| 3647 | 15342937 | CD1a+ DCs generated could be identified on the basis of DC-specific intracellular adhesion molecule-grabbing nonintegrin (DC-SIGN) expression, a novel C-type lectin receptor expressed on dermal DCs but not on Langerhans cells. |
| 3648 | 15342937 | CD1a+ DCs generated could be identified on the basis of DC-specific intracellular adhesion molecule-grabbing nonintegrin (DC-SIGN) expression, a novel C-type lectin receptor expressed on dermal DCs but not on Langerhans cells. |
| 3649 | 15342937 | In addition, the inclusion of IL-3 to the culture medium induced the appearance of CD13- cells that differentiated into plasmacytoid DC (DC2) on the addition of TNF-alpha, allowing the identification of developmental stages of DC2. |
| 3650 | 15342937 | In addition, the inclusion of IL-3 to the culture medium induced the appearance of CD13- cells that differentiated into plasmacytoid DC (DC2) on the addition of TNF-alpha, allowing the identification of developmental stages of DC2. |
| 3651 | 15342937 | In addition, the inclusion of IL-3 to the culture medium induced the appearance of CD13- cells that differentiated into plasmacytoid DC (DC2) on the addition of TNF-alpha, allowing the identification of developmental stages of DC2. |
| 3652 | 15342370 | We show that IFN-alpha and polyinosinic:polycytidylic acid (p-I:C) synergize with the "classical" type-1-polarizing cytokine cocktail [tumor necrosis factor alpha (TNFalpha)/IL-1beta/IFNgamma], allowing for serum-free generation of fully mature type-1-polarized DCs (DC1). |
| 3653 | 15342370 | We show that IFN-alpha and polyinosinic:polycytidylic acid (p-I:C) synergize with the "classical" type-1-polarizing cytokine cocktail [tumor necrosis factor alpha (TNFalpha)/IL-1beta/IFNgamma], allowing for serum-free generation of fully mature type-1-polarized DCs (DC1). |
| 3654 | 15342370 | Such "alpha-type-1-polarized DC(s)" (alphaDC1) show high migratory responses to the CCR7 ligand, 6C-kine but produce much higher levels of IL-12p70 as compared to TNFalpha/IL-1beta/IL-6/prostaglandin E2 (PGE2)-matured DCs (sDC), the current "gold standard" in DC-based cancer vaccination. |
| 3655 | 15342370 | Such "alpha-type-1-polarized DC(s)" (alphaDC1) show high migratory responses to the CCR7 ligand, 6C-kine but produce much higher levels of IL-12p70 as compared to TNFalpha/IL-1beta/IL-6/prostaglandin E2 (PGE2)-matured DCs (sDC), the current "gold standard" in DC-based cancer vaccination. |
| 3656 | 15342370 | A single round of in vitro sensitization with alphaDC1 (versus sDCs) induces up to 40-fold higher numbers of long-lived CTLs against melanoma-associated antigens: MART-1, gp100, and tyrosinase. |
| 3657 | 15342370 | A single round of in vitro sensitization with alphaDC1 (versus sDCs) induces up to 40-fold higher numbers of long-lived CTLs against melanoma-associated antigens: MART-1, gp100, and tyrosinase. |
| 3658 | 15331707 | Recombinant interleukin-7 induces proliferation of naive macaque CD4+ and CD8+ T cells in vivo. |
| 3659 | 15331707 | Naive CD8+ T cells transferred to lymphopenic mice acquire a memory-like phenotype, raising the possibility that IL-7 is the biological mediator of this effect. |
| 3660 | 15331707 | Here, we provide direct evidence that IL-7 induces the acquisition of memory-cell markers not only in CD8+ T cells but also in CD4+ T-cell subsets in immune-competent Indian rhesus macaques. |
| 3661 | 15331707 | Memory-like CD4+ and CD8+ T cells acquired the ability to secrete tumor necrosis factor alpha and, to a lesser extent, gamma interferon following stimulation with a cognate antigen. |
| 3662 | 15331707 | Importantly, IL-7 induced cycling of both CD4+ and CD8+ central memory and effector memory T cells, demonstrating its contribution to the maintenance of the entire T-cell pool. |
| 3663 | 15322018 | Murine bone marrow-derived dendritic cells were activated to secrete interleukin-6 (IL-6), IL-12, and tumor necrosis factor upon exposure to antigen-free TPL liposomes. |
| 3664 | 15322018 | Although the activity of phosphatidylinositol dimannoside was little influenced by palmitoylation of mannose at C-6, a further palmitoylation at inositol C-3 diminished the induction levels of IL-6 and IL-12. |
| 3665 | 15321988 | The role of CD4(+) T cells in the pathogenesis of ocular toxoplasmosis was investigated in murine models utilizing inbred C57BL/6 mice deficient either in CD4(+), CD8(+), or B cells (microMT). |
| 3666 | 15321988 | As expected, there were no increases in the levels of immunoglobulin G in serum or aqueous humor in microMT mice, and there was no increase in the levels of gamma interferon and tumor necrosis factor alpha in the sera of CD4 KO mice after both infection and challenge. |
| 3667 | 15321988 | Mice deficient in CD8(+) CD4(+) T cells or B cells exhibit diminished vaccine-induced resistance and increased ocular parasite burden after challenge. |
| 3668 | 15315837 | OX40 ligand (OX40L), a member of TNF superfamily, is a co-stimulatory molecule involved in T cell activation. |
| 3669 | 15315837 | Vaccination with OX40L was significantly enhanced by combination treatment with intra-tumour injection of a disabled infectious single cycle-herpes simplex virus (DISC-HSV) vector encoding murine granulocyte macrophage-colony stimulating factor (mGM-CSF). |
| 3670 | 15315837 | Tumour rejection in response to OX40L therapy required functional CD4+ and CD8+ T cells and correlated with splenocyte cytotoxic T lymphocytes (CTLs) activity against the AH-1 gp70 peptide of the tumour associated antigen expressed by CT26 cells. |
| 3671 | 15314040 | Furthermore, the UV-inactivated virion induced regional lymph node T-cell proliferation and significant levels of cytokine production (IL-2, IL-4, IL-5, IFN-gamma and TNF-alpha) upon restimulation with inactivated SARS-CoV virion in vitro. |
| 3672 | 15295005 | In the presence of GM-CSF, TNF-alpha, and/or IL-4, leukemia-derived DC are obtained that display features of immature DC (i-DC). |
| 3673 | 15295005 | Using CD40L as maturating agent, we show that leukemic i-DC can differentiate into cells that fulfill the phenotypic criteria of m-DC and, compared with normal counterparts, are functionally competent in vitro in terms of: 1) production of cytokines that support T cell activation and proliferation and drive Th1 polarization; 2) generation of autologous CD8(+) CTLs and CD4(+) T cells that are MHC-restricted and leukemia-specific; 3) migration from tissues to lymph nodes; 4) amplification of Ag presentation by monocyte attraction; 5) attraction of naive/resting and activated T cells. |
| 3674 | 15294953 | After adoptive transfer and in vivo activation of TCR transgenic CD8(+) T cells, an increased number of activated CD8(+) T cells was observed in the lymph nodes, spleen, and liver of mice treated with anti-TNF-alpha. |
| 3675 | 15294953 | After adoptive transfer and in vivo activation of TCR transgenic CD8(+) T cells, an increased number of activated CD8(+) T cells was observed in the lymph nodes, spleen, and liver of mice treated with anti-TNF-alpha. |
| 3676 | 15294953 | These results indicate that TNF-alpha is responsible for inducing apoptosis in the liver and suggest that CD8(+) T cells escaping this mechanism of deletion can recirculate into the periphery. |
| 3677 | 15294953 | These results indicate that TNF-alpha is responsible for inducing apoptosis in the liver and suggest that CD8(+) T cells escaping this mechanism of deletion can recirculate into the periphery. |
| 3678 | 15280475 | The immunogenic properties of baculovirus as vaccine vector were not restricted to E2 because a CEA-specific CD4(+) T-cell response was observed upon intramuscular injection of Bac-CEA. |
| 3679 | 15280475 | Induction of inflammatory cytokines such as gamma interferon, tumor necrosis factor alpha, and interleukin-6 was detected as early as 6 h postinjection of Bac-G-E2. |
| 3680 | 15273801 | With the purpose of understanding the immunological mechanisms involved in this protection, the lymphoproliferative response, IFN-gamma and other cytokines like interleukin (IL-5, IL-10), and tumor necrosis factor alpha (TNF-alpha) were evaluated before and after the use of anti-TB drugs on 30 patients with active TB disease, 24 healthy household contacts of active TB patients, with positive purified protein derivative (PPD) skin tests (induration > 10 mm), and 34 asymptomatic individuals with negative PPD skin test results (induration < 5 mm). |
| 3681 | 15273801 | With the purpose of understanding the immunological mechanisms involved in this protection, the lymphoproliferative response, IFN-gamma and other cytokines like interleukin (IL-5, IL-10), and tumor necrosis factor alpha (TNF-alpha) were evaluated before and after the use of anti-TB drugs on 30 patients with active TB disease, 24 healthy household contacts of active TB patients, with positive purified protein derivative (PPD) skin tests (induration > 10 mm), and 34 asymptomatic individuals with negative PPD skin test results (induration < 5 mm). |
| 3682 | 15273801 | The positive lymphoproliferative response among peripheral blood mononuclear cells of patients showed high levels of IFN-gamma, TNF-alpha, and IL-10. |
| 3683 | 15273801 | The positive lymphoproliferative response among peripheral blood mononuclear cells of patients showed high levels of IFN-gamma, TNF-alpha, and IL-10. |
| 3684 | 15270693 | However, the C-terminal portion (amino acids 359-610) stimulates the production of CC chemokines, IL-12 (interleukin-12), TNFalpha(tumour necrosis factor alpha), NO and maturation of dendritic cells and also functions as an adjuvant in the induction of immune responses. |
| 3685 | 15270693 | Since the receptor for HSP70 is CD40, which with its CD40 ligand constitutes a major co-stimulatory pathway in the interaction between antigen-presenting cells and T-cells, HSP70 may function as an alternative ligand to CD40L. |
| 3686 | 15265929 | There was also approximately 40% more specific lysis of the HIV Env-expressing target cells in chimeric HA/SHIV VLP-immunized than in SHIV VLP-immunized CD4 KO mouse splenocytes. |
| 3687 | 15265929 | Moreover, we have found that chimeric HA/SHIV VLPs could efficiently bind and activate dendritic cells and stimulate the activated dendritic cells to secret TNF-alpha and IFN-gamma. |
| 3688 | 15254748 | They can be repaired, at least partially and in vitro, by cytokines (IFNgamma, TNFalpha) or by DNA demethylation/histone hyperacetylation procedures. |
| 3689 | 15254748 | The innate and adaptive antitumour immunity may be under some conditions interconnected: primary activation of the MHC class I-unrestricted surveillance mechanisms may lead to the production of IFNgamma by the activated NK/gammadelta T cells; the in situ produced IFNgamma may then up-regulate the MHC class I molecule expression on the tumour cell surface and in this way it may stimulate the more efficient, MHC class I-restricted, adaptive immunity. |
| 3690 | 15254748 | Either therapeutic procedures aiming at up-regulation of MHC class I expression, or enhancement of MHC class I-unrestricted (CD4+, NK, NKT, gammadelta T) tumour defence effector mechanisms by dendritic cell-based therapeutic vaccines, by cytokines (IL-2, IL-12, IFNgamma, GM-CSF), or by the cytokine gene-based, genetically modified tumour vaccines should be considered. |
| 3691 | 15254744 | OK432 and PSK were examined in vitro, and compared with lipopolysaccharide (LPS) and a cytokine cocktail (IL-1beta, TNF-alpha, IL-6 and PGE2). |
| 3692 | 15254744 | In the immunophenotypical analysis, the expression of CD80 and CD83 of DCs stimulated with OK-432 increased significantly compared with PSK and medium, and this up-regulation was the same as levels of DCs stimulated with cytokine cocktail. |
| 3693 | 15254744 | DCs stimulated with OK-432 showed significantly higher production of IL-12 and Th1-type cytokines (IL-2 and IFN-gamma) compared with DCs stimulated with LPS or cytokine cocktail. |
| 3694 | 15242811 | Human monocytes were cultured with GM-CSF and IL-4 for 6 days, followed by another 2 days in the presence of M1, M4 or TNF-alpha as a maturation stimulus. |
| 3695 | 15242811 | Human monocytes were cultured with GM-CSF and IL-4 for 6 days, followed by another 2 days in the presence of M1, M4 or TNF-alpha as a maturation stimulus. |
| 3696 | 15242811 | Stimulation with 20 microM of M1 or M4 increased expression level of CD80, CD83 and CD86 as expressed by mean fluorescence intensity (MFI) and decreased endocytic activity. |
| 3697 | 15242811 | Stimulation with 20 microM of M1 or M4 increased expression level of CD80, CD83 and CD86 as expressed by mean fluorescence intensity (MFI) and decreased endocytic activity. |
| 3698 | 15242811 | In CTL assay, the production of IFN-gamma and 51Cr release on M4-primed mature DCs was more augmented than of immature DCs or TNF-alpha-primed mature DCs. |
| 3699 | 15242811 | In CTL assay, the production of IFN-gamma and 51Cr release on M4-primed mature DCs was more augmented than of immature DCs or TNF-alpha-primed mature DCs. |
| 3700 | 15240755 | We found that monocytes infected with BCG differentiate into CD1a- DCs (BCG-DCs) in the presence of granulocyte macrophage-colony stimulating factor and interleukin (IL)-4 and acquired a mature phenotype in the absence of maturation stimuli. |
| 3701 | 15240755 | In addition, BCG-DCs produced proinflammatory cytokines (tumor necrosis factor alpha, IL-1beta, IL-6) and IL-10 but not IL-12. |
| 3702 | 15214052 | In this study, we demonstrate that pretreatment of monocytes with human HSP60 results in a suppression of TNF-alpha production on restimulation with HSP60. |
| 3703 | 15214052 | In this study, we demonstrate that pretreatment of monocytes with human HSP60 results in a suppression of TNF-alpha production on restimulation with HSP60. |
| 3704 | 15214052 | In this study, we demonstrate that pretreatment of monocytes with human HSP60 results in a suppression of TNF-alpha production on restimulation with HSP60. |
| 3705 | 15214052 | Furthermore, desensitization with HSP60 inhibits TNF-alpha expression in these cells in response to LPS stimulation, thereby inducing "cross-tolerance". |
| 3706 | 15214052 | Furthermore, desensitization with HSP60 inhibits TNF-alpha expression in these cells in response to LPS stimulation, thereby inducing "cross-tolerance". |
| 3707 | 15214052 | Furthermore, desensitization with HSP60 inhibits TNF-alpha expression in these cells in response to LPS stimulation, thereby inducing "cross-tolerance". |
| 3708 | 15214052 | In contrast to TNF-alpha suppression, IL-1beta expression was augmented in HSP60-pretreated monocytes on restimulation, while being suppressed in THP-1 cells. |
| 3709 | 15214052 | In contrast to TNF-alpha suppression, IL-1beta expression was augmented in HSP60-pretreated monocytes on restimulation, while being suppressed in THP-1 cells. |
| 3710 | 15214052 | In contrast to TNF-alpha suppression, IL-1beta expression was augmented in HSP60-pretreated monocytes on restimulation, while being suppressed in THP-1 cells. |
| 3711 | 15214052 | Addition of an anti-IL-10 neutralizing antibody had no significant effect on HSP60- or LPS-induced tolerance.HSP60 priming of monocytes also results in significant down-regulation of HLA-DR, CD86 and Toll-like receptor 4 expression, but minimally up-regulates CD80 expression, similar to that previously reported with LPS. |
| 3712 | 15214052 | Addition of an anti-IL-10 neutralizing antibody had no significant effect on HSP60- or LPS-induced tolerance.HSP60 priming of monocytes also results in significant down-regulation of HLA-DR, CD86 and Toll-like receptor 4 expression, but minimally up-regulates CD80 expression, similar to that previously reported with LPS. |
| 3713 | 15214052 | Addition of an anti-IL-10 neutralizing antibody had no significant effect on HSP60- or LPS-induced tolerance.HSP60 priming of monocytes also results in significant down-regulation of HLA-DR, CD86 and Toll-like receptor 4 expression, but minimally up-regulates CD80 expression, similar to that previously reported with LPS. |
| 3714 | 15214052 | By identifying a previously unrecognized "tolerizing" effect of extended exposure to autologous HSP60 on the innate immune system, as opposed to its recently identified pro-inflammatory stimulatory capacity, this study highlights a further level of complexity of our understanding of the biological activities of HSP. |
| 3715 | 15214052 | By identifying a previously unrecognized "tolerizing" effect of extended exposure to autologous HSP60 on the innate immune system, as opposed to its recently identified pro-inflammatory stimulatory capacity, this study highlights a further level of complexity of our understanding of the biological activities of HSP. |
| 3716 | 15214052 | By identifying a previously unrecognized "tolerizing" effect of extended exposure to autologous HSP60 on the innate immune system, as opposed to its recently identified pro-inflammatory stimulatory capacity, this study highlights a further level of complexity of our understanding of the biological activities of HSP. |
| 3717 | 15210831 | Elderly individuals had a similar frequency of CD69+CD4+ T cells producing IFN-gamma and TNF-alpha at 1 wk, but a lower frequency of these CD4+ T cells at 3 mo after influenza vaccination. |
| 3718 | 15210831 | Although the elderly had a higher frequency of central memory (CM; CCR7+CD45RA-) CD4+ T cells, they had a significantly lower frequency of effector memory (EM; CCR7-CD45RA-) CD4+ T cells, and the frequency of the latter memory CD4+ T cells positively correlated with the frequency of influenza virus-specific CD69+CD4+ T cells producing IFN-gamma at 3 mo. |
| 3719 | 15210831 | This failure probably stems from the alteration in the frequency of CM and EM CD4+ T cells in the elderly that is related to alteration in IL-7 levels. |
| 3720 | 15205385 | Involvement of interleukin-6 and tumor necrosis factor alpha in CYP3A11 and 2C29 down-regulation by Bacillus Calmette-Guerin and lipopolysaccharide in mouse liver. |
| 3721 | 15205385 | Involvement of interleukin-6 and tumor necrosis factor alpha in CYP3A11 and 2C29 down-regulation by Bacillus Calmette-Guerin and lipopolysaccharide in mouse liver. |
| 3722 | 15205385 | Involvement of interleukin-6 and tumor necrosis factor alpha in CYP3A11 and 2C29 down-regulation by Bacillus Calmette-Guerin and lipopolysaccharide in mouse liver. |
| 3723 | 15205385 | Bacillus Calmette-Guérin (BCG) and lipopolysaccharide (LPS) are well known potent activators of the cell-mediated immune system and thus lead to the decreases in cytochrome P450 (P450). |
| 3724 | 15205385 | Bacillus Calmette-Guérin (BCG) and lipopolysaccharide (LPS) are well known potent activators of the cell-mediated immune system and thus lead to the decreases in cytochrome P450 (P450). |
| 3725 | 15205385 | Bacillus Calmette-Guérin (BCG) and lipopolysaccharide (LPS) are well known potent activators of the cell-mediated immune system and thus lead to the decreases in cytochrome P450 (P450). |
| 3726 | 15205385 | In this study we used interleukin (IL)-1alpha/beta, IL-6, or tumor necrosis factor alpha (TNFalpha) knockout (KO) mice to investigate how each cytokine is involved in P450 down-regulation, especially CYP3A11 and 2C29. |
| 3727 | 15205385 | In this study we used interleukin (IL)-1alpha/beta, IL-6, or tumor necrosis factor alpha (TNFalpha) knockout (KO) mice to investigate how each cytokine is involved in P450 down-regulation, especially CYP3A11 and 2C29. |
| 3728 | 15205385 | In this study we used interleukin (IL)-1alpha/beta, IL-6, or tumor necrosis factor alpha (TNFalpha) knockout (KO) mice to investigate how each cytokine is involved in P450 down-regulation, especially CYP3A11 and 2C29. |
| 3729 | 15205385 | The present study has shown that IL-6 and TNFalpha are likely to be major factors involved in the down-regulation of CYP3A11 and 2C29 mRNAs in mice. |
| 3730 | 15205385 | The present study has shown that IL-6 and TNFalpha are likely to be major factors involved in the down-regulation of CYP3A11 and 2C29 mRNAs in mice. |
| 3731 | 15205385 | The present study has shown that IL-6 and TNFalpha are likely to be major factors involved in the down-regulation of CYP3A11 and 2C29 mRNAs in mice. |
| 3732 | 15196240 | IFN-gamma production by splenocytes was eliminated by addition of neutralizing anti-IL-18 antibody. |
| 3733 | 15196240 | IFN-gamma production by splenocytes was eliminated by addition of neutralizing anti-IL-18 antibody. |
| 3734 | 15196240 | Endogenous IL-12 played a favourable role whereas IL-10 played an adverse role in rBCG-mIL-18-induced IFN-gamma production. |
| 3735 | 15196240 | Endogenous IL-12 played a favourable role whereas IL-10 played an adverse role in rBCG-mIL-18-induced IFN-gamma production. |
| 3736 | 15196240 | Further, splenocytes from rBCG-mIL-18-infected mice, in response to BCG antigen, displayed increased production of IFN-gamma and GMCSF, decreased production of IL-10, elevated cellular proliferation and higher differentiation of IFN-gamma-secreting cells. rBCG-mIL-18 also enhanced BCG-induced macrophage cytotoxicity against bladder cancer MBT-2 cells in a dose-dependent manner. |
| 3737 | 15196240 | Further, splenocytes from rBCG-mIL-18-infected mice, in response to BCG antigen, displayed increased production of IFN-gamma and GMCSF, decreased production of IL-10, elevated cellular proliferation and higher differentiation of IFN-gamma-secreting cells. rBCG-mIL-18 also enhanced BCG-induced macrophage cytotoxicity against bladder cancer MBT-2 cells in a dose-dependent manner. |
| 3738 | 15196240 | Neutralizing all endogenous macrophage-derived cytokines tested (IL-12, IL-18 and TNF-alpha) as well as IFN-gamma severely diminished the rBCG-mIL-18-induced macrophage cytolytic activity, indicating a critical role for these cytokines in this process. |
| 3739 | 15196240 | Neutralizing all endogenous macrophage-derived cytokines tested (IL-12, IL-18 and TNF-alpha) as well as IFN-gamma severely diminished the rBCG-mIL-18-induced macrophage cytolytic activity, indicating a critical role for these cytokines in this process. |
| 3740 | 15196240 | Cytokine analysis for supernatants of macrophage-BCG mixture cultures manifested higher levels of IFN-gamma and TNF-alpha in rBCG-mIL-18 cultures than in control BCG cultures. |
| 3741 | 15196240 | Cytokine analysis for supernatants of macrophage-BCG mixture cultures manifested higher levels of IFN-gamma and TNF-alpha in rBCG-mIL-18 cultures than in control BCG cultures. |
| 3742 | 15194169 | Induction of these autoantibodies appeared to be associated with the hydrocarbon's ability to induce IL-12, IL-6, and TNF-alpha, suggesting a relationship with hydrocarbon's adjuvanticity. |
| 3743 | 15193387 | The immunogens, as well as the reference vaccine drastically inhibited increases in TNF-alpha and IL-6 plasma levels after challenge. |
| 3744 | 15186399 | We show here that optimal IL-12 and TNF-alpha production by human monocyte derived DC in response to killed serogroup B N. meningitidis depends on physical contact and internalization of the bacteria by DC. |
| 3745 | 15186399 | We show here that optimal IL-12 and TNF-alpha production by human monocyte derived DC in response to killed serogroup B N. meningitidis depends on physical contact and internalization of the bacteria by DC. |
| 3746 | 15186399 | The majority of DC producing cytokines had internalized N. meningitidis while inhibition of bacterial internalization markedly impaired IL-12 and TNF-alpha, but not IL-6 production. |
| 3747 | 15186399 | The majority of DC producing cytokines had internalized N. meningitidis while inhibition of bacterial internalization markedly impaired IL-12 and TNF-alpha, but not IL-6 production. |
| 3748 | 15186399 | Restoration of LOS biosynthesis in a LOS regulatory strain also restored both internalization and cytokine production and was enhanced in the presence of LPS binding protein (LBP). |
| 3749 | 15186399 | Restoration of LOS biosynthesis in a LOS regulatory strain also restored both internalization and cytokine production and was enhanced in the presence of LPS binding protein (LBP). |
| 3750 | 15181282 | CD137 (4-1BB), is an inducible T-cell costimulatory receptor and a member of the tumor necrosis factor receptor (TNFR) superfamily. |
| 3751 | 15181282 | The natural counter receptor for CD137 is 4-1BB ligand, a member of the TNF superfamily that is weakly expressed on naïve or resting B cells, macrophages, and DCs. |
| 3752 | 15181282 | In T cells CD137-induced signals lead to the recruitment of TRAF family members and activation of several kinases, including ASK-1, MKK, MAPK3/ MAPK4, p38, and JNK/SAPK. |
| 3753 | 15181282 | Kinase activation is then followed by the activation and nuclear translocation of several transcription factors, including ATF-2, Jun, and NF-kappaB. |
| 3754 | 15181282 | In addition to augmenting suboptimal TCR-induced proliferation, CD137-mediated signaling protects T cells, and in particular, CD8+ T cells from activation-induced cell death (AICD). |
| 3755 | 15163503 | LTR72, a genetically detoxified heat-labile toxin from Escherichia coli with a strong adjuvant effect in EPI, was found to bind the keratinocytes of the epidermis, but not the LCs, and caused the production of elevated TNF-alpha and IL-12 cytokines in emigrating epidermal cells. |
| 3756 | 15161079 | To examine the effects of cytokine environment at the time of antigenic exposure on T-cell cytokine profiles following T-cell-antigen presenting cell (APC) interaction, pig monocyte-derived dendritic cells (mDCs) were treated with hen egg white lysozyme (HEWL) or killed Mycobacterium tuberculosis (Mtb) alone or with a recombinant pig cytokine (TNF-alpha, interleukin (IL)-12, IL-10, interferon (IFN)-gamma or IL-6) and then incubated with autologous T-cell-enriched lymphocytes. |
| 3757 | 15161079 | To examine the effects of cytokine environment at the time of antigenic exposure on T-cell cytokine profiles following T-cell-antigen presenting cell (APC) interaction, pig monocyte-derived dendritic cells (mDCs) were treated with hen egg white lysozyme (HEWL) or killed Mycobacterium tuberculosis (Mtb) alone or with a recombinant pig cytokine (TNF-alpha, interleukin (IL)-12, IL-10, interferon (IFN)-gamma or IL-6) and then incubated with autologous T-cell-enriched lymphocytes. |
| 3758 | 15161079 | Messenger RNA was isolated from the T-cells and used to evaluate the effects of treatment on IL-12p35, IFN-gamma, IL-4, IL-10 and IL-13 expression using RT-PCR. |
| 3759 | 15161079 | Messenger RNA was isolated from the T-cells and used to evaluate the effects of treatment on IL-12p35, IFN-gamma, IL-4, IL-10 and IL-13 expression using RT-PCR. |
| 3760 | 15161079 | T-cells exposed to HEWL-treated mDCs expressed high IL-13 and moderate IL-10 and IFN-gamma, suggesting T-helper 2 (Th-2) bias. |
| 3761 | 15161079 | T-cells exposed to HEWL-treated mDCs expressed high IL-13 and moderate IL-10 and IFN-gamma, suggesting T-helper 2 (Th-2) bias. |
| 3762 | 15161079 | Addition of any cytokine during HEWL treatment of mDCs reduced subsequent expression of IL-10 and IL-13 by T-cells. |
| 3763 | 15161079 | Addition of any cytokine during HEWL treatment of mDCs reduced subsequent expression of IL-10 and IL-13 by T-cells. |
| 3764 | 15161079 | Added IL-12 increased IFN-gamma mRNA. |
| 3765 | 15161079 | Added IL-12 increased IFN-gamma mRNA. |
| 3766 | 15161079 | T-cells exposed to Mtb-treated mDCs expressed increased IFN-gamma and decreased IL-10 suggesting Th-1 bias. |
| 3767 | 15161079 | T-cells exposed to Mtb-treated mDCs expressed increased IFN-gamma and decreased IL-10 suggesting Th-1 bias. |
| 3768 | 15161079 | Addition of cytokines to mDCs treated with Mtb altered T-cell cytokine mRNA expression such that TNF-alpha, IFN-gamma or IL-12 increased IFN-gamma; IL-12 and IFN-gamma suppressed IL-10, while IL-10 and IL-12 enhanced IL-13. |
| 3769 | 15161079 | Addition of cytokines to mDCs treated with Mtb altered T-cell cytokine mRNA expression such that TNF-alpha, IFN-gamma or IL-12 increased IFN-gamma; IL-12 and IFN-gamma suppressed IL-10, while IL-10 and IL-12 enhanced IL-13. |
| 3770 | 15158187 | In this work, we used a murine model of systemic C. albicans infection, in which resistance to reinfection with virulent wild-type cells is induced by prior exposure of mice to a low-virulence agerminative strain of C. albicans (primary sublethal infection), to study the influence of TLR2 gene deletion on (i) the ability to develop an acquired resistance upon vaccination; (ii) the development of the acquired humoral response; and (iii) the production of Th1 cytokines IFN-gamma, IL-12 and TNF-alpha. |
| 3771 | 15150328 | Transfer of specific antibodies results in increased expression of TNF-alpha and IL12 and recruitment of neutrophils to the site of a cutaneous Francisella tularensis infection. |
| 3772 | 15150328 | Transfer of specific antibodies results in increased expression of TNF-alpha and IL12 and recruitment of neutrophils to the site of a cutaneous Francisella tularensis infection. |
| 3773 | 15150328 | Recipient mice showed stronger staining for TNF-alpha and IL12, and larger numbers of neutrophils in skin samples after infection than control mice. |
| 3774 | 15150328 | Recipient mice showed stronger staining for TNF-alpha and IL12, and larger numbers of neutrophils in skin samples after infection than control mice. |
| 3775 | 15150089 | Recent studies have shown CpG oligodeoxynucleotide induce tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) expression via IFN production. |
| 3776 | 15150089 | Using ELISA, urine IFN-gamma, and TRAIL levels were initially undetectable in BCG therapy patients but were high after later induction treatments. |
| 3777 | 15147040 | These analyses revealed that the expansion of antigen specific CD8+T cells is the most effective when T cells were activated by fully maturated DCs by culturing monocytes for 5 days in the presence of GM-CSF and IL-4, followed by 2-3 days of maturation with pro-inflammatory mediators including TNFalpha, IL-6, IL-1beta and PGE2. |
| 3778 | 15146996 | Whole blood was stimulated with complete vaccine suspension, and TNF-alpha, IL-1beta, IL-6, and IL-8 were determined from heparin/EDTA-plasma and culture supernatants. |
| 3779 | 15146996 | Whole blood was stimulated with complete vaccine suspension, and TNF-alpha, IL-1beta, IL-6, and IL-8 were determined from heparin/EDTA-plasma and culture supernatants. |
| 3780 | 15146996 | It was shown that Ticovac and the new Encepur Kinder can induce relatively high amounts of TNF-alpha and lower amounts of IL-1beta. |
| 3781 | 15146996 | It was shown that Ticovac and the new Encepur Kinder can induce relatively high amounts of TNF-alpha and lower amounts of IL-1beta. |
| 3782 | 15146294 | Primed DCs were assessed by the in vitro activation of B3Z OVA-specific CD8 T cells and the proliferation of OVA-specific CD8 and CD4 T cells from OT-I and OT-II TCR transgenic mice, respectively. |
| 3783 | 15146294 | Primed DCs were assessed by the in vitro activation of B3Z OVA-specific CD8 T cells and the proliferation of OVA-specific CD8 and CD4 T cells from OT-I and OT-II TCR transgenic mice, respectively. |
| 3784 | 15146294 | Quantification of IL-2, IL-4, IL-5, IFN-gamma, and TNF-alpha by cytometric bead array (CBA) assay determined the polarization of TH1/TH2 responses, whereas H-2 Kb/SIINFEKL tetramers monitored the expansion of OVA-specific T cells. |
| 3785 | 15146294 | Quantification of IL-2, IL-4, IL-5, IFN-gamma, and TNF-alpha by cytometric bead array (CBA) assay determined the polarization of TH1/TH2 responses, whereas H-2 Kb/SIINFEKL tetramers monitored the expansion of OVA-specific T cells. |
| 3786 | 15146294 | The hybrids also induced the most potent CTLs, offered the highest protection against established EG7 tumors and also induced the highest stimulation of IFN-gamma and TNF-alpha production. |
| 3787 | 15146294 | The hybrids also induced the most potent CTLs, offered the highest protection against established EG7 tumors and also induced the highest stimulation of IFN-gamma and TNF-alpha production. |
| 3788 | 15138584 | The secondary response in the peritoneal cavity involved a >80-fold enrichment of epitope specific CD8+ T cells and the release of various cytokines, including IL-12 and TNF-alpha. |
| 3789 | 15128817 | Bone marrow-derived DC (BMDC) that had been activated by TNF-alpha or CD40 ligation were not able to induce protection against leishmaniasis in susceptible BALB/c mice. |
| 3790 | 15128786 | Both vectors induced IL-12 and TNF-alpha, but only Lm-LLO-E7 induced IL-2 production by DCs. |
| 3791 | 15128786 | Lm-LLO-E7 also induced significantly higher levels of MHC class II molecules, CD40, and B7 costimulatory molecules (CD86, B7-H1, and B7-DC) on DCs than Lm-E7. |
| 3792 | 15128786 | A similar shift is also observed for B7-H1 and B7-DC molecules. |
| 3793 | 15123153 | The most noteworthy changes were in tumor necrosis factor-alpha (TNF-alpha) and interferon gamma (IFN-gamma) levels. |
| 3794 | 15123153 | The most noteworthy changes were in tumor necrosis factor-alpha (TNF-alpha) and interferon gamma (IFN-gamma) levels. |
| 3795 | 15123153 | Our preliminary findings suggest that immunity against FIP is associated with TNF-alpha and IFN-gamma response imbalance, with high TNF-alpha/low IFN-gamma mRNA responses favouring disease and low TNF-alpha/high IFN-gamma mRNA responses being indicative of immunity. |
| 3796 | 15123153 | Our preliminary findings suggest that immunity against FIP is associated with TNF-alpha and IFN-gamma response imbalance, with high TNF-alpha/low IFN-gamma mRNA responses favouring disease and low TNF-alpha/high IFN-gamma mRNA responses being indicative of immunity. |
| 3797 | 15122754 | HCs upregulate surface expression of major histocompatibility complex (MHC) class I molecules and CD1d but not MHC class II molecules Qa-1, CD80, CD86, CD54, or CD95; in addition, they expressed/secreted interleukin (IL)-10 and IL-4 but not IL-1, IL-6, IL-13, interferon (IFN)-gamma, tumor necrosis factor (TNF), IL-4, or IL-27 (i.e., they acquire the HC* phenotype). |
| 3798 | 15122754 | HCs upregulate surface expression of major histocompatibility complex (MHC) class I molecules and CD1d but not MHC class II molecules Qa-1, CD80, CD86, CD54, or CD95; in addition, they expressed/secreted interleukin (IL)-10 and IL-4 but not IL-1, IL-6, IL-13, interferon (IFN)-gamma, tumor necrosis factor (TNF), IL-4, or IL-27 (i.e., they acquire the HC* phenotype). |
| 3799 | 15122754 | HCs* (but not HCs) induced specific activation, proliferation, and IFN-gamma, TNF, and IL-13 release of cocultured naïve CD8(+) T cells. |
| 3800 | 15122754 | HCs* (but not HCs) induced specific activation, proliferation, and IFN-gamma, TNF, and IL-13 release of cocultured naïve CD8(+) T cells. |
| 3801 | 15122754 | Only recently activated CD8(+) T blasts (but not recently activated CD4(+) T blasts or activated cells of the innate immune system, including natural killer T [NKT] cells) induced the HC* phenotype that is prominent from day 10 to day 20 postvaccination (i.e., time points at which peak numbers of recently primed CD8(+) T blasts are found in the liver). |
| 3802 | 15122754 | Only recently activated CD8(+) T blasts (but not recently activated CD4(+) T blasts or activated cells of the innate immune system, including natural killer T [NKT] cells) induced the HC* phenotype that is prominent from day 10 to day 20 postvaccination (i.e., time points at which peak numbers of recently primed CD8(+) T blasts are found in the liver). |
| 3803 | 15121298 | Analysis of cytokine mRNA in GALT and lymphoid organs showed early induction of IFN-gamma, a Th1 cytokine, as well as the pro-inflammatory cytokine TNF-alpha. |
| 3804 | 15121297 | Acute Trypanosoma cruzi infection: IL-12, IL-18, TNF, sTNFR and NO in T. rangeli-vaccinated mice. |
| 3805 | 15121297 | Acute Trypanosoma cruzi infection: IL-12, IL-18, TNF, sTNFR and NO in T. rangeli-vaccinated mice. |
| 3806 | 15121297 | The aim of the present work was to complete our previous study on the production of IFN-gamma and IL-10 in this vaccination model by investigating the production of IL-12p35 and p40, IL-18, TNF, TNF soluble receptors (sTNFR), and nitric oxide (NO), factors known to play a key role in the outcome of T. cruzi infection. |
| 3807 | 15121297 | The aim of the present work was to complete our previous study on the production of IFN-gamma and IL-10 in this vaccination model by investigating the production of IL-12p35 and p40, IL-18, TNF, TNF soluble receptors (sTNFR), and nitric oxide (NO), factors known to play a key role in the outcome of T. cruzi infection. |
| 3808 | 15120157 | Previous studies have shown that IFN-gamma, TNF-alpha and NOS-2, but not B cells, are crucial for host defense against primary systemic infection with the attenuated live vaccine strain (LVS) of Francisella tularensis. |
| 3809 | 15120157 | Wild-type (WT) mice and mice deficient in IFN-gamma, TNFR1R2, NOS-2, or B cells were equally susceptible to low dose ( approximately 10 colony forming units) aerosol or intradermal challenge with virulent type B F. tularensis, and succumbed to the infection between days 6 and 8 post-inoculation. |
| 3810 | 15109052 | Analysis of chicken TLR4, CD28, MIF, MD-2, and LITAF genes in a Salmonella enteritidis resource population. |
| 3811 | 15109052 | Five candidate genes were selected for study, based on their biological function as possibly affecting response to SE: toll-like receptor 4 (TLR4), T-cell specific surface protein (CD28), macrophage migration inhibitory factor (MIF), MD-2, and lipopolysaccharide-induced tumor necrosis factor (TNF)-alpha factor (LITAF). |
| 3812 | 15109052 | The LITAF and MIF genes were homozygous for all sires. |
| 3813 | 15109052 | Single nucleotide polymorphisms (SNP) were identified in 3 genes (TLR4, CD28, and MD-2) and were used to test for associations of sire SNP with SE response. |
| 3814 | 15103504 | In these studies, we demonstrate that exogenous soluble LIGHT or soluble CD40 ligand (CD40L) can promote monocyte-derived dendritic cell maturation in vitro by the up-regulation of CD86, CD80, CD83, and HLA-DR antigen expression. |
| 3815 | 15103504 | However, upon induction of maturation by LIGHT or CD40L, the expression of costimulatory and HLA-DR molecules is comparable between DCs from MDS and normal subjects. |
| 3816 | 15103504 | Exogenous LIGHT- and CD40L-stimulated mature DCs (mDCs) also displayed increased antigen presentation to autologous T lymphocytes (tetanus toxin) or allogeneic T lymphocytes in mixed lymphocyte reactions. |
| 3817 | 15103504 | DCs matured by LIGHT showed increased secretion of IL-6, IL-12p75, and TNF-alpha, but not IL-1beta. |
| 3818 | 15103504 | We conclude that both LIGHT and CD40L are immunoregulating factors that induce monocyte-derived iDCs from MDS patients to undergo maturation resulting in increased antigen presentation and T-cell activation. |
| 3819 | 15100273 | CY plus IL-2 treatment not only enhances proliferation and accumulation of effector CD4 cells, but also preserves the ability of these cells to express the effector cytokine IFN-gamma (and to a lesser extent TNF-alpha) in proportion to the level of parenchymal self-Ag expression. |
| 3820 | 15100273 | Although effector CD4 cells in CY plus IL-2-treated self-Ag-expressing mice eventually succumb to tolerization, this delay results in an increased level of in situ IFN-gamma expression in cognate Ag-expressing parenchymal tissues as well as death via a mechanism that requires direct parenchymal Ag presentation. |
| 3821 | 15099760 | The ingestion of MS did not change the cell surface expression of CD80, CD83, CD86 and HLA-DR of immature and mature DC, suggesting that MS uptake did not induce DC maturation but that maturation by cytokines or LPS was unaltered in the presence of MS. |
| 3822 | 15099760 | Furthermore, MS-loaded mature MoDC expressed normal levels of the chemokine receptor CCR7 and migrated as efficiently towards CCL19 or CCL21 as unloaded MoDC. |
| 3823 | 15099760 | DC viability and the secretion of TNF-alpha and IL-12 was not significantly changed by MS loading. |
| 3824 | 15096181 | The present work demonstrated that the CpG oligonucleotides (CpG-ODN) 2216, D32 and D19 induce high amounts of interferon-alpha (IFN-alpha), tumour-necrosis factor-alpha (TNF-alpha) and interleukin (IL)-12 in porcine peripheral blood mononuclear cells (PBMCs). |
| 3825 | 15096181 | The present work demonstrated that the CpG oligonucleotides (CpG-ODN) 2216, D32 and D19 induce high amounts of interferon-alpha (IFN-alpha), tumour-necrosis factor-alpha (TNF-alpha) and interleukin (IL)-12 in porcine peripheral blood mononuclear cells (PBMCs). |
| 3826 | 15096181 | These cells did not express CD6, CD8 or CD45RA. |
| 3827 | 15096181 | These cells did not express CD6, CD8 or CD45RA. |
| 3828 | 15096181 | Importantly, monocyte-derived DC did not respond to CpG-ODN by secretion of IFN-alpha or TNF-alpha or by the up-regulation of costimulatory molecule expression. |
| 3829 | 15096181 | Importantly, monocyte-derived DC did not respond to CpG-ODN by secretion of IFN-alpha or TNF-alpha or by the up-regulation of costimulatory molecule expression. |
| 3830 | 15094367 | After intravenous administration, OVA mRNA expression and MHC class I-restricted antigen presentation on CD11c+ cells and inflammatory cytokines, such as TNF-alpha, IL-12, and IFN-gamma, that can enhance the Th1 response of the Man liposome/pCMV-OVA complex were higher than that of naked pCMV-OVA and that complexed with DC-Chol liposomes. |
| 3831 | 15076142 | Phase I trial of antigen-specific gene therapy using a recombinant vaccinia virus encoding MUC-1 and IL-2 in MUC-1-positive patients with advanced prostate cancer. |
| 3832 | 15076142 | The purpose of this phase 1 clinical trial was to determine the maximum tolerated dose, safety of a multiple-dose regimen, and the immunologic effect of vaccinia virus expressing MUC-1 and IL-2 genes (VV/MUC-1/IL-2) in patients with advanced prostate cancer. |
| 3833 | 15076142 | Systemic immune modulation in this patient included (1) up-regulation of IL-2 (CD25) and T cell (TcR alphabeta) receptors, (2) increase in the CD4/CD8 ratio (2.5-fold) (3) augmentation of T-helper type 1 cell (TH1) (interferon-gamma and tumor necrosis factor-alpha) but not TH2 (IL-4) cytokine mRNA expression, (4) induction of natural killer cell activity and MHC independent MUC-1 specific cytotoxic T-cell activity, and (5) normalization of mRNA expression of T-cell-associated signal transduction molecules TcR-zeta and p56lck. |
| 3834 | 15076142 | These results suggest that VV/MUC-1/IL-2 gene therapy with a maximum tolerated dose of 5 x 10(7) pfu is safe and well tolerated. |
| 3835 | 15070823 | Our results show that both apoptotic preparations were equivalent regarding the responsiveness of DCs to combined treatment with tumor necrosis factor-alpha and poly(inosinic-cytidylic) acid, as determined by similar increased expression of costimulatory molecules and interleukin-12 production. |
| 3836 | 15070685 | The presence of PDCs synergistically enhanced CD86 expression, cytokine production (interleukin 6 [IL-6], tumor necrosis factor alpha, and IL-10) and plasma cell differentiation of isolated human peripheral blood B cells stimulated through CpG-C and B-cell antigen receptor (BCR) ligation. |
| 3837 | 15057902 | Further associations were observed with single nucleotide polymorphisms (SNPs) at the IL2 and IL4 loci along with insertion/deletion variants at the IL12B locus (P =.003-.01). |
| 3838 | 15057902 | Host genetic associations were independent of one another as well as other HLA (A, B, C, and DQB1) and cytokine gene (IL4R, IL6, IL10, and TNF) variants. |
| 3839 | 15053398 | Gametocytes are capable of inducing specific humoral IgG, and cellular responses, which include induction of TNFalpha, IFNgamma and gammadelta+ lymphocyte proliferation, in addition to immune responses to other stages of the parasite (sporozoite, exo-erythrocytic stages, erythrocytic stages). |
| 3840 | 15045561 | Peripheral blood mononuclear cells (PBMC) isolated from vaccinated macaques were stimulated with inactivated viral particles for 24 h, and the production of IL-2, IL-4, IL-6, IL-10, IL-12, TNF-alpha and IFN-gamma was determined by ELISA and flow cytometry. |
| 3841 | 15004179 | Cellular responses were monitored by evaluating blood-derived virus-specific IFN-gamma-secreting cells and TNF-alpha-expressing CD8+ T cells, and blood- and rectally derived p11C tetramer-positive T cells. |
| 3842 | 14999431 | The vaccine used mature DCs (CD1a+++, CD40++, CD80++, CD83+, and CD86+++) generated from peripheral blood monocytes in the presence of GM-CSF and IL-4. |
| 3843 | 14999431 | After 7 days, DCs were matured with a defined cocktail of cytokines (IL-1+IL-6+TNF-alpha+PGE2) and simultaneously pulsed with lysates of heterologous melanoma cell lines, for 2 days. |
| 3844 | 14984494 | Retroviral transduction of acute myeloid leukaemia-derived dendritic cells with OX40 ligand augments their antigen presenting activity. |
| 3845 | 14984494 | Retroviral transduction of acute myeloid leukaemia-derived dendritic cells with OX40 ligand augments their antigen presenting activity. |
| 3846 | 14984494 | In the present study, we examined whether the transduction of leukaemia-DCs with OX40 ligand (OX40L), a member of the tumour necrosis factor (TNF) family, resulted in augmentation of their antigen presenting activity. |
| 3847 | 14984494 | In the present study, we examined whether the transduction of leukaemia-DCs with OX40 ligand (OX40L), a member of the tumour necrosis factor (TNF) family, resulted in augmentation of their antigen presenting activity. |
| 3848 | 14984494 | Fresh leukaemic cells from five patients with acute myeloid leukaemia (AML) were isolated and retrovirally transduced with OX40L during the culture with a combination of cytokines from stem cell factor, fms-like tyrosine kinase (Flt)-3 ligand, granulocyte-macrophage colony stimulating factor (GM-CSF), interleukin-4 (IL-4) and TNF-alpha. |
| 3849 | 14984494 | Fresh leukaemic cells from five patients with acute myeloid leukaemia (AML) were isolated and retrovirally transduced with OX40L during the culture with a combination of cytokines from stem cell factor, fms-like tyrosine kinase (Flt)-3 ligand, granulocyte-macrophage colony stimulating factor (GM-CSF), interleukin-4 (IL-4) and TNF-alpha. |
| 3850 | 14984494 | After 7 d, the majority of cells showed DC-like morphology, and expressed higher levels of CD80, CD86 and HLA-DR than fresh leukaemic cells. |
| 3851 | 14984494 | After 7 d, the majority of cells showed DC-like morphology, and expressed higher levels of CD80, CD86 and HLA-DR than fresh leukaemic cells. |
| 3852 | 14984494 | Co-culture of allogeneic CD4+ T cells with OX40L-transduced leukaemia-DCs was superior in the generation of interferon (IFN)-gamma producing CD4+ T cells and in production of IFN-gamma. |
| 3853 | 14984494 | Co-culture of allogeneic CD4+ T cells with OX40L-transduced leukaemia-DCs was superior in the generation of interferon (IFN)-gamma producing CD4+ T cells and in production of IFN-gamma. |
| 3854 | 14977992 | Mycobacterial purified protein derivatives stimulate innate immunity: Malawians show enhanced tumor necrosis factor alpha, interleukin-1beta (IL-1beta), and IL-10 responses compared to those of adolescents in the United Kingdom. |
| 3855 | 14977992 | Mycobacterial purified protein derivatives stimulate innate immunity: Malawians show enhanced tumor necrosis factor alpha, interleukin-1beta (IL-1beta), and IL-10 responses compared to those of adolescents in the United Kingdom. |
| 3856 | 14977992 | To investigate the role of innate immunity in variable efficacy of Mycobacterium bovis BCG vaccination in Malawi and the United Kingdom, we examined 24-h tumor necrosis factor alpha, interleukin-1beta (IL-1beta), and IL-10 responses to mycobacterial purified protein derivatives (PPDs). |
| 3857 | 14977992 | To investigate the role of innate immunity in variable efficacy of Mycobacterium bovis BCG vaccination in Malawi and the United Kingdom, we examined 24-h tumor necrosis factor alpha, interleukin-1beta (IL-1beta), and IL-10 responses to mycobacterial purified protein derivatives (PPDs). |
| 3858 | 14977983 | MP-immunized animals had increased brain levels of tumor necrosis factor alpha, gamma interferon, and interleukin-2. |
| 3859 | 14764714 | We found that OMPC and Hib-OMPC engaged human Toll-like receptor 2 (TLR2) expressed in human embryonic kidney (HEK) cells, inducing IL-8 production, and engaged mouse TLR2 on bone marrow-derived dendritic cells, inducing TNF release. |
| 3860 | 14764714 | We found that OMPC and Hib-OMPC engaged human Toll-like receptor 2 (TLR2) expressed in human embryonic kidney (HEK) cells, inducing IL-8 production, and engaged mouse TLR2 on bone marrow-derived dendritic cells, inducing TNF release. |
| 3861 | 14764714 | We found that OMPC and Hib-OMPC engaged human Toll-like receptor 2 (TLR2) expressed in human embryonic kidney (HEK) cells, inducing IL-8 production, and engaged mouse TLR2 on bone marrow-derived dendritic cells, inducing TNF release. |
| 3862 | 14764714 | Engagement of TLR2 by Hib-OMPC was MyD88 dependent, as Hib-OMPC-induced TNF production was ablated in MyD88 knockout (KO) mice. |
| 3863 | 14764714 | Engagement of TLR2 by Hib-OMPC was MyD88 dependent, as Hib-OMPC-induced TNF production was ablated in MyD88 knockout (KO) mice. |
| 3864 | 14764714 | Engagement of TLR2 by Hib-OMPC was MyD88 dependent, as Hib-OMPC-induced TNF production was ablated in MyD88 knockout (KO) mice. |
| 3865 | 14764714 | Splenocytes from OMPC-immunized TLR2 KO mice also produced significantly less IL-6 and TNF-alpha than those from wild-type mice. |
| 3866 | 14764714 | Splenocytes from OMPC-immunized TLR2 KO mice also produced significantly less IL-6 and TNF-alpha than those from wild-type mice. |
| 3867 | 14764714 | Splenocytes from OMPC-immunized TLR2 KO mice also produced significantly less IL-6 and TNF-alpha than those from wild-type mice. |
| 3868 | 14764714 | Hib-OMPC is unique among glycoconjugate vaccines by engaging TLR2, and the ability of Hib-OMPC to elicit protective levels of Abs after one dose may be related to TLR2-mediated induction and regulation of cytokines produced by T cells and macrophages in addition to the peptide/MHC II-dependent recruitment of T cell help commonly afforded by carrier proteins. |
| 3869 | 14764714 | Hib-OMPC is unique among glycoconjugate vaccines by engaging TLR2, and the ability of Hib-OMPC to elicit protective levels of Abs after one dose may be related to TLR2-mediated induction and regulation of cytokines produced by T cells and macrophages in addition to the peptide/MHC II-dependent recruitment of T cell help commonly afforded by carrier proteins. |
| 3870 | 14764714 | Hib-OMPC is unique among glycoconjugate vaccines by engaging TLR2, and the ability of Hib-OMPC to elicit protective levels of Abs after one dose may be related to TLR2-mediated induction and regulation of cytokines produced by T cells and macrophages in addition to the peptide/MHC II-dependent recruitment of T cell help commonly afforded by carrier proteins. |
| 3871 | 14744795 | BCG-CWS was capable of activating DCs ex vivo by the criteria of CD80/CD86 up-regulation and cytokine (interleukin-12, tumor necrosis factor-alpha) induction. |
| 3872 | 14742547 | Mucosal vaccination increases endothelial expression of mucosal addressin cell adhesion molecule 1 in the human gastrointestinal tract. |
| 3873 | 14742547 | Mucosal vaccination increases endothelial expression of mucosal addressin cell adhesion molecule 1 in the human gastrointestinal tract. |
| 3874 | 14742547 | Using different immunization routes with an oral cholera vaccine, we show that the endothelial expression of mucosal addressin cell adhesion molecule 1 (MAdCAM-1) is increased in the gastric and upper small intestinal mucosae after immunization through various local routes in the upper gastrointestinal tract. |
| 3875 | 14742547 | Using different immunization routes with an oral cholera vaccine, we show that the endothelial expression of mucosal addressin cell adhesion molecule 1 (MAdCAM-1) is increased in the gastric and upper small intestinal mucosae after immunization through various local routes in the upper gastrointestinal tract. |
| 3876 | 14742547 | Furthermore, we show that MAdCAM-1 can be induced on human endothelial cells by tumor necrosis factor alpha (TNF-alpha) and gamma interferon. |
| 3877 | 14742547 | Furthermore, we show that MAdCAM-1 can be induced on human endothelial cells by tumor necrosis factor alpha (TNF-alpha) and gamma interferon. |
| 3878 | 14742547 | The vaccine component cholera toxin B subunit (CTB) increased MAdCAM-1 expression on endothelial cells in cultured human gastric explants, an effect that seemed to be mediated by TNF-alpha. |
| 3879 | 14742547 | The vaccine component cholera toxin B subunit (CTB) increased MAdCAM-1 expression on endothelial cells in cultured human gastric explants, an effect that seemed to be mediated by TNF-alpha. |
| 3880 | 14742545 | The replication-promoting effect of IFN-gamma on amastigotes was independent of the source and genetic background of Mphis, was apparently not affected by surface opsonization of amastigotes, was not mediated by interleukin-10 or transforming growth factor beta, and was observed at different temperatures. |
| 3881 | 14742545 | On the other hand, IFN-gamma could stimulate Mphis to limit amastigote replication when it was coupled with lipopolysaccharides but not when it was coupled with tumor necrosis factor alpha. |
| 3882 | 14741165 | The addition of interferon-gamma (IFN-gamma) augmented IL-12 production. |
| 3883 | 14741165 | RT-PCR showed that SAKRA induced not only expression of IL-12 p40 mRNA, but expression of tumor necrosis factor (TNF)-alpha and inducible nitric oxide synthase (iNOS) mRNA at least 6 h after stimulation, suggesting that SAKRA activates the bactericidal activity of macrophages. |
| 3884 | 14741150 | Avipox-based simian immunodeficiency virus (SIV) vaccines elicit a high frequency of SIV-specific CD4+ and CD8+ T-cell responses in vaccinia-experienced SIVmac251-infected macaques. |
| 3885 | 14741150 | Avipox-based simian immunodeficiency virus (SIV) vaccines elicit a high frequency of SIV-specific CD4+ and CD8+ T-cell responses in vaccinia-experienced SIVmac251-infected macaques. |
| 3886 | 14741150 | The ability of ALVAC- or fowlpox-based simian immunodeficiency virus (SIV) vaccines to boost SIV-specific CD4+ and CD8+ T-cell responses was tested in 10 vaccinia-experienced macaques infected with SIVmac251. |
| 3887 | 14741150 | The ability of ALVAC- or fowlpox-based simian immunodeficiency virus (SIV) vaccines to boost SIV-specific CD4+ and CD8+ T-cell responses was tested in 10 vaccinia-experienced macaques infected with SIVmac251. |
| 3888 | 14741150 | The overall CD8+ T-cell response to Gag was assessed using a peptide pool encompassing the entire Gag protein followed by measurement of TNF-alpha production in ICS assay. |
| 3889 | 14741150 | The overall CD8+ T-cell response to Gag was assessed using a peptide pool encompassing the entire Gag protein followed by measurement of TNF-alpha production in ICS assay. |
| 3890 | 14741150 | Similarly, virus-specific CD4+ T-cell responses were measured by ICS for TNF-alpha following stimulation with the Gag-overlapping peptide and by proliferative response following stimulation with purified p27 Gag. |
| 3891 | 14741150 | Similarly, virus-specific CD4+ T-cell responses were measured by ICS for TNF-alpha following stimulation with the Gag-overlapping peptide and by proliferative response following stimulation with purified p27 Gag. |
| 3892 | 14741150 | The two vaccine modalities effectively boosted both CD4+ and CD8+ SIV-specific T-cell response despite prior exposure to the vaccinia-derivative NYVAC vector, suggesting that sequential boosting with either avipox-based vector vaccine candidate is a realistic approach in immune therapy of human immunodeficiency virus type 1 (HIV-1)-infected individuals. |
| 3893 | 14741150 | The two vaccine modalities effectively boosted both CD4+ and CD8+ SIV-specific T-cell response despite prior exposure to the vaccinia-derivative NYVAC vector, suggesting that sequential boosting with either avipox-based vector vaccine candidate is a realistic approach in immune therapy of human immunodeficiency virus type 1 (HIV-1)-infected individuals. |
| 3894 | 14738463 | IL-12 enhances the generation of tumour antigen-specific Th1 CD4 T cells during ex vivo expansion. |
| 3895 | 14738463 | The effects of IL-12, along with IL-2, on the ex vivo generation of HER-2/neu antigen-specific T cells were examined. |
| 3896 | 14738463 | The resulting p776-790-specific T cells responded readily to antigen by proliferating and producing type I cytokines (IFN-gamma and TNF-alpha). |
| 3897 | 14738463 | These results suggest that IL-12 is an important cytokine for ex vivo recovery and maintenance of antigen-specific CD4+ T lymphocytes that would otherwise be lost by using IL-2 alone in combination with antigen. |
| 3898 | 14734732 | IL-21 induces tumor rejection by specific CTL and IFN-gamma-dependent CXC chemokines in syngeneic mice. |
| 3899 | 14734732 | IL-21 is an immune-stimulatory four alpha helix cytokine produced by activated T cells. |
| 3900 | 14734732 | Five days after injection, TS/A-IL-21 tumors showed numerous infiltrating granulocytes, NK cells, and to a lesser extent CD8(+) T cells, along with the expression of TNF-alpha, IFN-gamma, and endothelial adhesion molecules ICAM-1 and VCAM-1. |
| 3901 | 14734732 | At day 7, CD8(+) and CD4(+) T cells increased together with IFN-gamma, and the CXC chemokines IFN-gamma-inducible protein 10, monokine induced by IFN-gamma, and IFN-inducible T cell alpha-chemoattractant. |
| 3902 | 14734732 | In vivo depletion experiments by specific Abs showed that rejection of TS/A-IL-21 cells required CD8(+) T lymphocytes and granulocytes. |
| 3903 | 14734732 | When injected in IFN-gamma-deficient mice, TS/A-IL-21 cells formed tumors that regressed in only 29% of animals, indicating a role for IFN-gamma in IL-21-mediated antitumor response, but also the existence of IFN-gamma-independent effects. |
| 3904 | 14704372 | T cells from mice immunized with antigen in the presence of CT produced high levels of interleukin (IL)-10 and IL-5 and low levels of IL-4 and interferon-gamma (IFN-gamma). |
| 3905 | 14704372 | Here, we demonstrate that immunization with antigen in the presence of CT induced a population of antigen-specific CD4(+) T cells that produced IL-10 in the absence of IL-4, in addition to cells that coexpressed IL-4 and IL-10 or produced IL-4 only. |
| 3906 | 14704372 | Previous data showed that CT can modulate the expression of costimulatory molecules and inhibit the production of chemokines and cytokines, including IL-12 and tumor necrosis factor alpha and enhance IL-10 production. |
| 3907 | 14704372 | Here, we show that CT synergizes with LPS to induce IL-6 and IL-1beta in addition to IL-10 production by immature DC. |
| 3908 | 14688317 | In the present study, we demonstrate that immature DC are rapidly eliminated by NK cells in vivo via a pathway dependent on the TNF-related apoptosis-inducing ligand (TRAIL). |
| 3909 | 14685154 | However, in EBV-positive Hodgkin's disease (HD) the efficacy of adoptively transferred EBV-specific CTL may be limited by tumor-derived immunosuppressive factors, such as T-cell growth factor (TGF) beta, interleukin (IL)13 and the chemokine TARC. |
| 3910 | 14685154 | EBV-specific CTL transduced with a retrovirus vector expressing the p40 and p35 subunits of IL12 as a single molecule (Flexi-IL12), produced IL12 following antigenic stimulation. |
| 3911 | 14685154 | This resulted in an elevated production of Th1 cytokines, including interferon gamma and tumor necrosis factor alpha, and a reduction in the Th2 cytokines IL4 and IL5. |
| 3912 | 14685154 | Flexi-IL12-transduced CTL resisted the antiproliferative and anticytotoxic effects of exogenous TGFbeta, likely by antagonizing the TGFbeta-induced downregulation of the Th1 transcriptional factor T-bet. |
| 3913 | 14673108 | Herein, we report that Ebola VLPs (eVLPs) were immunogenic in vitro as eVLPs matured and activated mouse bone marrow-derived dendritic cells, assessed by increases in cell-surface markers CD40, CD80, CD86, and MHC class I and II and secretion of IL-6, IL-10, macrophage inflammatory protein (MIP)-1alpha, and tumor necrosis factor alpha by the dendritic cells. |
| 3914 | 14673108 | Further, vaccinating mice with eVLPs activated CD4+ and CD8+ T cells, as well as CD19+ B cells. |
| 3915 | 14671675 | These include the more recently described 4-1BB:4-1BB ligand (4-1BBL) molecules. 4-1BB:4-1BBL are a member of the TNFR:TNF ligand family, which are expressed on T cells and antigen-presenting cells (APCs), respectively. |
| 3916 | 14670350 | These components include T cells (both CD4+ and CD8+), cytokines, including IFN-gamma, IL-12, TNF-alpha, and IL-6, and macrophages. |
| 3917 | 14670333 | IL-12 enhances protective immunity in mice engendered by immunization with recombinant 14 kDa Schistosoma mansoni fatty acid-binding protein through an IFN-gamma and TNF-alpha dependent pathway. |
| 3918 | 14670333 | IL-12 enhances protective immunity in mice engendered by immunization with recombinant 14 kDa Schistosoma mansoni fatty acid-binding protein through an IFN-gamma and TNF-alpha dependent pathway. |
| 3919 | 14670333 | IL-12 enhances protective immunity in mice engendered by immunization with recombinant 14 kDa Schistosoma mansoni fatty acid-binding protein through an IFN-gamma and TNF-alpha dependent pathway. |
| 3920 | 14670333 | Regarding other cytokines, significant amounts of IFN-gamma were measured in splenocyte culture supernatants of rSm14/IL-12 or rSm14 vaccinated mice and no IL-4 was detected. |
| 3921 | 14670333 | Regarding other cytokines, significant amounts of IFN-gamma were measured in splenocyte culture supernatants of rSm14/IL-12 or rSm14 vaccinated mice and no IL-4 was detected. |
| 3922 | 14670333 | Regarding other cytokines, significant amounts of IFN-gamma were measured in splenocyte culture supernatants of rSm14/IL-12 or rSm14 vaccinated mice and no IL-4 was detected. |
| 3923 | 14670333 | In an attempt to determine the role of IFN-gamma and TNF-alpha in IL-12 induced immunity, IFN-gamma and TNFR-p55 knockout mice were immunized with rSm14/IL-12 and no protection was achieved. |
| 3924 | 14670333 | In an attempt to determine the role of IFN-gamma and TNF-alpha in IL-12 induced immunity, IFN-gamma and TNFR-p55 knockout mice were immunized with rSm14/IL-12 and no protection was achieved. |
| 3925 | 14670333 | In an attempt to determine the role of IFN-gamma and TNF-alpha in IL-12 induced immunity, IFN-gamma and TNFR-p55 knockout mice were immunized with rSm14/IL-12 and no protection was achieved. |
| 3926 | 14670333 | Therefore, protection induced by rSm14/IL-12 was shown to be dependent on endogenous IFN-gamma and TNF-alpha. |
| 3927 | 14670333 | Therefore, protection induced by rSm14/IL-12 was shown to be dependent on endogenous IFN-gamma and TNF-alpha. |
| 3928 | 14670333 | Therefore, protection induced by rSm14/IL-12 was shown to be dependent on endogenous IFN-gamma and TNF-alpha. |
| 3929 | 14647233 | Concurrent delivery of tumor antigens and activation signals to dendritic cells by irradiated CD40 ligand-transfected tumor cells resulted in efficient activation of specific CD8+ T cells. |
| 3930 | 14647233 | To improve the efficacy of tumor cell-based and dendritic cell (DC)-based cancer vaccines, this study explored the potential of a new cancer vaccine strategy, that is, the use of CD40 ligand-transfected tumor (CD40L-tumor) cells to simultaneously deliver both tumor-derived antigens (Ag) and maturation stimuli to DCs. |
| 3931 | 14647233 | However, during the internalization process, only coculturing with irradiated CD40L-tumor cells resulted in concurrent, optimal DC maturation and production of proinflammatory chemokines and pro-Th1 cytokines, such as IL-6, IL-8, IL-12, IFN-gamma, and TNF-alpha. |
| 3932 | 14638790 | Nevertheless, bacterial counts in infected lungs, immunohistochemistry, and reverse transcription-PCR analysis of mRNAs for tumor necrosis factor alpha (TNF-alpha), gamma interferon (IFN-gamma), interleukin-1beta (IL-1beta), IL-6, IL-12, and inducible nitric oxide synthase (iNOS) revealed significant differences among the strains. |
| 3933 | 14638790 | Nevertheless, bacterial counts in infected lungs, immunohistochemistry, and reverse transcription-PCR analysis of mRNAs for tumor necrosis factor alpha (TNF-alpha), gamma interferon (IFN-gamma), interleukin-1beta (IL-1beta), IL-6, IL-12, and inducible nitric oxide synthase (iNOS) revealed significant differences among the strains. |
| 3934 | 14638790 | At 72 h postinfection, M90T guaBA purHD still induced proinflammatory cytokines and factors such as IL-1beta, IL-6, TNF-alpha, and iNOS, along with cytokines such as IL-12 and IFN-gamma. |
| 3935 | 14638790 | At 72 h postinfection, M90T guaBA purHD still induced proinflammatory cytokines and factors such as IL-1beta, IL-6, TNF-alpha, and iNOS, along with cytokines such as IL-12 and IFN-gamma. |
| 3936 | 14627128 | Immature monocyte-derived dendritic cells (imMo-DCs) isolated from human peripheral blood monocytes stimulated with granulocyte-macrophage colony stimulating factor and interleukin-4 were exposed to maturation factors, i.e., lipopolysaccharide (LPS), tumor necrosis factor alpha (TNF-alpha) plus prostaglandin E2 (PGE2), and OK-432 for 2 days. |
| 3937 | 14627128 | Immature monocyte-derived dendritic cells (imMo-DCs) isolated from human peripheral blood monocytes stimulated with granulocyte-macrophage colony stimulating factor and interleukin-4 were exposed to maturation factors, i.e., lipopolysaccharide (LPS), tumor necrosis factor alpha (TNF-alpha) plus prostaglandin E2 (PGE2), and OK-432 for 2 days. |
| 3938 | 14627128 | OK-432 increased expression of activation- and maturation-related molecules such as HLA-DR, CD80, CD83, and CD86 in imMo-DCs at levels similar to that of TNF-alpha plus PGE2, and higher than that of LPS. |
| 3939 | 14627128 | OK-432 increased expression of activation- and maturation-related molecules such as HLA-DR, CD80, CD83, and CD86 in imMo-DCs at levels similar to that of TNF-alpha plus PGE2, and higher than that of LPS. |
| 3940 | 14627128 | Only OK-432 caused significant production of interleukin-12 (IL-12) p70 and interferon gamma (IFN-gamma) at both the mRNA and protein levels in imMo-DCs. |
| 3941 | 14627128 | Only OK-432 caused significant production of interleukin-12 (IL-12) p70 and interferon gamma (IFN-gamma) at both the mRNA and protein levels in imMo-DCs. |
| 3942 | 14627128 | Neutralizing antibody against IL-12 p70 blocked IFN-gamma secretion from OK-432-stimulated Mo-DCs. |
| 3943 | 14627128 | Neutralizing antibody against IL-12 p70 blocked IFN-gamma secretion from OK-432-stimulated Mo-DCs. |
| 3944 | 14627128 | IL-12 p70 produced by OK-432-stimulated imMo-DCs induced secretion of IFN-gamma by CD4+ T cells. |
| 3945 | 14627128 | IL-12 p70 produced by OK-432-stimulated imMo-DCs induced secretion of IFN-gamma by CD4+ T cells. |
| 3946 | 14627128 | Both secretion of IL-12 p70 and IFN-gamma and activation of NF-kappaB induced by OK-432 were suppressed when imMo-DCs were pretreated with cytochalasin B. |
| 3947 | 14627128 | Both secretion of IL-12 p70 and IFN-gamma and activation of NF-kappaB induced by OK-432 were suppressed when imMo-DCs were pretreated with cytochalasin B. |
| 3948 | 14627128 | These results indicate that uptake of OK-432 by imMo-DCs is an early critical event for IL-12 p70 production and that NF-kappaB activation induced by OK-432 also contributes partially to IL-12 p70 production. |
| 3949 | 14627128 | These results indicate that uptake of OK-432 by imMo-DCs is an early critical event for IL-12 p70 production and that NF-kappaB activation induced by OK-432 also contributes partially to IL-12 p70 production. |
| 3950 | 14611813 | Function of CD80 and CD86 on monocyte- and stem cell-derived dendritic cells. |
| 3951 | 14611813 | Dendritic cells (DCs) consist of a heterogeneous population of hematopoietic cells characterized by their unique dendritic morphology, their efficient antigen-presenting capability to activate naïve CD4+ and CD8+ T cells, as well as their lack of lineage-specific markers. |
| 3952 | 14611813 | Human umbilical cord blood CD14+ monocytes and CD34+ stem cells were induced to differentiate into dendritic cells using 100 ng/mL granulocyte-macrophage colony-stimulating factor (GM-CSF), 25 ng/mL interleukin (II)-4, 2.5 ng/mL tumor necrosis factor alpha (TNF-alpha) and 100 ng/mL GM-CSF, 25 ng/mL stem cell factor, and 2.5 ng/mL TNF-alpha, respectively. |
| 3953 | 14611813 | Differentiated dendritic cells were CD80+, CD86+, CD83+, CD54+, CD1a+, CD11b+, CD11c+, HLA-DR+, CD34-, CD3-, CD19-, CD14-, and CD16-. |
| 3954 | 14611813 | Reverse transcription polymerase chain reaction revealed that differentiating monocytes initially expressed CD86 mRNA while CD80 mRNA appeared on Day 2. |
| 3955 | 14611813 | Differentiating stem cells expressed both CD80 and CD86 mRNA on Day 2 of culture. |
| 3956 | 14611813 | Monoclonal antibodies (mabs) to CD80 and CD86 were employed to assess their costimulatory roles. |
| 3957 | 14611813 | CD14 and CD34 derived DCs prior to the functional assay were stimulated for 18 h with 0.1 and 1.0 mg/mL Escherichia coli lipopolyssacharide, respectively. |
| 3958 | 14611813 | A decrease in stimulation as depicted by decreased T-cell activation was significant with mabs to both CD80 and CD86 on monocyte-derived DCs while only mabs to CD86 induced decreased T-cell activation by stem cell-derived DCs. |
| 3959 | 14611813 | The varied functional role of CD80 and CD86 costimulatory molecules is associated with DC differentiation from distinct cord blood-isolated hematopoietic lineages. |
| 3960 | 14607947 | C57BL/6 mice infected with a nonlethal (Py17X) strain of Plasmodium yoelii produce TGF-beta from 5 days postinfection; this correlates with resolution of parasitemia, down-regulation of TNF-alpha, and full recovery. |
| 3961 | 14607947 | C57BL/6 mice infected with a nonlethal (Py17X) strain of Plasmodium yoelii produce TGF-beta from 5 days postinfection; this correlates with resolution of parasitemia, down-regulation of TNF-alpha, and full recovery. |
| 3962 | 14607947 | C57BL/6 mice infected with a nonlethal (Py17X) strain of Plasmodium yoelii produce TGF-beta from 5 days postinfection; this correlates with resolution of parasitemia, down-regulation of TNF-alpha, and full recovery. |
| 3963 | 14607947 | C57BL/6 mice infected with a nonlethal (Py17X) strain of Plasmodium yoelii produce TGF-beta from 5 days postinfection; this correlates with resolution of parasitemia, down-regulation of TNF-alpha, and full recovery. |
| 3964 | 14607947 | In contrast, infection with the lethal strain Py17XL induces high levels of circulating TGF-beta within 24 h; this is associated with delayed and blunted IFN-gamma and TNF-alpha responses, failure to clear parasites, and 100% mortality. |
| 3965 | 14607947 | In contrast, infection with the lethal strain Py17XL induces high levels of circulating TGF-beta within 24 h; this is associated with delayed and blunted IFN-gamma and TNF-alpha responses, failure to clear parasites, and 100% mortality. |
| 3966 | 14607947 | In contrast, infection with the lethal strain Py17XL induces high levels of circulating TGF-beta within 24 h; this is associated with delayed and blunted IFN-gamma and TNF-alpha responses, failure to clear parasites, and 100% mortality. |
| 3967 | 14607947 | In contrast, infection with the lethal strain Py17XL induces high levels of circulating TGF-beta within 24 h; this is associated with delayed and blunted IFN-gamma and TNF-alpha responses, failure to clear parasites, and 100% mortality. |
| 3968 | 14607947 | Neutralization of early TGF-beta in Py17XL infection leads to a compensatory increase in IL-10 production, while simultaneous neutralization of TGF-beta and IL-10R signaling leads to up-regulation of TNF-alpha and IFN-gamma, prolonged survival in all, and ultimate resolution of infection in 40% of Py17XL-infected animals. |
| 3969 | 14607947 | Neutralization of early TGF-beta in Py17XL infection leads to a compensatory increase in IL-10 production, while simultaneous neutralization of TGF-beta and IL-10R signaling leads to up-regulation of TNF-alpha and IFN-gamma, prolonged survival in all, and ultimate resolution of infection in 40% of Py17XL-infected animals. |
| 3970 | 14607947 | Neutralization of early TGF-beta in Py17XL infection leads to a compensatory increase in IL-10 production, while simultaneous neutralization of TGF-beta and IL-10R signaling leads to up-regulation of TNF-alpha and IFN-gamma, prolonged survival in all, and ultimate resolution of infection in 40% of Py17XL-infected animals. |
| 3971 | 14607947 | Neutralization of early TGF-beta in Py17XL infection leads to a compensatory increase in IL-10 production, while simultaneous neutralization of TGF-beta and IL-10R signaling leads to up-regulation of TNF-alpha and IFN-gamma, prolonged survival in all, and ultimate resolution of infection in 40% of Py17XL-infected animals. |
| 3972 | 14607947 | TGF-beta production can be induced in an Ag-specific manner from splenocytes of infected mice, and by cross-linking surface CTLA-4. |
| 3973 | 14607947 | TGF-beta production can be induced in an Ag-specific manner from splenocytes of infected mice, and by cross-linking surface CTLA-4. |
| 3974 | 14607947 | TGF-beta production can be induced in an Ag-specific manner from splenocytes of infected mice, and by cross-linking surface CTLA-4. |
| 3975 | 14607947 | TGF-beta production can be induced in an Ag-specific manner from splenocytes of infected mice, and by cross-linking surface CTLA-4. |
| 3976 | 14607947 | CD25(+) and CD8(+) cells are the primary source of TGF-beta following Py17X stimulation of splenocytes, whereas Py17XL induces significant production of TGF-beta from adherent cells. |
| 3977 | 14607947 | CD25(+) and CD8(+) cells are the primary source of TGF-beta following Py17X stimulation of splenocytes, whereas Py17XL induces significant production of TGF-beta from adherent cells. |
| 3978 | 14607947 | CD25(+) and CD8(+) cells are the primary source of TGF-beta following Py17X stimulation of splenocytes, whereas Py17XL induces significant production of TGF-beta from adherent cells. |
| 3979 | 14607947 | CD25(+) and CD8(+) cells are the primary source of TGF-beta following Py17X stimulation of splenocytes, whereas Py17XL induces significant production of TGF-beta from adherent cells. |
| 3980 | 14607947 | In mice immunized against Py17XL, the early TGF-beta response is inhibited and is accompanied by significant up-regulation of IFN-gamma and TNF-alpha and rapid resolution of challenge infections. |
| 3981 | 14607947 | In mice immunized against Py17XL, the early TGF-beta response is inhibited and is accompanied by significant up-regulation of IFN-gamma and TNF-alpha and rapid resolution of challenge infections. |
| 3982 | 14607947 | In mice immunized against Py17XL, the early TGF-beta response is inhibited and is accompanied by significant up-regulation of IFN-gamma and TNF-alpha and rapid resolution of challenge infections. |
| 3983 | 14607947 | In mice immunized against Py17XL, the early TGF-beta response is inhibited and is accompanied by significant up-regulation of IFN-gamma and TNF-alpha and rapid resolution of challenge infections. |
| 3984 | 14604550 | TNF-alpha and IFN-gamma production from memory CD4+ T cells were measured and compared to a control group who never received the anthrax vaccine. |
| 3985 | 14604550 | TNF-alpha and IFN-gamma production from memory CD4+ T cells were measured and compared to a control group who never received the anthrax vaccine. |
| 3986 | 14604550 | The optimal antigen concentration for TNF-alpha was determined to be around 7.5 microg/ml and IFN-gamma production was not detected. |
| 3987 | 14604550 | The optimal antigen concentration for TNF-alpha was determined to be around 7.5 microg/ml and IFN-gamma production was not detected. |
| 3988 | 14594508 | Differentiation of CD14(+) cells into mature monocyte-derived DC was induced by incubation with IL-4, GM-CSF, TNF-alpha, PGE(2), IL-1 beta, and IL-6. |
| 3989 | 14594508 | Mature DC showed a high expression of CD83, HLA-DR, and the co-stimulatory molecules CD80 and CD86. |
| 3990 | 14592822 | Here, we report that Hsp70-like protein 1 (Hsp70L1), a novel HSP derived from human dendritic cells (DCs), has potent adjuvant effects that polarize responses toward Th1. |
| 3991 | 14592822 | With a calculated molecular weight of 54.8 kDa, Hsp70L1 is smaller in size than Hsp70 but resembles it both structurally and functionally. |
| 3992 | 14592822 | Hsp70L1 shares common receptors on DCs with Hsp70 and can interact with DCs, promoting DC maturation and stimulating secretion of the proinflammatory cytokines interleukin 12p70 (IL-12p70), IL-1beta, tumor necrosis factor-alpha (TNF-alpha), and the chemokines IP-10, macrophage inflammatory protein-1alpha (MIP-1alpha), MIP-1beta, and normal T cell expressed and secreted (RANTES). |
| 3993 | 14592822 | The induction of interferon-gamma-inducible protein 10 (IP-10) secretion by Hsp70L1 is not shared by Hsp70, and other functional differences include more potent stimulation of DC IL-12p70, CC-chemokine, and CCR7 and CXCR4 expression by Hsp70L1. |
| 3994 | 14579266 | We show that E. coli LPS-pulsed MDDC released Th1-biasing cytokines - consisting of high levels of IL-12 p70, IFN-gamma-inducible protein 10 (IP-10) - but also TNF-alpha, IL-10, IL-6 and IL-1beta. |
| 3995 | 14579266 | We show that E. coli LPS-pulsed MDDC released Th1-biasing cytokines - consisting of high levels of IL-12 p70, IFN-gamma-inducible protein 10 (IP-10) - but also TNF-alpha, IL-10, IL-6 and IL-1beta. |
| 3996 | 14579266 | In contrast, no IL-12 p70 or IP-10, and lower levels of TNF-alpha and IL-10 were induced by P. gingivalis LPS. |
| 3997 | 14579266 | In contrast, no IL-12 p70 or IP-10, and lower levels of TNF-alpha and IL-10 were induced by P. gingivalis LPS. |
| 3998 | 14579266 | These differences were sustained at LPS doses that yielded nearly equivalent maturation of MDDC; moreover the T cell response was consistent: E. coli LPS-pulsed MDDC induced higher T cell proliferation, and T cells released more IFN-gamma and IL-2, but less IL-5 than T cells co-cultured with P. gingivalis LPS pulsed-MDDC. |
| 3999 | 14579266 | These differences were sustained at LPS doses that yielded nearly equivalent maturation of MDDC; moreover the T cell response was consistent: E. coli LPS-pulsed MDDC induced higher T cell proliferation, and T cells released more IFN-gamma and IL-2, but less IL-5 than T cells co-cultured with P. gingivalis LPS pulsed-MDDC. |
| 4000 | 14577973 | A single chain antibody scFv-pDL1.0, which recognizes the human ovarian cancer antigen CA125 was formulated in microspheres and injected to mice alone or in the presence of colony stimulating factor (GM-CSF) or tumor necrosis factor (TNF-alpha). |
| 4001 | 14577973 | A single chain antibody scFv-pDL1.0, which recognizes the human ovarian cancer antigen CA125 was formulated in microspheres and injected to mice alone or in the presence of colony stimulating factor (GM-CSF) or tumor necrosis factor (TNF-alpha). |
| 4002 | 14577973 | These results raise the possibility of cancer immunotherapy by administration of single chain antibody encapsulated in microspheres with GM-CSF or TNF-alpha. |
| 4003 | 14577973 | These results raise the possibility of cancer immunotherapy by administration of single chain antibody encapsulated in microspheres with GM-CSF or TNF-alpha. |
| 4004 | 14557666 | DD identified eight differentially expressed cDNAs, including inhibitor of apoptosis-1, 2'-5' oligoadenylate synthetase (OAS), a 2'-5' OAS-like (OASL) gene, galectin-9, myxovirus protein A (MxA), regulator of G-protein signaling, endothelial and smooth muscle cell-derived neuropilin-like protein, and phospholipid scramblase 1. |
| 4005 | 14557666 | Tumor necrosis factor alpha, OASL, and MxA and h-IAP1 genes were induced within the first 8 to 12 h after infection, suggesting a direct effect of DV infection. |
| 4006 | 14517689 | Macrophages isolated from mice immunised with native or plant-expressed CTB showed enhanced secretion of interleukin-10 but secretion of lipopolysaccharide-induced interleukin-12 and tumor necrosis factor alpha was inhibited. |
| 4007 | 14507024 | Priming of neutrophils by TNF-alpha, IFN-gamma, or C5adesArg did not promote an oxidative burst or uptake of sIgA-opsonized S. aureus to a greater extent than with IgG1-opsonized bacteria. |
| 4008 | 14506743 | Examination of the cytokines produced by these Th-cells showed that a majority of the proliferative p53-specific T cell cultures produced none of the key cytokines (IFNgamma, TNFalpha, IL-4, IL-5 or IL-10), indicating that these p53-specific Th-responses are not polarized. |
| 4009 | 14506743 | In patients who exhibited p53-specific reactivity against multiple p53-epitopes, non-polarized responses could be found side by side with polarized Th-responses that produced INFgamma or other cytokines such as IL-10. |
| 4010 | 12972343 | The effect of mycobacterial virulence and viability on MAP kinase signalling and TNF alpha production by human monocytes. |
| 4011 | 12969546 | CD1a and CD1c cell sorting yields a homogeneous population of immature human Langerhans cells. |
| 4012 | 12969546 | CD1c selection yielded a homogeneous population of pure and viable HLA-DR(+)/CD1a(+) DCs, with the ultrastructural features, surface antigen expression and cytokine profile, characteristic of epidermis-resident immature LCs. |
| 4013 | 12969546 | Characterizing the cells in more detail, we could demonstrate for the first time that normal human LCs express CXCR4, CD40 ligand (CD40L), and Fas and Fas ligand (FasL). |
| 4014 | 12969546 | LPS and IFN-omega stimulated the expression of the inflammatory cytokines TNF-alpha and IL-1beta, and there was secretion of IL-12p70 after CD40 ligation. |
| 4015 | 12966542 | The production of high levels of interferon-gamma (IFN-gamma) and tumor necrosis factor-alpha (TNF-alpha) by antigen-specific T cells was found in six patients (46.0%) who showed significantly lower HBV DNA levels in serum at 6 (P = 0.04) and 18 months (P = 0.005) after completion of therapy than those without high levels of cytokine production. |
| 4016 | 12959322 | During the course of HIV-1 infection secretion of T-helper type 1 (Th1) cytokines, such as interleukin (IL)-2, and antiviral interferon (IFN)-gamma, is generally decreased, whereas production of T helper type 2 (Th2) cytokines, IL-4, IL-10, proinflammatory cytokines (IL-1, IL-6, IL-8) and tumour necrosis factor (TNF)-alpha, is increased. |
| 4017 | 12959322 | During the course of HIV-1 infection secretion of T-helper type 1 (Th1) cytokines, such as interleukin (IL)-2, and antiviral interferon (IFN)-gamma, is generally decreased, whereas production of T helper type 2 (Th2) cytokines, IL-4, IL-10, proinflammatory cytokines (IL-1, IL-6, IL-8) and tumour necrosis factor (TNF)-alpha, is increased. |
| 4018 | 12959322 | HIV-inductive cytokines include: TNF-alpha, TNF-beta, IL-1 and IL-6, which stimulate HIV-1 replication in T cells and monocyte-derived macrophages (MDM), IL-2, IL-7 and IL-15, which upregulate HIV-1 in T cells, and macrophage-colony stimulating factor, which stimulates HIV-1 in MDM. |
| 4019 | 12959322 | HIV-inductive cytokines include: TNF-alpha, TNF-beta, IL-1 and IL-6, which stimulate HIV-1 replication in T cells and monocyte-derived macrophages (MDM), IL-2, IL-7 and IL-15, which upregulate HIV-1 in T cells, and macrophage-colony stimulating factor, which stimulates HIV-1 in MDM. |
| 4020 | 12959322 | HIV-suppressive cytokines include: IFN-alpha, IFN-beta and IL-16, which inhibit HIV-1 replication in T cells and MDM, and IL-10 and IL-13, which inhibit HIV-1 in MDM. |
| 4021 | 12959322 | HIV-suppressive cytokines include: IFN-alpha, IFN-beta and IL-16, which inhibit HIV-1 replication in T cells and MDM, and IL-10 and IL-13, which inhibit HIV-1 in MDM. |
| 4022 | 12959322 | Bifunctional cytokines such as IFN-gamma, IL-4 and granulocyte-macrophage colony-stimulating factor have been shown to have both inhibitory and stimulatory effects on HIV-1. |
| 4023 | 12959322 | Bifunctional cytokines such as IFN-gamma, IL-4 and granulocyte-macrophage colony-stimulating factor have been shown to have both inhibitory and stimulatory effects on HIV-1. |
| 4024 | 12959322 | The beta-chemokines, macrophage-inflammatory protein (MIP)-1alpha, MIP-1beta and RANTES are important inhibitors of macrophage-tropic strains of HIV-1, whereas the alpha-chemokine stromal-derived factor-1 suppresses infection of T-tropic strains of HIV-1. |
| 4025 | 12959322 | The beta-chemokines, macrophage-inflammatory protein (MIP)-1alpha, MIP-1beta and RANTES are important inhibitors of macrophage-tropic strains of HIV-1, whereas the alpha-chemokine stromal-derived factor-1 suppresses infection of T-tropic strains of HIV-1. |
| 4026 | 12957792 | To understand the pathogenesis of vaccine-modified measles (VMM), we measured plasma levels of IFN-gamma and IL-2 (Th1 cytokines), IL-4 and IL-10 (Th2 cytokines), IL-12, TNF-alpha and TGF-beta1 in children with uncomplicated measles, who had anti-measles IgG antibodies and with a history of immunization on admission (day 0), day 14 and day 60. |
| 4027 | 12957792 | Plasma levels of IFN-gamma, IL-2 and IL-12 were significantly higher in VMM patients on day 0 compared to healthy controls (p = 0.023; p = 0.018; p = 0.001) respectively. |
| 4028 | 12957792 | Kinetically, IFN-gamma and IL-10 levels decreased consistently from day 0 to days 14 and 60 in VMM patients. |
| 4029 | 12951895 | In vitro effects of 1,25-dihydroxyvitamin D3 on interferon-gamma and tumor necrosis factor-alpha secretion by blood leukocytes from young and adult cattle vaccinated with Mycobacterium bovis BCG. |
| 4030 | 12951895 | In vitro effects of 1,25-dihydroxyvitamin D3 on interferon-gamma and tumor necrosis factor-alpha secretion by blood leukocytes from young and adult cattle vaccinated with Mycobacterium bovis BCG. |
| 4031 | 12951895 | In vitro effects of 1,25-dihydroxyvitamin D3 on interferon-gamma and tumor necrosis factor-alpha secretion by blood leukocytes from young and adult cattle vaccinated with Mycobacterium bovis BCG. |
| 4032 | 12951895 | In vitro effects of 1,25-dihydroxyvitamin D3 on interferon-gamma and tumor necrosis factor-alpha secretion by blood leukocytes from young and adult cattle vaccinated with Mycobacterium bovis BCG. |
| 4033 | 12951895 | In vitro effects of 1,25-dihydroxyvitamin D3 on interferon-gamma and tumor necrosis factor-alpha secretion by blood leukocytes from young and adult cattle vaccinated with Mycobacterium bovis BCG. |
| 4034 | 12951895 | In vitro effects of 1,25-dihydroxyvitamin D3 on interferon-gamma and tumor necrosis factor-alpha secretion by blood leukocytes from young and adult cattle vaccinated with Mycobacterium bovis BCG. |
| 4035 | 12951895 | In vitro effects of 1,25-dihydroxyvitamin D3 on interferon-gamma and tumor necrosis factor-alpha secretion by blood leukocytes from young and adult cattle vaccinated with Mycobacterium bovis BCG. |
| 4036 | 12951895 | In vitro effects of 1,25-dihydroxyvitamin D3 on interferon-gamma and tumor necrosis factor-alpha secretion by blood leukocytes from young and adult cattle vaccinated with Mycobacterium bovis BCG. |
| 4037 | 12951895 | In vitro effects of 1,25-dihydroxyvitamin D3 on interferon-gamma and tumor necrosis factor-alpha secretion by blood leukocytes from young and adult cattle vaccinated with Mycobacterium bovis BCG. |
| 4038 | 12951895 | Interferon-gamma (IFN-gamma) and tumor necrosis factor-alpha (TNF-alpha) are critical in the development of an effective immune response. |
| 4039 | 12951895 | Interferon-gamma (IFN-gamma) and tumor necrosis factor-alpha (TNF-alpha) are critical in the development of an effective immune response. |
| 4040 | 12951895 | Interferon-gamma (IFN-gamma) and tumor necrosis factor-alpha (TNF-alpha) are critical in the development of an effective immune response. |
| 4041 | 12951895 | Interferon-gamma (IFN-gamma) and tumor necrosis factor-alpha (TNF-alpha) are critical in the development of an effective immune response. |
| 4042 | 12951895 | Interferon-gamma (IFN-gamma) and tumor necrosis factor-alpha (TNF-alpha) are critical in the development of an effective immune response. |
| 4043 | 12951895 | Interferon-gamma (IFN-gamma) and tumor necrosis factor-alpha (TNF-alpha) are critical in the development of an effective immune response. |
| 4044 | 12951895 | Interferon-gamma (IFN-gamma) and tumor necrosis factor-alpha (TNF-alpha) are critical in the development of an effective immune response. |
| 4045 | 12951895 | Interferon-gamma (IFN-gamma) and tumor necrosis factor-alpha (TNF-alpha) are critical in the development of an effective immune response. |
| 4046 | 12951895 | Interferon-gamma (IFN-gamma) and tumor necrosis factor-alpha (TNF-alpha) are critical in the development of an effective immune response. |
| 4047 | 12951895 | Ten weeks after primary vaccination, cells from vaccinated calves and adults, and nonvaccinated, age-matched calves (n = 4) were evaluated in vitro for their capacity to produce IFN-gamma and TNF-alpha. |
| 4048 | 12951895 | Ten weeks after primary vaccination, cells from vaccinated calves and adults, and nonvaccinated, age-matched calves (n = 4) were evaluated in vitro for their capacity to produce IFN-gamma and TNF-alpha. |
| 4049 | 12951895 | Ten weeks after primary vaccination, cells from vaccinated calves and adults, and nonvaccinated, age-matched calves (n = 4) were evaluated in vitro for their capacity to produce IFN-gamma and TNF-alpha. |
| 4050 | 12951895 | Ten weeks after primary vaccination, cells from vaccinated calves and adults, and nonvaccinated, age-matched calves (n = 4) were evaluated in vitro for their capacity to produce IFN-gamma and TNF-alpha. |
| 4051 | 12951895 | Ten weeks after primary vaccination, cells from vaccinated calves and adults, and nonvaccinated, age-matched calves (n = 4) were evaluated in vitro for their capacity to produce IFN-gamma and TNF-alpha. |
| 4052 | 12951895 | Ten weeks after primary vaccination, cells from vaccinated calves and adults, and nonvaccinated, age-matched calves (n = 4) were evaluated in vitro for their capacity to produce IFN-gamma and TNF-alpha. |
| 4053 | 12951895 | Ten weeks after primary vaccination, cells from vaccinated calves and adults, and nonvaccinated, age-matched calves (n = 4) were evaluated in vitro for their capacity to produce IFN-gamma and TNF-alpha. |
| 4054 | 12951895 | Ten weeks after primary vaccination, cells from vaccinated calves and adults, and nonvaccinated, age-matched calves (n = 4) were evaluated in vitro for their capacity to produce IFN-gamma and TNF-alpha. |
| 4055 | 12951895 | Ten weeks after primary vaccination, cells from vaccinated calves and adults, and nonvaccinated, age-matched calves (n = 4) were evaluated in vitro for their capacity to produce IFN-gamma and TNF-alpha. |
| 4056 | 12951895 | IFN-gamma and TNF-alpha concentrations in culture supernatants harvested at these times were quantified by enzyme-linked immunosorbent assay (ELISA). |
| 4057 | 12951895 | IFN-gamma and TNF-alpha concentrations in culture supernatants harvested at these times were quantified by enzyme-linked immunosorbent assay (ELISA). |
| 4058 | 12951895 | IFN-gamma and TNF-alpha concentrations in culture supernatants harvested at these times were quantified by enzyme-linked immunosorbent assay (ELISA). |
| 4059 | 12951895 | IFN-gamma and TNF-alpha concentrations in culture supernatants harvested at these times were quantified by enzyme-linked immunosorbent assay (ELISA). |
| 4060 | 12951895 | IFN-gamma and TNF-alpha concentrations in culture supernatants harvested at these times were quantified by enzyme-linked immunosorbent assay (ELISA). |
| 4061 | 12951895 | IFN-gamma and TNF-alpha concentrations in culture supernatants harvested at these times were quantified by enzyme-linked immunosorbent assay (ELISA). |
| 4062 | 12951895 | IFN-gamma and TNF-alpha concentrations in culture supernatants harvested at these times were quantified by enzyme-linked immunosorbent assay (ELISA). |
| 4063 | 12951895 | IFN-gamma and TNF-alpha concentrations in culture supernatants harvested at these times were quantified by enzyme-linked immunosorbent assay (ELISA). |
| 4064 | 12951895 | IFN-gamma and TNF-alpha concentrations in culture supernatants harvested at these times were quantified by enzyme-linked immunosorbent assay (ELISA). |
| 4065 | 12951895 | PPD-induced IFN-gamma and TNF-alpha responses of cells from vaccinated calves and adults were greater than responses of autologous unstimulated cells. |
| 4066 | 12951895 | PPD-induced IFN-gamma and TNF-alpha responses of cells from vaccinated calves and adults were greater than responses of autologous unstimulated cells. |
| 4067 | 12951895 | PPD-induced IFN-gamma and TNF-alpha responses of cells from vaccinated calves and adults were greater than responses of autologous unstimulated cells. |
| 4068 | 12951895 | PPD-induced IFN-gamma and TNF-alpha responses of cells from vaccinated calves and adults were greater than responses of autologous unstimulated cells. |
| 4069 | 12951895 | PPD-induced IFN-gamma and TNF-alpha responses of cells from vaccinated calves and adults were greater than responses of autologous unstimulated cells. |
| 4070 | 12951895 | PPD-induced IFN-gamma and TNF-alpha responses of cells from vaccinated calves and adults were greater than responses of autologous unstimulated cells. |
| 4071 | 12951895 | PPD-induced IFN-gamma and TNF-alpha responses of cells from vaccinated calves and adults were greater than responses of autologous unstimulated cells. |
| 4072 | 12951895 | PPD-induced IFN-gamma and TNF-alpha responses of cells from vaccinated calves and adults were greater than responses of autologous unstimulated cells. |
| 4073 | 12951895 | PPD-induced IFN-gamma and TNF-alpha responses of cells from vaccinated calves and adults were greater than responses of autologous unstimulated cells. |
| 4074 | 12951895 | Incubation period also influenced the magnitude of both IFN-gamma and TNF-alpha, responses in PPD- and PWM-stimulated cultures. |
| 4075 | 12951895 | Incubation period also influenced the magnitude of both IFN-gamma and TNF-alpha, responses in PPD- and PWM-stimulated cultures. |
| 4076 | 12951895 | Incubation period also influenced the magnitude of both IFN-gamma and TNF-alpha, responses in PPD- and PWM-stimulated cultures. |
| 4077 | 12951895 | Incubation period also influenced the magnitude of both IFN-gamma and TNF-alpha, responses in PPD- and PWM-stimulated cultures. |
| 4078 | 12951895 | Incubation period also influenced the magnitude of both IFN-gamma and TNF-alpha, responses in PPD- and PWM-stimulated cultures. |
| 4079 | 12951895 | Incubation period also influenced the magnitude of both IFN-gamma and TNF-alpha, responses in PPD- and PWM-stimulated cultures. |
| 4080 | 12951895 | Incubation period also influenced the magnitude of both IFN-gamma and TNF-alpha, responses in PPD- and PWM-stimulated cultures. |
| 4081 | 12951895 | Incubation period also influenced the magnitude of both IFN-gamma and TNF-alpha, responses in PPD- and PWM-stimulated cultures. |
| 4082 | 12951895 | Incubation period also influenced the magnitude of both IFN-gamma and TNF-alpha, responses in PPD- and PWM-stimulated cultures. |
| 4083 | 12951895 | Effects of 1,25-(OH)2D3 on antigen-induced secretion of IFN-gamma and TNF-alpha were marginal. |
| 4084 | 12951895 | Effects of 1,25-(OH)2D3 on antigen-induced secretion of IFN-gamma and TNF-alpha were marginal. |
| 4085 | 12951895 | Effects of 1,25-(OH)2D3 on antigen-induced secretion of IFN-gamma and TNF-alpha were marginal. |
| 4086 | 12951895 | Effects of 1,25-(OH)2D3 on antigen-induced secretion of IFN-gamma and TNF-alpha were marginal. |
| 4087 | 12951895 | Effects of 1,25-(OH)2D3 on antigen-induced secretion of IFN-gamma and TNF-alpha were marginal. |
| 4088 | 12951895 | Effects of 1,25-(OH)2D3 on antigen-induced secretion of IFN-gamma and TNF-alpha were marginal. |
| 4089 | 12951895 | Effects of 1,25-(OH)2D3 on antigen-induced secretion of IFN-gamma and TNF-alpha were marginal. |
| 4090 | 12951895 | Effects of 1,25-(OH)2D3 on antigen-induced secretion of IFN-gamma and TNF-alpha were marginal. |
| 4091 | 12951895 | Effects of 1,25-(OH)2D3 on antigen-induced secretion of IFN-gamma and TNF-alpha were marginal. |
| 4092 | 12951895 | Vitamin D caused a concentration-dependent decrease in IFN-gamma response and an increase in TNF-alpha response in PWM-stimulated cultures. |
| 4093 | 12951895 | Vitamin D caused a concentration-dependent decrease in IFN-gamma response and an increase in TNF-alpha response in PWM-stimulated cultures. |
| 4094 | 12951895 | Vitamin D caused a concentration-dependent decrease in IFN-gamma response and an increase in TNF-alpha response in PWM-stimulated cultures. |
| 4095 | 12951895 | Vitamin D caused a concentration-dependent decrease in IFN-gamma response and an increase in TNF-alpha response in PWM-stimulated cultures. |
| 4096 | 12951895 | Vitamin D caused a concentration-dependent decrease in IFN-gamma response and an increase in TNF-alpha response in PWM-stimulated cultures. |
| 4097 | 12951895 | Vitamin D caused a concentration-dependent decrease in IFN-gamma response and an increase in TNF-alpha response in PWM-stimulated cultures. |
| 4098 | 12951895 | Vitamin D caused a concentration-dependent decrease in IFN-gamma response and an increase in TNF-alpha response in PWM-stimulated cultures. |
| 4099 | 12951895 | Vitamin D caused a concentration-dependent decrease in IFN-gamma response and an increase in TNF-alpha response in PWM-stimulated cultures. |
| 4100 | 12951895 | Vitamin D caused a concentration-dependent decrease in IFN-gamma response and an increase in TNF-alpha response in PWM-stimulated cultures. |
| 4101 | 12951895 | These results indicate that animal maturity (i.e., age) and antigenic experience affect IFN-gamma and TNF-alpha secretion by bovine leukocytes and suggest that 1,25-(OH)2D3 can alter secretion of both cytokines under specific conditions of culture. |
| 4102 | 12951895 | These results indicate that animal maturity (i.e., age) and antigenic experience affect IFN-gamma and TNF-alpha secretion by bovine leukocytes and suggest that 1,25-(OH)2D3 can alter secretion of both cytokines under specific conditions of culture. |
| 4103 | 12951895 | These results indicate that animal maturity (i.e., age) and antigenic experience affect IFN-gamma and TNF-alpha secretion by bovine leukocytes and suggest that 1,25-(OH)2D3 can alter secretion of both cytokines under specific conditions of culture. |
| 4104 | 12951895 | These results indicate that animal maturity (i.e., age) and antigenic experience affect IFN-gamma and TNF-alpha secretion by bovine leukocytes and suggest that 1,25-(OH)2D3 can alter secretion of both cytokines under specific conditions of culture. |
| 4105 | 12951895 | These results indicate that animal maturity (i.e., age) and antigenic experience affect IFN-gamma and TNF-alpha secretion by bovine leukocytes and suggest that 1,25-(OH)2D3 can alter secretion of both cytokines under specific conditions of culture. |
| 4106 | 12951895 | These results indicate that animal maturity (i.e., age) and antigenic experience affect IFN-gamma and TNF-alpha secretion by bovine leukocytes and suggest that 1,25-(OH)2D3 can alter secretion of both cytokines under specific conditions of culture. |
| 4107 | 12951895 | These results indicate that animal maturity (i.e., age) and antigenic experience affect IFN-gamma and TNF-alpha secretion by bovine leukocytes and suggest that 1,25-(OH)2D3 can alter secretion of both cytokines under specific conditions of culture. |
| 4108 | 12951895 | These results indicate that animal maturity (i.e., age) and antigenic experience affect IFN-gamma and TNF-alpha secretion by bovine leukocytes and suggest that 1,25-(OH)2D3 can alter secretion of both cytokines under specific conditions of culture. |
| 4109 | 12951895 | These results indicate that animal maturity (i.e., age) and antigenic experience affect IFN-gamma and TNF-alpha secretion by bovine leukocytes and suggest that 1,25-(OH)2D3 can alter secretion of both cytokines under specific conditions of culture. |
| 4110 | 12938230 | Astrocytes produced both IL-6 and TNF-alpha in response to L-OspA and Pam(3)Cys. |
| 4111 | 12938230 | Astrocytes produced both IL-6 and TNF-alpha in response to L-OspA and Pam(3)Cys. |
| 4112 | 12938230 | Astrocytes produced both IL-6 and TNF-alpha in response to L-OspA and Pam(3)Cys. |
| 4113 | 12938230 | Proliferation induced by L-OspA was diminished in the presence of an excess of anti-IL-6 antibody, and apoptosis induced by this lipoprotein was completely suppressed with anti-TNF-alpha antibody. |
| 4114 | 12938230 | Proliferation induced by L-OspA was diminished in the presence of an excess of anti-IL-6 antibody, and apoptosis induced by this lipoprotein was completely suppressed with anti-TNF-alpha antibody. |
| 4115 | 12938230 | Proliferation induced by L-OspA was diminished in the presence of an excess of anti-IL-6 antibody, and apoptosis induced by this lipoprotein was completely suppressed with anti-TNF-alpha antibody. |
| 4116 | 12938230 | Hence, IL-6 contributes to, and TNF-alpha determines, astrocyte proliferation and apoptosis, respectively, as elicited by lipoproteins. |
| 4117 | 12938230 | Hence, IL-6 contributes to, and TNF-alpha determines, astrocyte proliferation and apoptosis, respectively, as elicited by lipoproteins. |
| 4118 | 12938230 | Hence, IL-6 contributes to, and TNF-alpha determines, astrocyte proliferation and apoptosis, respectively, as elicited by lipoproteins. |
| 4119 | 12934191 | Interferon (IFN)-gamma production in the serum samples and spleens from vaccinated mice was significantly decreased compared with that in controls, whereas interleukin-10 titers were significantly higher in vaccinated mice. |
| 4120 | 12934191 | IFN-gamma and tumor necrosis factor-alpha production in vitro were significantly inhibited by serum samples from mTSST-1-immunized mice but not from control mice. |
| 4121 | 12927083 | Association of INOS, TRAIL, TGF-beta2, TGF-beta3, and IgL genes with response to Salmonella enteritidis in poultry. |
| 4122 | 12927083 | The candidate genes were: inducible nitric oxide synthase (INOS), tumor necrosis factor related apoptosis inducing ligand (TRAIL), transforming growth factor beta2 (TGF-beta2), transforming growth factor beta3 (TGF-beta3), and immunoglobulin G light chain (IgL). |
| 4123 | 12927083 | This is the first reported study on the association of SNP in INOS, TRAIL, TGF-beta2, TGF-beta3, and IgL with the chicken response to SE. |
| 4124 | 12922130 | To gain further insight into the cytokine production profile in response to measles vaccination, we studied interferon-gamma (IFN-gamma), tumor necrosis factor (TNF-alpha), soluble IL-2 receptor (sIL-2R), interleukin-2 (IL-2), interleukin-4 (IL-4), and interleukin-6 (IL-6) in both supernatants from peripheral blood mononuclear cells (PBMC) stimulated with phytohaemagglutinin (PHA), and plasma. |
| 4125 | 12922130 | To gain further insight into the cytokine production profile in response to measles vaccination, we studied interferon-gamma (IFN-gamma), tumor necrosis factor (TNF-alpha), soluble IL-2 receptor (sIL-2R), interleukin-2 (IL-2), interleukin-4 (IL-4), and interleukin-6 (IL-6) in both supernatants from peripheral blood mononuclear cells (PBMC) stimulated with phytohaemagglutinin (PHA), and plasma. |
| 4126 | 12922130 | However, plasma levels of Th1 cytokines (IFN-gamma, sIL-2R and TNF-alpha) were preferentially activated by measles virus after the first dose of measles vaccination. |
| 4127 | 12922130 | However, plasma levels of Th1 cytokines (IFN-gamma, sIL-2R and TNF-alpha) were preferentially activated by measles virus after the first dose of measles vaccination. |
| 4128 | 12922116 | The anti-hemagglutinins (HI), tumour necrosis factor alpha (TNFalpha), interleukin (IL) 1beta, IL6, IL10, ACTH/cortisol axis, anti-CMV antibodies and CD28+CD57- lymphocytes were assessed. |
| 4129 | 12922116 | The anti-hemagglutinins (HI), tumour necrosis factor alpha (TNFalpha), interleukin (IL) 1beta, IL6, IL10, ACTH/cortisol axis, anti-CMV antibodies and CD28+CD57- lymphocytes were assessed. |
| 4130 | 12922116 | The anti-hemagglutinins (HI), tumour necrosis factor alpha (TNFalpha), interleukin (IL) 1beta, IL6, IL10, ACTH/cortisol axis, anti-CMV antibodies and CD28+CD57- lymphocytes were assessed. |
| 4131 | 12922116 | Non-responders of both ages we characterised by higher levels of anti-CMV IgG and higher percentages of CD57+CD28- lymphocytes (known to be associated with CMV carrier status) together with increased concentrations of TNFalpha and IL6 and decreased levels of cortisol. |
| 4132 | 12922116 | Non-responders of both ages we characterised by higher levels of anti-CMV IgG and higher percentages of CD57+CD28- lymphocytes (known to be associated with CMV carrier status) together with increased concentrations of TNFalpha and IL6 and decreased levels of cortisol. |
| 4133 | 12922116 | Non-responders of both ages we characterised by higher levels of anti-CMV IgG and higher percentages of CD57+CD28- lymphocytes (known to be associated with CMV carrier status) together with increased concentrations of TNFalpha and IL6 and decreased levels of cortisol. |
| 4134 | 12922116 | The anti-influenza vaccine induced increase in TNFalpha and IL10 in the all non-responders, while cortisol increased only in the young. |
| 4135 | 12922116 | The anti-influenza vaccine induced increase in TNFalpha and IL10 in the all non-responders, while cortisol increased only in the young. |
| 4136 | 12922116 | The anti-influenza vaccine induced increase in TNFalpha and IL10 in the all non-responders, while cortisol increased only in the young. |
| 4137 | 12911520 | We found Max decreased the secretion of interferon (IFN)-gamma and IL-12p40 by PBMC and TNF-alpha by monocytes. |
| 4138 | 12909408 | In order to investigate these effects on the canine immune system and to elucidate possible mechanisms we determined the following immune parameters in the blood of 33 clinically sound German shepherd dogs before and after standard vaccination with a polyvalent vaccine against distemper, parvovirus, viral hepatitis, leptospirosis, kennel cough and rabies: white and differential blood cell count, the serum concentrations and/or activities of IL-1, IL-2, IFN-gamma, TNF-alpha, neopterin and IgG, natural killer (NK) cell activity, bactericidal activity and complement hemolytic activity, lymphocyte proliferation test (LPT) and nitroblue tetrazolium test (NBT). |
| 4139 | 12892730 | However, high levels of IL-6, IL-12, and TNFalpha production 2-3 months after intraperitoneal injection appeared to be associated with the ability to induce lupus autoantibodies. |
| 4140 | 12890631 | A therapeutic vaccine for individuals infected with HIV-1 and treated with antiretroviral therapy (ART) should be able to replenish virus-specific CD4+ T-cells and broaden the virus-specific CD8+ T-cell response in order to maintain CD8+ T-cell function and minimize viral immune escape after ART cessation. |
| 4141 | 12890631 | Importantly, the combination of these vaccine modalities also induced a sizeable expansion in most macaques of Gag-specific CD8-(CD4+) T-cells able to produce TNF-alpha. |
| 4142 | 12885891 | Neutralizing antibodies against human RANTES, MIP-1alpha, MIP-1beta, alpha interferon (IFN-alpha), IFN-beta, IFN-gamma, interleukin-4 (IL-4), IL-10, IL-13, IL-16, MCP-1, MCP-3, tumor necrosis factor alpha (TNF-alpha), or TNF-beta failed to reverse the HIV-1-suppressive activity. |
| 4143 | 12885873 | Further, a unique population of Thy1+alphabeta+CD4-CD8- cells that was previously suggested to operate during secondary immunity to LVS in vivo strongly controlled LVS intracellular growth in vitro. |
| 4144 | 12885873 | Thus, T cell mechanisms exist that control LVS intracellular growth without acting through the IFN-gamma receptor; such control is due in large part to TNF-alpha, and is partially mediated by a unique double negative T cell subpopulation. |
| 4145 | 12874236 | Heat-killed Brucella abortus induces TNF and IL-12p40 by distinct MyD88-dependent pathways: TNF, unlike IL-12p40 secretion, is Toll-like receptor 2 dependent. |
| 4146 | 12874236 | Heat-killed Brucella abortus induces TNF and IL-12p40 by distinct MyD88-dependent pathways: TNF, unlike IL-12p40 secretion, is Toll-like receptor 2 dependent. |
| 4147 | 12874236 | Heat-killed Brucella abortus induces TNF and IL-12p40 by distinct MyD88-dependent pathways: TNF, unlike IL-12p40 secretion, is Toll-like receptor 2 dependent. |
| 4148 | 12874236 | Heat-killed Brucella abortus induces TNF and IL-12p40 by distinct MyD88-dependent pathways: TNF, unlike IL-12p40 secretion, is Toll-like receptor 2 dependent. |
| 4149 | 12874236 | Our results show that HKBA-mediated induction of IL-12p40 and TNF is dependent on the adapter molecule MyD88. |
| 4150 | 12874236 | Our results show that HKBA-mediated induction of IL-12p40 and TNF is dependent on the adapter molecule MyD88. |
| 4151 | 12874236 | Our results show that HKBA-mediated induction of IL-12p40 and TNF is dependent on the adapter molecule MyD88. |
| 4152 | 12874236 | Our results show that HKBA-mediated induction of IL-12p40 and TNF is dependent on the adapter molecule MyD88. |
| 4153 | 12874236 | To identify the TLR involved in HKBA recognition, we examined HKBA responses in TLR2- and TLR4-deficient animals. |
| 4154 | 12874236 | To identify the TLR involved in HKBA recognition, we examined HKBA responses in TLR2- and TLR4-deficient animals. |
| 4155 | 12874236 | To identify the TLR involved in HKBA recognition, we examined HKBA responses in TLR2- and TLR4-deficient animals. |
| 4156 | 12874236 | To identify the TLR involved in HKBA recognition, we examined HKBA responses in TLR2- and TLR4-deficient animals. |
| 4157 | 12874236 | TNF responses to HKBA were TLR4 independent; however, the response in TLR2-deficient mice was significantly delayed and reduced, although not completely abolished. |
| 4158 | 12874236 | TNF responses to HKBA were TLR4 independent; however, the response in TLR2-deficient mice was significantly delayed and reduced, although not completely abolished. |
| 4159 | 12874236 | TNF responses to HKBA were TLR4 independent; however, the response in TLR2-deficient mice was significantly delayed and reduced, although not completely abolished. |
| 4160 | 12874236 | TNF responses to HKBA were TLR4 independent; however, the response in TLR2-deficient mice was significantly delayed and reduced, although not completely abolished. |
| 4161 | 12874236 | Studies using Chinese hamster ovary/CD14 reporter cell lines stably transfected with either human TLR2 or human TLR4 confirmed the results seen with knockout mice, namely TLR2, but not TLR4, can mediate cellular activation by HKBA. |
| 4162 | 12874236 | Studies using Chinese hamster ovary/CD14 reporter cell lines stably transfected with either human TLR2 or human TLR4 confirmed the results seen with knockout mice, namely TLR2, but not TLR4, can mediate cellular activation by HKBA. |
| 4163 | 12874236 | Studies using Chinese hamster ovary/CD14 reporter cell lines stably transfected with either human TLR2 or human TLR4 confirmed the results seen with knockout mice, namely TLR2, but not TLR4, can mediate cellular activation by HKBA. |
| 4164 | 12874236 | Studies using Chinese hamster ovary/CD14 reporter cell lines stably transfected with either human TLR2 or human TLR4 confirmed the results seen with knockout mice, namely TLR2, but not TLR4, can mediate cellular activation by HKBA. |
| 4165 | 12874236 | In addition, human embryonic kidney 293 cells, which do not respond to HKBA, were made responsive by transfecting TLR2, but not TLR4 or TLR9. |
| 4166 | 12874236 | In addition, human embryonic kidney 293 cells, which do not respond to HKBA, were made responsive by transfecting TLR2, but not TLR4 or TLR9. |
| 4167 | 12874236 | In addition, human embryonic kidney 293 cells, which do not respond to HKBA, were made responsive by transfecting TLR2, but not TLR4 or TLR9. |
| 4168 | 12874236 | In addition, human embryonic kidney 293 cells, which do not respond to HKBA, were made responsive by transfecting TLR2, but not TLR4 or TLR9. |
| 4169 | 12874236 | Taken together, our data demonstrate that MyD88-dependent pathways are crucial for activation by HKBA and that TLR2 plays a role in TNF, but not IL-12p40 pathways activated by this microbial product. |
| 4170 | 12874236 | Taken together, our data demonstrate that MyD88-dependent pathways are crucial for activation by HKBA and that TLR2 plays a role in TNF, but not IL-12p40 pathways activated by this microbial product. |
| 4171 | 12874236 | Taken together, our data demonstrate that MyD88-dependent pathways are crucial for activation by HKBA and that TLR2 plays a role in TNF, but not IL-12p40 pathways activated by this microbial product. |
| 4172 | 12874236 | Taken together, our data demonstrate that MyD88-dependent pathways are crucial for activation by HKBA and that TLR2 plays a role in TNF, but not IL-12p40 pathways activated by this microbial product. |
| 4173 | 12865071 | Unlike exposure to the native toxin, the vaccine did not trigger the release of inflammatory cytokines (TNF alpha, IL6, or IFN gamma). |
| 4174 | 12850812 | Granulocyte-macrophage colony-stimulating factor (GM-CSF) enhances immune responses by inducing the proliferation, maturation, and migration of dendritic cells, and the expansion and differentiation of B and T lymphocytes. |
| 4175 | 12850812 | The early response was characterized by high levels of inflammatory molecules, including IL-1beta, IL-6, TNFalpha, RANTES, MIP-1alpha and MCP-1, later followed by expression of precursor Th1 cytokines, IL-12 and IL-18, concomitant with IFNgamma production. |
| 4176 | 12834622 | Costimulatory function of umbilical cord blood CD14+ and CD34+ derived dendritic cells. |
| 4177 | 12834622 | Dendritic cells (DCs) consist of a heterogeneous population of hematopoietic cells characterized by their unique dendritic morphology, their efficient antigen-presenting capability to activate naive CD4(+) and CD8(+) T cells, and their lack of lineage specific markers. |
| 4178 | 12834622 | CD14(+) monocytes and CD34(+) stem cells were isolated from human umbilical cord blood and were induced to differentiate into dendritic cells using 100 ng/mL granulocyte-macrophage colony stimulating factor (GM-CSF), 25 ng/mL IL-4, 2.5 ng/mL tumor necrosis factor-alpha (TNF-alpha), 100 ng/mL GM-CSF, 25 ng/mL stem cell factor, and 2.5 ng/mL TNF-alpha, respectively. |
| 4179 | 12834622 | Flow cytometric analysis revealed that the 14-day-old dendritic cells were CD80(+), CD86(+), CD83(+), CD54(+), CD1a(+), CD11b(+), CD11c(+), HLA-DR(+), CD34(-), CD3(-), CD19(-), CD14(-), and CD16(-). |
| 4180 | 12834622 | Reverse transcription polymerase chain reaction was employed to detect expression of mRNA for CD80 and CD86. |
| 4181 | 12834622 | Differentiating monocytes initially expressed CD86 while CD80 appeared on day 2. |
| 4182 | 12834622 | Differentiating stem cells expressed CD80 and CD86 on day 2 of culture. |
| 4183 | 12834622 | The surface expression of CD80 and CD86 was studied over the course of differentiation. |
| 4184 | 12834622 | Prior to the functional assay, CD14(+) and CD34(+) derived DCs were stimulated for 18 h with 0.1 mg/mL and 1.0 mg/mL E. coli lipopolyssacharide, respectively. |
| 4185 | 12834622 | Monoclonal antibodies (mabs) to CD80 and CD86 were employed to assess their costimulatory roles. |
| 4186 | 12834622 | A decrease of stimulation as depicted by decreased T cell activation was significant with mabs to both CD80 and CD86 on monocyte-derived DCs while only mabs to CD86 induced decreased T cell activation by stem cell-derived DCs. |
| 4187 | 12834622 | The varied functional role of CD80 and CD86 costimulatory molecules is associated with DC differentiation from distinct cord blood isolated hematopoietic lineages. |
| 4188 | 12823275 | Compared with H37Rv, infections with Beijng strains were characterized by extensive pneumonia, early but ephemeral tumour necrosis factor-alpha (TNF-alpha) and inducible isoform of nitric oxide synthetase (iNOS) expression, and significantly higher earlier mortality. |
| 4189 | 12823275 | Compared with H37Rv, infections with Beijng strains were characterized by extensive pneumonia, early but ephemeral tumour necrosis factor-alpha (TNF-alpha) and inducible isoform of nitric oxide synthetase (iNOS) expression, and significantly higher earlier mortality. |
| 4190 | 12823275 | Conversely, Canetti strains induced limited pneumonia, sustained TNF-alpha and iNOS expression in lungs, and almost 100% survival. |
| 4191 | 12823275 | Conversely, Canetti strains induced limited pneumonia, sustained TNF-alpha and iNOS expression in lungs, and almost 100% survival. |
| 4192 | 12810878 | This study shows that inactivated parapoxvirus ovis (Orf virus), strain D1701 (PPVO), induces an autoregulatory cytokine response that involves the upregulation of IL-12, IL-18, IFN-gamma and other T helper 1-type cytokines and their subsequent downregulation, which is accompanied by induction of IL-4. |
| 4193 | 12810878 | PPVO induces IL-12, TNF-alpha and, together with a suboptimal concentration of Concanavalin A, IFN-gamma in human peripheral blood leukocytes as well. |
| 4194 | 12803883 | Prostaglandins, interleukin-(IL-)10, and transforming growth factor-beta are other players of in vivo endotoxin tolerance. |
| 4195 | 12803883 | Cross-tolerance between LPS, TLR2 specific ligands, IL-1 and TNF has been regularly reported. |
| 4196 | 12794148 | Both lymphotoxin-alpha and TNF are crucial for control of Toxoplasma gondii in the central nervous system. |
| 4197 | 12794148 | Both lymphotoxin-alpha and TNF are crucial for control of Toxoplasma gondii in the central nervous system. |
| 4198 | 12794148 | Both lymphotoxin-alpha and TNF are crucial for control of Toxoplasma gondii in the central nervous system. |
| 4199 | 12794148 | Both lymphotoxin-alpha and TNF are crucial for control of Toxoplasma gondii in the central nervous system. |
| 4200 | 12794148 | Both lymphotoxin-alpha and TNF are crucial for control of Toxoplasma gondii in the central nervous system. |
| 4201 | 12794148 | Both lymphotoxin-alpha and TNF are crucial for control of Toxoplasma gondii in the central nervous system. |
| 4202 | 12794148 | Both lymphotoxin-alpha and TNF are crucial for control of Toxoplasma gondii in the central nervous system. |
| 4203 | 12794148 | Both lymphotoxin-alpha and TNF are crucial for control of Toxoplasma gondii in the central nervous system. |
| 4204 | 12794148 | Immunity to Toxoplasma gondii critically depends on TNFR type I-mediated immune reactions, but the precise role of the individual ligands of TNFR1, TNF and lymphotoxin-alpha (LTalpha), is still unknown. |
| 4205 | 12794148 | Immunity to Toxoplasma gondii critically depends on TNFR type I-mediated immune reactions, but the precise role of the individual ligands of TNFR1, TNF and lymphotoxin-alpha (LTalpha), is still unknown. |
| 4206 | 12794148 | Immunity to Toxoplasma gondii critically depends on TNFR type I-mediated immune reactions, but the precise role of the individual ligands of TNFR1, TNF and lymphotoxin-alpha (LTalpha), is still unknown. |
| 4207 | 12794148 | Immunity to Toxoplasma gondii critically depends on TNFR type I-mediated immune reactions, but the precise role of the individual ligands of TNFR1, TNF and lymphotoxin-alpha (LTalpha), is still unknown. |
| 4208 | 12794148 | Immunity to Toxoplasma gondii critically depends on TNFR type I-mediated immune reactions, but the precise role of the individual ligands of TNFR1, TNF and lymphotoxin-alpha (LTalpha), is still unknown. |
| 4209 | 12794148 | Immunity to Toxoplasma gondii critically depends on TNFR type I-mediated immune reactions, but the precise role of the individual ligands of TNFR1, TNF and lymphotoxin-alpha (LTalpha), is still unknown. |
| 4210 | 12794148 | Immunity to Toxoplasma gondii critically depends on TNFR type I-mediated immune reactions, but the precise role of the individual ligands of TNFR1, TNF and lymphotoxin-alpha (LTalpha), is still unknown. |
| 4211 | 12794148 | Immunity to Toxoplasma gondii critically depends on TNFR type I-mediated immune reactions, but the precise role of the individual ligands of TNFR1, TNF and lymphotoxin-alpha (LTalpha), is still unknown. |
| 4212 | 12794148 | Upon oral infection with T. gondii, TNF(-/-), LTalpha(-/-), and TNF/LTalpha(-/-) mice failed to control intracerebral T. gondii and succumbed to an acute necrotizing Toxoplasma encephalitis, whereas wild-type (WT) mice survived. |
| 4213 | 12794148 | Upon oral infection with T. gondii, TNF(-/-), LTalpha(-/-), and TNF/LTalpha(-/-) mice failed to control intracerebral T. gondii and succumbed to an acute necrotizing Toxoplasma encephalitis, whereas wild-type (WT) mice survived. |
| 4214 | 12794148 | Upon oral infection with T. gondii, TNF(-/-), LTalpha(-/-), and TNF/LTalpha(-/-) mice failed to control intracerebral T. gondii and succumbed to an acute necrotizing Toxoplasma encephalitis, whereas wild-type (WT) mice survived. |
| 4215 | 12794148 | Upon oral infection with T. gondii, TNF(-/-), LTalpha(-/-), and TNF/LTalpha(-/-) mice failed to control intracerebral T. gondii and succumbed to an acute necrotizing Toxoplasma encephalitis, whereas wild-type (WT) mice survived. |
| 4216 | 12794148 | Upon oral infection with T. gondii, TNF(-/-), LTalpha(-/-), and TNF/LTalpha(-/-) mice failed to control intracerebral T. gondii and succumbed to an acute necrotizing Toxoplasma encephalitis, whereas wild-type (WT) mice survived. |
| 4217 | 12794148 | Upon oral infection with T. gondii, TNF(-/-), LTalpha(-/-), and TNF/LTalpha(-/-) mice failed to control intracerebral T. gondii and succumbed to an acute necrotizing Toxoplasma encephalitis, whereas wild-type (WT) mice survived. |
| 4218 | 12794148 | Upon oral infection with T. gondii, TNF(-/-), LTalpha(-/-), and TNF/LTalpha(-/-) mice failed to control intracerebral T. gondii and succumbed to an acute necrotizing Toxoplasma encephalitis, whereas wild-type (WT) mice survived. |
| 4219 | 12794148 | Upon oral infection with T. gondii, TNF(-/-), LTalpha(-/-), and TNF/LTalpha(-/-) mice failed to control intracerebral T. gondii and succumbed to an acute necrotizing Toxoplasma encephalitis, whereas wild-type (WT) mice survived. |
| 4220 | 12794148 | Additionally, peritoneal macrophages produced reduced levels of NO upon infection with T. gondii and had significantly reduced toxoplasmastatic activity in TNF(-/-), LTalpha(-/-), and TNF/LTalpha(-/-) mice as compared with WT animals. |
| 4221 | 12794148 | Additionally, peritoneal macrophages produced reduced levels of NO upon infection with T. gondii and had significantly reduced toxoplasmastatic activity in TNF(-/-), LTalpha(-/-), and TNF/LTalpha(-/-) mice as compared with WT animals. |
| 4222 | 12794148 | Additionally, peritoneal macrophages produced reduced levels of NO upon infection with T. gondii and had significantly reduced toxoplasmastatic activity in TNF(-/-), LTalpha(-/-), and TNF/LTalpha(-/-) mice as compared with WT animals. |
| 4223 | 12794148 | Additionally, peritoneal macrophages produced reduced levels of NO upon infection with T. gondii and had significantly reduced toxoplasmastatic activity in TNF(-/-), LTalpha(-/-), and TNF/LTalpha(-/-) mice as compared with WT animals. |
| 4224 | 12794148 | Additionally, peritoneal macrophages produced reduced levels of NO upon infection with T. gondii and had significantly reduced toxoplasmastatic activity in TNF(-/-), LTalpha(-/-), and TNF/LTalpha(-/-) mice as compared with WT animals. |
| 4225 | 12794148 | Additionally, peritoneal macrophages produced reduced levels of NO upon infection with T. gondii and had significantly reduced toxoplasmastatic activity in TNF(-/-), LTalpha(-/-), and TNF/LTalpha(-/-) mice as compared with WT animals. |
| 4226 | 12794148 | Additionally, peritoneal macrophages produced reduced levels of NO upon infection with T. gondii and had significantly reduced toxoplasmastatic activity in TNF(-/-), LTalpha(-/-), and TNF/LTalpha(-/-) mice as compared with WT animals. |
| 4227 | 12794148 | Additionally, peritoneal macrophages produced reduced levels of NO upon infection with T. gondii and had significantly reduced toxoplasmastatic activity in TNF(-/-), LTalpha(-/-), and TNF/LTalpha(-/-) mice as compared with WT animals. |
| 4228 | 12794148 | Frequencies of parasite-specific IFN-gamma-producing T cells, intracerebral and splenic IFN-gamma production, and T. gondii-specific IgM and IgG titers in LTalpha(-/-) and TNF/LTalpha(-/-) mice were reduced only early after infection. |
| 4229 | 12794148 | Frequencies of parasite-specific IFN-gamma-producing T cells, intracerebral and splenic IFN-gamma production, and T. gondii-specific IgM and IgG titers in LTalpha(-/-) and TNF/LTalpha(-/-) mice were reduced only early after infection. |
| 4230 | 12794148 | Frequencies of parasite-specific IFN-gamma-producing T cells, intracerebral and splenic IFN-gamma production, and T. gondii-specific IgM and IgG titers in LTalpha(-/-) and TNF/LTalpha(-/-) mice were reduced only early after infection. |
| 4231 | 12794148 | Frequencies of parasite-specific IFN-gamma-producing T cells, intracerebral and splenic IFN-gamma production, and T. gondii-specific IgM and IgG titers in LTalpha(-/-) and TNF/LTalpha(-/-) mice were reduced only early after infection. |
| 4232 | 12794148 | Frequencies of parasite-specific IFN-gamma-producing T cells, intracerebral and splenic IFN-gamma production, and T. gondii-specific IgM and IgG titers in LTalpha(-/-) and TNF/LTalpha(-/-) mice were reduced only early after infection. |
| 4233 | 12794148 | Frequencies of parasite-specific IFN-gamma-producing T cells, intracerebral and splenic IFN-gamma production, and T. gondii-specific IgM and IgG titers in LTalpha(-/-) and TNF/LTalpha(-/-) mice were reduced only early after infection. |
| 4234 | 12794148 | Frequencies of parasite-specific IFN-gamma-producing T cells, intracerebral and splenic IFN-gamma production, and T. gondii-specific IgM and IgG titers in LTalpha(-/-) and TNF/LTalpha(-/-) mice were reduced only early after infection. |
| 4235 | 12794148 | Frequencies of parasite-specific IFN-gamma-producing T cells, intracerebral and splenic IFN-gamma production, and T. gondii-specific IgM and IgG titers in LTalpha(-/-) and TNF/LTalpha(-/-) mice were reduced only early after infection. |
| 4236 | 12794148 | In contrast, intracerebral IL-10 and IL-12p40 mRNA expression and splenic IL-2, IL-4, and IL-12 production were identical in all genotypes. |
| 4237 | 12794148 | In contrast, intracerebral IL-10 and IL-12p40 mRNA expression and splenic IL-2, IL-4, and IL-12 production were identical in all genotypes. |
| 4238 | 12794148 | In contrast, intracerebral IL-10 and IL-12p40 mRNA expression and splenic IL-2, IL-4, and IL-12 production were identical in all genotypes. |
| 4239 | 12794148 | In contrast, intracerebral IL-10 and IL-12p40 mRNA expression and splenic IL-2, IL-4, and IL-12 production were identical in all genotypes. |
| 4240 | 12794148 | In contrast, intracerebral IL-10 and IL-12p40 mRNA expression and splenic IL-2, IL-4, and IL-12 production were identical in all genotypes. |
| 4241 | 12794148 | In contrast, intracerebral IL-10 and IL-12p40 mRNA expression and splenic IL-2, IL-4, and IL-12 production were identical in all genotypes. |
| 4242 | 12794148 | In contrast, intracerebral IL-10 and IL-12p40 mRNA expression and splenic IL-2, IL-4, and IL-12 production were identical in all genotypes. |
| 4243 | 12794148 | In contrast, intracerebral IL-10 and IL-12p40 mRNA expression and splenic IL-2, IL-4, and IL-12 production were identical in all genotypes. |
| 4244 | 12794148 | In addition, TNF(-/-), LTalpha(-/-), and TNF/LTalpha(-/-), but not WT, mice succumbed to infection with the highly attenuated ts-4 strain of T. gondii or to a subsequent challenge infection with virulent RH toxoplasms, although they had identical frequencies of IFN-gamma-producing T cells as compared with WT mice. |
| 4245 | 12794148 | In addition, TNF(-/-), LTalpha(-/-), and TNF/LTalpha(-/-), but not WT, mice succumbed to infection with the highly attenuated ts-4 strain of T. gondii or to a subsequent challenge infection with virulent RH toxoplasms, although they had identical frequencies of IFN-gamma-producing T cells as compared with WT mice. |
| 4246 | 12794148 | In addition, TNF(-/-), LTalpha(-/-), and TNF/LTalpha(-/-), but not WT, mice succumbed to infection with the highly attenuated ts-4 strain of T. gondii or to a subsequent challenge infection with virulent RH toxoplasms, although they had identical frequencies of IFN-gamma-producing T cells as compared with WT mice. |
| 4247 | 12794148 | In addition, TNF(-/-), LTalpha(-/-), and TNF/LTalpha(-/-), but not WT, mice succumbed to infection with the highly attenuated ts-4 strain of T. gondii or to a subsequent challenge infection with virulent RH toxoplasms, although they had identical frequencies of IFN-gamma-producing T cells as compared with WT mice. |
| 4248 | 12794148 | In addition, TNF(-/-), LTalpha(-/-), and TNF/LTalpha(-/-), but not WT, mice succumbed to infection with the highly attenuated ts-4 strain of T. gondii or to a subsequent challenge infection with virulent RH toxoplasms, although they had identical frequencies of IFN-gamma-producing T cells as compared with WT mice. |
| 4249 | 12794148 | In addition, TNF(-/-), LTalpha(-/-), and TNF/LTalpha(-/-), but not WT, mice succumbed to infection with the highly attenuated ts-4 strain of T. gondii or to a subsequent challenge infection with virulent RH toxoplasms, although they had identical frequencies of IFN-gamma-producing T cells as compared with WT mice. |
| 4250 | 12794148 | In addition, TNF(-/-), LTalpha(-/-), and TNF/LTalpha(-/-), but not WT, mice succumbed to infection with the highly attenuated ts-4 strain of T. gondii or to a subsequent challenge infection with virulent RH toxoplasms, although they had identical frequencies of IFN-gamma-producing T cells as compared with WT mice. |
| 4251 | 12794148 | In addition, TNF(-/-), LTalpha(-/-), and TNF/LTalpha(-/-), but not WT, mice succumbed to infection with the highly attenuated ts-4 strain of T. gondii or to a subsequent challenge infection with virulent RH toxoplasms, although they had identical frequencies of IFN-gamma-producing T cells as compared with WT mice. |
| 4252 | 12794148 | Generation and infection of bone marrow reconstitution chimeras demonstrated an exclusive role of hematogeneously produced TNF and LTalpha for survival of toxoplasmosis. |
| 4253 | 12794148 | Generation and infection of bone marrow reconstitution chimeras demonstrated an exclusive role of hematogeneously produced TNF and LTalpha for survival of toxoplasmosis. |
| 4254 | 12794148 | Generation and infection of bone marrow reconstitution chimeras demonstrated an exclusive role of hematogeneously produced TNF and LTalpha for survival of toxoplasmosis. |
| 4255 | 12794148 | Generation and infection of bone marrow reconstitution chimeras demonstrated an exclusive role of hematogeneously produced TNF and LTalpha for survival of toxoplasmosis. |
| 4256 | 12794148 | Generation and infection of bone marrow reconstitution chimeras demonstrated an exclusive role of hematogeneously produced TNF and LTalpha for survival of toxoplasmosis. |
| 4257 | 12794148 | Generation and infection of bone marrow reconstitution chimeras demonstrated an exclusive role of hematogeneously produced TNF and LTalpha for survival of toxoplasmosis. |
| 4258 | 12794148 | Generation and infection of bone marrow reconstitution chimeras demonstrated an exclusive role of hematogeneously produced TNF and LTalpha for survival of toxoplasmosis. |
| 4259 | 12794148 | Generation and infection of bone marrow reconstitution chimeras demonstrated an exclusive role of hematogeneously produced TNF and LTalpha for survival of toxoplasmosis. |
| 4260 | 12794148 | These findings demonstrate the crucial role of both LTalpha and TNF for control of intracerebral toxoplasms. |
| 4261 | 12794148 | These findings demonstrate the crucial role of both LTalpha and TNF for control of intracerebral toxoplasms. |
| 4262 | 12794148 | These findings demonstrate the crucial role of both LTalpha and TNF for control of intracerebral toxoplasms. |
| 4263 | 12794148 | These findings demonstrate the crucial role of both LTalpha and TNF for control of intracerebral toxoplasms. |
| 4264 | 12794148 | These findings demonstrate the crucial role of both LTalpha and TNF for control of intracerebral toxoplasms. |
| 4265 | 12794148 | These findings demonstrate the crucial role of both LTalpha and TNF for control of intracerebral toxoplasms. |
| 4266 | 12794148 | These findings demonstrate the crucial role of both LTalpha and TNF for control of intracerebral toxoplasms. |
| 4267 | 12794148 | These findings demonstrate the crucial role of both LTalpha and TNF for control of intracerebral toxoplasms. |
| 4268 | 12782709 | Vaccine immunity to pathogenic fungi overcomes the requirement for CD4 help in exogenous antigen presentation to CD8+ T cells: implications for vaccine development in immune-deficient hosts. |
| 4269 | 12782709 | In the absence of T helper cells, exogenous fungal antigens activated memory CD8+ cells in a major histocompatibility complex class I-restricted manner and CD8+ T cell-derived cytokines tumor necrosis factor alpha, interferon gamma, and granulocyte/macrophage colony-stimulating factor-mediated durable vaccine immunity. |
| 4270 | 12763682 | Long pentraxins consist of a C-terminal pentraxin domain, which has sequence similarity to C-reactive protein (CRP) and serum amyloid P (SAP) component (the classic short pentraxins), and of an unrelated N-terminal portion. |
| 4271 | 12763682 | PTX3 is made by diverse cell types, most prominently endothelial cells, macrophages and dendritic cells, in response to primary inflammatory signals (e.g. interleukin-1 (IL-1), tumour necrosis factor (TNF), lipopolysaccharide (LPS)). |
| 4272 | 12763679 | There are over 300,000 patients worldwide being treated with agents that specifically block the biological activities of interleukin-1 (IL-1) or tumor necrosis factor (TNF) for reducing the severity of autoimmune diseases such as rheumatoid arthritis, Crohn's disease or psoriasis. |
| 4273 | 12763679 | There are over 300,000 patients worldwide being treated with agents that specifically block the biological activities of interleukin-1 (IL-1) or tumor necrosis factor (TNF) for reducing the severity of autoimmune diseases such as rheumatoid arthritis, Crohn's disease or psoriasis. |
| 4274 | 12763679 | There are over 300,000 patients worldwide being treated with agents that specifically block the biological activities of interleukin-1 (IL-1) or tumor necrosis factor (TNF) for reducing the severity of autoimmune diseases such as rheumatoid arthritis, Crohn's disease or psoriasis. |
| 4275 | 12763679 | Those patients receiving anti-TNF-alpha or IL-1 blocking therapies are treated on a chronic basis. |
| 4276 | 12763679 | Those patients receiving anti-TNF-alpha or IL-1 blocking therapies are treated on a chronic basis. |
| 4277 | 12763679 | Those patients receiving anti-TNF-alpha or IL-1 blocking therapies are treated on a chronic basis. |
| 4278 | 12763679 | Blockade of IL-1 activity with the IL-1 receptor antagonist (IL-1Ra) appears, at present, to be relatively safe. |
| 4279 | 12763679 | Blockade of IL-1 activity with the IL-1 receptor antagonist (IL-1Ra) appears, at present, to be relatively safe. |
| 4280 | 12763679 | Blockade of IL-1 activity with the IL-1 receptor antagonist (IL-1Ra) appears, at present, to be relatively safe. |
| 4281 | 12763679 | From a wealth of rodent studies using live infection models, the following conclusions can be drawn: (1) neutralization or gene deletion for TNF-alpha is frequently associated with reduction of host defense in models of live Gram-positive or Gram-negative infections as well as infection by intracellular microbes such as Salmonella and Listeria; (2) absence of the IL-1 receptor can also result in decreased resistance to Listeria or Gram-positive bacteria and (3) TNF-alpha and IFN-gamma are required for defense against infection caused by Mycobacterium tuberculosis. |
| 4282 | 12763679 | From a wealth of rodent studies using live infection models, the following conclusions can be drawn: (1) neutralization or gene deletion for TNF-alpha is frequently associated with reduction of host defense in models of live Gram-positive or Gram-negative infections as well as infection by intracellular microbes such as Salmonella and Listeria; (2) absence of the IL-1 receptor can also result in decreased resistance to Listeria or Gram-positive bacteria and (3) TNF-alpha and IFN-gamma are required for defense against infection caused by Mycobacterium tuberculosis. |
| 4283 | 12763679 | From a wealth of rodent studies using live infection models, the following conclusions can be drawn: (1) neutralization or gene deletion for TNF-alpha is frequently associated with reduction of host defense in models of live Gram-positive or Gram-negative infections as well as infection by intracellular microbes such as Salmonella and Listeria; (2) absence of the IL-1 receptor can also result in decreased resistance to Listeria or Gram-positive bacteria and (3) TNF-alpha and IFN-gamma are required for defense against infection caused by Mycobacterium tuberculosis. |
| 4284 | 12737995 | Murine bone marrow macrophages treated in vitro with F. novicida LPS produced IL12 and TNF-alpha, but did not produce detectable interferon-gamma, IL10, or nitric oxide; in contrast, murine macrophages treated with F. tularensis LVS LPS produced none of these mediators. |
| 4285 | 12737995 | Murine bone marrow macrophages treated in vitro with F. novicida LPS produced IL12 and TNF-alpha, but did not produce detectable interferon-gamma, IL10, or nitric oxide; in contrast, murine macrophages treated with F. tularensis LVS LPS produced none of these mediators. |
| 4286 | 12737995 | Thus, although LPS recognition may not be a major factor in engendering protection, the ability of F. novicida LPS to stimulate the production of proinflammatory cytokines including TNF-alpha likely contributes to the increased virulence for mice of F. novicida compared to F. tularensis LVS. |
| 4287 | 12737995 | Thus, although LPS recognition may not be a major factor in engendering protection, the ability of F. novicida LPS to stimulate the production of proinflammatory cytokines including TNF-alpha likely contributes to the increased virulence for mice of F. novicida compared to F. tularensis LVS. |
| 4288 | 12733599 | We report here the standardized conditions for stimulation of macaque whole blood samples with various protein or peptide antigens, and production of significant intracellular levels of interferon gamma (IFN-gamma) and tumor necrosis factor alpha (TNF-alpha) in CD4+ as well as CD8+ T lymphocytes. |
| 4289 | 12733599 | We report here the standardized conditions for stimulation of macaque whole blood samples with various protein or peptide antigens, and production of significant intracellular levels of interferon gamma (IFN-gamma) and tumor necrosis factor alpha (TNF-alpha) in CD4+ as well as CD8+ T lymphocytes. |
| 4290 | 12733599 | We report here the standardized conditions for stimulation of macaque whole blood samples with various protein or peptide antigens, and production of significant intracellular levels of interferon gamma (IFN-gamma) and tumor necrosis factor alpha (TNF-alpha) in CD4+ as well as CD8+ T lymphocytes. |
| 4291 | 12733599 | We observed significantly higher levels of TNF-alpha compared with IFN-gamma in both CD4+ and CD8+ T lymphocytes from all the macaque whole blood samples stimulated with staphylococcal enterotoxin B (SEB) as an antigen. |
| 4292 | 12733599 | We observed significantly higher levels of TNF-alpha compared with IFN-gamma in both CD4+ and CD8+ T lymphocytes from all the macaque whole blood samples stimulated with staphylococcal enterotoxin B (SEB) as an antigen. |
| 4293 | 12733599 | We observed significantly higher levels of TNF-alpha compared with IFN-gamma in both CD4+ and CD8+ T lymphocytes from all the macaque whole blood samples stimulated with staphylococcal enterotoxin B (SEB) as an antigen. |
| 4294 | 12733599 | Similarly, when whole blood samples from rhesus macaques immunized with an HIV envelope peptide cocktail vaccine were stimulated with either the peptide cocktail or recombinant gp160, we observed production of significant levels of TNF-alpha by both CD4+ and CD8+ T lymphocytes. |
| 4295 | 12733599 | Similarly, when whole blood samples from rhesus macaques immunized with an HIV envelope peptide cocktail vaccine were stimulated with either the peptide cocktail or recombinant gp160, we observed production of significant levels of TNF-alpha by both CD4+ and CD8+ T lymphocytes. |
| 4296 | 12733599 | Similarly, when whole blood samples from rhesus macaques immunized with an HIV envelope peptide cocktail vaccine were stimulated with either the peptide cocktail or recombinant gp160, we observed production of significant levels of TNF-alpha by both CD4+ and CD8+ T lymphocytes. |
| 4297 | 12719704 | Serum levels of IL-6, IL-10, tumor necrosis factor-alpha, and interferon-gamma increased within 6 hours of viral infusion, suggesting immune activation. |
| 4298 | 12706680 | This effect was due to activation of MHC class I-restricted CD8(+) T cells coupled with an increased secretion of proinflammatory cytokines IFN-gamma, TNF-alpha and IL-2. |
| 4299 | 12706680 | Also, specific activation of dendritic cells was indicated by a two-three-fold upregulation of their costimulatory CD80 and MHC class II molecules. |
| 4300 | 12706410 | Interestingly, there was a negative correlation between binding intensity and CD83 expression in DCs, suggesting that the main receptor for binding of VLPs may be downregulated during maturation. |
| 4301 | 12706410 | For each cell type, the patterns of interleukin-1beta, interleukin-12, tumor necrosis factor-alpha, and interleukin-6 production were distinct from the pattern induced by lipopolysaccharide (LPS), a bacterial activator of myeloid antigen-presenting cells. |
| 4302 | 12699364 | Cytokine and chemokine combinations can potentially help target antigen to the appropriate antigen presenting cell and initiate maturation of these presenting cells, attract cells expressing different chemokine receptors, steer cellular immune responses toward Th1 and CD8 CTL, and enhance systemic and mucosal IgG and secretory IgA antibodies and determine their isotype balance. |
| 4303 | 12699364 | For example, GM-CSF has been shown to be synergistic with IL-12 or CD40 ligand for induction of CTL and for antiviral protection, and the triple combination of GM-CSF, IL-12, and TNF alpha appears to induce the most effective protection in some mouse models. |
| 4304 | 12686724 | Among those signaling pathways, activation of NF-kappaB leads to up-regulation of IL-1beta, IL-8 and TNF-alpha, mucin MUC2 and Toll-like receptor 2 (TLR2), whereas activation of p38 MAP kinase mediates not only up-regulation of inflammatory mediators and mucin MUC5AC but also down-regulation of TLR2. |
| 4305 | 12686724 | Interestingly, NTHi-induced activation of the PI3K-Akt pathway, however, leads to inhibition of p38 mitogen-activated protein (MAP) kinase. |
| 4306 | 12686724 | Moreover, the TGF-beta-Smad signaling pathway cooperates with NF-kappaB to mediate up-regulation of mucin MUC2. |
| 4307 | 12686724 | Finally, glucocorticoids synergistically enhance NTHi-induced TLR2 expression via specific up-regulation of the MAP kinase phosphatase-1 that, in turn, leads to inactivation of p38 MAP kinase, the negative regulator for TLR2 expression. |
| 4308 | 12683420 | Rotavirus-specific subclass antibody responses and cytokines, tumour necrosis factor-alpha (TNF-alpha), interferon-gamma (IFN-gamma), interleukin-8 (IL-8), and IL-10, were measured in children 7-24 months of age with rotavirus diarrhoea (n = 29); the responses were compared with children with watery diarrhoea from whom no enteric pathogens were isolated (controls; n = 11). |
| 4309 | 12683420 | The numbers of children with rotavirus-specific IgA and IgA1 responses in stool were similar in the two groups of children. |
| 4310 | 12683420 | In the plasma, more children with rotavirus diarrhoea had rotavirus-specific IgA, IgA1, IgG, IgG1, and IgG3 responses than did control children (P = 0.049, 0.007, 0.001, 0.002, and 0.012, respectively). |
| 4311 | 12683337 | The single deletion of IFN-gamma or TNF alpha resulted in a severe lesion of multiple necrosis without granuloma, and cytokine mRNA level other than knocked out cytokine was normal, suggesting that IFN-gamma and TNF alpha are principally important cytokines. |
| 4312 | 12683337 | The single deletion of IFN-gamma or TNF alpha resulted in a severe lesion of multiple necrosis without granuloma, and cytokine mRNA level other than knocked out cytokine was normal, suggesting that IFN-gamma and TNF alpha are principally important cytokines. |
| 4313 | 12683337 | In knockout mice for IL-12 or IL-18, necrotic lesion was not induced after infection and the pathological change was not so significant as in IFN-gamma/TNF alpha knockout mice. |
| 4314 | 12683337 | In knockout mice for IL-12 or IL-18, necrotic lesion was not induced after infection and the pathological change was not so significant as in IFN-gamma/TNF alpha knockout mice. |
| 4315 | 12683337 | By using IL-12, IL-18 knockout mice or double knockout mice, it was shown that IL-12 exhibits more important role than IL-18 in the protection. |
| 4316 | 12683337 | By using IL-12, IL-18 knockout mice or double knockout mice, it was shown that IL-12 exhibits more important role than IL-18 in the protection. |
| 4317 | 12683337 | In most of the clinical cases of tuberculosis, the production of IL-12, IL-18 and IFN-gamma is increased, however, the group of relatively lower cytokine production did not respond well to the treatment. |
| 4318 | 12683337 | In most of the clinical cases of tuberculosis, the production of IL-12, IL-18 and IFN-gamma is increased, however, the group of relatively lower cytokine production did not respond well to the treatment. |
| 4319 | 12683337 | As immunizing antigens, a-Ag, ESAT-6, HSP65, 38kD-lipoprotein and so on have been employed. |
| 4320 | 12683337 | As immunizing antigens, a-Ag, ESAT-6, HSP65, 38kD-lipoprotein and so on have been employed. |
| 4321 | 12672905 | We showed that BCG could promote cord blood monocyte-derived DC maturation by up-regulation of CD80, CD83, CD86, CD40, and MHC class II molecules and down-regulation of mannose receptor. |
| 4322 | 12672905 | BCG was able to induce similar levels of tumor necrosis factor-alpha and IL-10 but no bioactive IL-12p70 production from cord blood DCs as from adult blood DCs. |
| 4323 | 12672905 | Both non-BCG-treated and BCG-treated cord blood DCs efficiently induced a high level of IL-10, medium level of interferon-gamma, but little IL-4 production by cord blood naïve CD4+ T cells. |
| 4324 | 12672905 | Heat shock protein 65, a key component of BCG, had no effect on cord blood DC maturation in terms of CD86, MHC class II, and mannose receptor up-regulation. |
| 4325 | 12668155 | Functional abolishment of any one of these cytokines (IL-2, IL-6, IL-12, IL-18, GMCSF, TNF-alpha, or IFN-alpha, except IL-10) by neutralizing antibodies leads to reduced IFN-gamma production (19-82% inhibition in mouse and 44-77% inhibition in human systems, respectively). |
| 4326 | 12668155 | Functional abolishment of any one of these cytokines (IL-2, IL-6, IL-12, IL-18, GMCSF, TNF-alpha, or IFN-alpha, except IL-10) by neutralizing antibodies leads to reduced IFN-gamma production (19-82% inhibition in mouse and 44-77% inhibition in human systems, respectively). |
| 4327 | 12668155 | In mice cytokines IL-2, IL-12, IL-18, and GMCSF are observed to synergize with BCG for IFN-gamma production, whereas in human cytokines IL-2, IL-12, TNF-alpha, and IFN-alpha exhibit similar synergistic effects. |
| 4328 | 12668155 | In mice cytokines IL-2, IL-12, IL-18, and GMCSF are observed to synergize with BCG for IFN-gamma production, whereas in human cytokines IL-2, IL-12, TNF-alpha, and IFN-alpha exhibit similar synergistic effects. |
| 4329 | 12668155 | Rational combinations of these Th1-stimulating cytokines (IL-12 plus IL-18 in mice and IL-2 plus IL-12 in humans, respectively) dramatically up-regulate IFN-gamma production that is incomparably superior to BCG for induction of this cytokine. |
| 4330 | 12668155 | Rational combinations of these Th1-stimulating cytokines (IL-12 plus IL-18 in mice and IL-2 plus IL-12 in humans, respectively) dramatically up-regulate IFN-gamma production that is incomparably superior to BCG for induction of this cytokine. |
| 4331 | 12663797 | Production of interleukin 2 and the ability to lyse target cells in vitro were the first functions compromised, followed by the ability to make tumor necrosis factor alpha, while gamma interferon production was most resistant to functional exhaustion. |
| 4332 | 12654790 | Increases in tumor necrosis factor alpha, interleukin-6, transforming growth factor beta, and vascular endothelial growth factor mRNA expression were associated with the enhancement of intracellular BCG growth. |
| 4333 | 12654790 | Increases in gamma interferon, FAS, FAS ligand, perforin, granzyme, and granulysin mRNA expression were associated with intracellular BCG inhibition. |
| 4334 | 12639819 | OM-197 upregulated the expression of HLA-DR, CD80, CD86, CD83, CD40 and CD54 at the surface of myeloid DC naturally present in blood as well as of DC generated in vitro from monocytes using IL-4 and GM-CSF. |
| 4335 | 12639819 | OM-197 also induced the release of IL-12 and TNF-alpha from DC. |
| 4336 | 12639819 | Finally, DC incubated with OM-197 after pulsing with hepatitis B surface antigen (HBs Ag) induced in vitro expansion of IFN-gamma-secreting HBs Ag-specific CD4(+) T lymphocytes from naive individuals. |
| 4337 | 12626603 | For all volunteers, single nucleotide polymorphisms were determined for the following UV response-related cytokines: IL-1 receptor antagonist (+2018), IL-1 alpha (+4845), IL-1 beta (+3953), TNF-alpha (-308), and TNF-alpha (-238). |
| 4338 | 12626542 | Members of the TNF ligand superfamily and the TNFR superfamily contribute to this costimulatory molecule signaling. |
| 4339 | 12626542 | Coexpression of 4-1BBL in these E7-expressing DCs increased effector and memory CTL responses when they were used for immunization. 4-1BBL expression up-regulated CD80 and CD86 second signaling molecules in DCs. |
| 4340 | 12626542 | We also report an additive effect of 4-1BBL and receptor activator of NF-kappa B/receptor activator of NF-kappa B ligand coexpression in E7-transduced DC immunogens on E7-directed effector and memory CTL responses and on MHC class II and CD80/86 expression in DCs. |
| 4341 | 12594570 | The purpose of this work was to optimize the ex-vivo production of functional TAA-loaded DC that would produce interleukin-2 (IL-12) and enhance the T cell response. |
| 4342 | 12594570 | The purpose of this work was to optimize the ex-vivo production of functional TAA-loaded DC that would produce interleukin-2 (IL-12) and enhance the T cell response. |
| 4343 | 12594570 | We generated ex-vivo DC from human monocytes with granulocyte macrophage-colony stimulating factor (GM-CSF) and IL-4, and whole necrotic tumor cells (cell lysates) of cancer cell lines were used as model TAA. |
| 4344 | 12594570 | We generated ex-vivo DC from human monocytes with granulocyte macrophage-colony stimulating factor (GM-CSF) and IL-4, and whole necrotic tumor cells (cell lysates) of cancer cell lines were used as model TAA. |
| 4345 | 12594570 | TNF-alpha matured DC phenotypically, but additional interferon-gamma (IFN-gamma) treatment was necessary to achieve functional maturation, the production of significant amounts of IL-12. |
| 4346 | 12594570 | TNF-alpha matured DC phenotypically, but additional interferon-gamma (IFN-gamma) treatment was necessary to achieve functional maturation, the production of significant amounts of IL-12. |
| 4347 | 12594570 | Our results suggest that after allowing 4 h of tumor lysate uptake by immature DC, further treatment with TNF-alpha and IFN-gamma for 24 h provides the optimal conditions to obtain functional TAA-loaded DC. |
| 4348 | 12594570 | Our results suggest that after allowing 4 h of tumor lysate uptake by immature DC, further treatment with TNF-alpha and IFN-gamma for 24 h provides the optimal conditions to obtain functional TAA-loaded DC. |
| 4349 | 12594331 | We generated CD4(+) T cell lines to fractions of native antigens from the blood stages of the rodent parasite, Plasmodium yoelii, and identified fraction-specific T cells that had a Th1 phenotype (producing IL-2, IFN-gamma, and tumor necrosis factor-alpha, but not IL-4, after antigenic stimulation). |
| 4350 | 12594271 | Immediate early effector functions of virus-specific CD8+CCR7+ memory cells in humans defined by HLA and CC chemokine ligand 19 tetramers. |
| 4351 | 12594271 | To identify CCR7(+) cells, we engineered a fluorescent ligand for CCR7; results with the new CC chemokine ligand 19 chemotetramer were verified by staining with a CCR7 mAb. |
| 4352 | 12594271 | Staining with the CC chemokine ligand 19 chemotetramer reveals two subsets within CCR7(+) cells: a CCR7(int) population containing memory cells and a CCR7(high) population containing naive T cells. |
| 4353 | 12594271 | Phenotypic analysis of MHC class I/peptide tetramer-positive cells revealed that HLA-A2-restricted CMV-specific CD8 T cells exhibit the lowest percentage of CCR7(+) cells (0.5-5%), while HLA-A2-restricted flu- and HLA-B8-restricted EBV-specific CD8 T cells showed the highest (45-70%). |
| 4354 | 12594271 | Intracellular staining of unstimulated cells revealed that both CCR7(int)- and CCR7(-)-specific CD8 T cells exhibit a detectable level of perforin. |
| 4355 | 12594271 | Both CCR7(int) and CCR7(-) Ag-specific CD8(+) T cells produced IFN-gamma and TNF-alpha following short-term peptide stimulation. |
| 4356 | 12594271 | Therefore, our finding that CCR7(+)CD8(+) T cells are able to exert immediate effector functions requires a substantial revision to the central and effector memory hypothesis. |
| 4357 | 12594246 | In this study, we show that human plasmacytoid DC, activated by either CpG oligodeoxynucleotides or viral infection, also respond to histamine through H2 receptors, leading to a marked down-regulation of IFN-alpha and TNF-alpha and a moderate switch in their capacity to polarize naive T cells. |
| 4358 | 12590704 | 4-1BB ligand stimulation enhances myeloid dendritic cell maturation from human umbilical cord blood CD34+ progenitor cells. |
| 4359 | 12590704 | We investigated whether 4-1BB ligand (4-1BBL), a member of the tumor necrosis factor (TNF) family, is involved in the maturation process to mature myeloid DCs during in vitro DC differentiation from immature DCs derived from human umbilical cord blood (CB) CD34(+) progenitor cells. |
| 4360 | 12590704 | Enhanced levels of CD11c as well as immunostimulatory molecules such as CD86, MHC class II, and 4-1BBL were induced in response to 4-1BBL stimulation. |
| 4361 | 12590704 | Stimulation of 4-1BBL on DCs with 4-1BB-Fc or with 4-1BB-transfected Jurkat cells resulted in acquisition of capacity for the immature DCs to produce interleukin-12 (IL-12). |
| 4362 | 12574370 | TNF plays an essential role in tumor regression after adoptive transfer of perforin/IFN-gamma double knockout effector T cells. |
| 4363 | 12574370 | TNF plays an essential role in tumor regression after adoptive transfer of perforin/IFN-gamma double knockout effector T cells. |
| 4364 | 12574370 | TNF plays an essential role in tumor regression after adoptive transfer of perforin/IFN-gamma double knockout effector T cells. |
| 4365 | 12574370 | Blocking TNF in vivo by administering soluble TNFR II fusion protein (TNFRII:Fc) significantly reduced the therapeutic efficacy of PKO/GKO, but not wild-type T(E). |
| 4366 | 12574370 | Blocking TNF in vivo by administering soluble TNFR II fusion protein (TNFRII:Fc) significantly reduced the therapeutic efficacy of PKO/GKO, but not wild-type T(E). |
| 4367 | 12574370 | Blocking TNF in vivo by administering soluble TNFR II fusion protein (TNFRII:Fc) significantly reduced the therapeutic efficacy of PKO/GKO, but not wild-type T(E). |
| 4368 | 12574370 | This study identifies perforin, IFN-gamma, and TNF as a critical triad of effector molecules that characterize therapeutic antitumor T cells. |
| 4369 | 12574370 | This study identifies perforin, IFN-gamma, and TNF as a critical triad of effector molecules that characterize therapeutic antitumor T cells. |
| 4370 | 12574370 | This study identifies perforin, IFN-gamma, and TNF as a critical triad of effector molecules that characterize therapeutic antitumor T cells. |
| 4371 | 12574345 | We failed to detect any effects on ex vivo MOG-peptide-induced IFN-gamma, TNF-alpha, IL-6, IL-4, IL-10, and brain-derived neurotropic factor expression in splenocytes or CNS-derived lymphocytes. |
| 4372 | 12574345 | In CNS-derived lymphocytes, Fas ligand expression was down-regulated in DNA-vaccinated rats compared with controls. |
| 4373 | 12562379 | IFN-gamma and TNF-alpha, the two major cytokines associated with DTH, were efficiently induced by BCG. |
| 4374 | 12562379 | Constitutive levels of IL4 and IL5 were observed, but neither IL4 nor IL5 were modulated by BCG. |
| 4375 | 12562379 | Production of Th1 (T helper type 1) cytokines (IFN-gamma, IL2 and IL12) preceded that of the Th2 (T helper type 2) cytokine IL10. |
| 4376 | 12562379 | A tendency toward higher ratios of IFN-gamma versus IL10 for BCG responders also was observed. |
| 4377 | 12562326 | Our data shows that transfection of DCs with recombinant adenovirus AdV-TNF-alpha resulted in greater maturation of the DCs than occurred with control DCs cultured in exogenous TNF-alpha, as determined by up-regulated expression of pro-inflammatory cytokines (e.g. interleukins 1beta and 18), chemokines [e.g. interferon-gamma-inducible protein-10 and macrophage inflammatory protein-1beta (MIP-1beta)], the CC chemokine receptor CCR7, and immunologically important cell surface molecules (CD40, CD86 and intercellular adhesion molecule-1). |
| 4378 | 12562326 | Our data shows that transfection of DCs with recombinant adenovirus AdV-TNF-alpha resulted in greater maturation of the DCs than occurred with control DCs cultured in exogenous TNF-alpha, as determined by up-regulated expression of pro-inflammatory cytokines (e.g. interleukins 1beta and 18), chemokines [e.g. interferon-gamma-inducible protein-10 and macrophage inflammatory protein-1beta (MIP-1beta)], the CC chemokine receptor CCR7, and immunologically important cell surface molecules (CD40, CD86 and intercellular adhesion molecule-1). |
| 4379 | 12562326 | Our data also demonstrate that vaccination of mice with Mut1 peptide-pulsed, AdV-TNF-alpha-transfected DCs stimulated more efficient in vitro Mut1-specific CD8+ cytotoxic T-cell responses and solid tumour immunity in vivo, when compared to the in vitro TNF-alpha-cultivated DCs. |
| 4380 | 12562326 | Our data also demonstrate that vaccination of mice with Mut1 peptide-pulsed, AdV-TNF-alpha-transfected DCs stimulated more efficient in vitro Mut1-specific CD8+ cytotoxic T-cell responses and solid tumour immunity in vivo, when compared to the in vitro TNF-alpha-cultivated DCs. |
| 4381 | 12547597 | The cells were cultured in a serum-free medium with different cytokine combinations including GM-CSF, TNF-alpha, Flt-3, CD40L, IFN-gamma, IL-1alpha, IL-6, PGE1, and IL-4. |
| 4382 | 12542469 | Francisella tularensis inhibits Toll-like receptor-mediated activation of intracellular signalling and secretion of TNF-alpha and IL-1 from murine macrophages. |
| 4383 | 12542469 | Francisella tularensis inhibits Toll-like receptor-mediated activation of intracellular signalling and secretion of TNF-alpha and IL-1 from murine macrophages. |
| 4384 | 12542469 | Francisella tularensis inhibits Toll-like receptor-mediated activation of intracellular signalling and secretion of TNF-alpha and IL-1 from murine macrophages. |
| 4385 | 12542469 | Infection with the live vaccine strain F. tularensis LVS rendered cells of the murine macrophage-like cell line J774A.1 incapable of secreting TNF-alpha or IL-1beta and mobilizing an antimicrobial activity in response to bacterial lipopeptide or Escherichia coli-derived LPS. |
| 4386 | 12542469 | Infection with the live vaccine strain F. tularensis LVS rendered cells of the murine macrophage-like cell line J774A.1 incapable of secreting TNF-alpha or IL-1beta and mobilizing an antimicrobial activity in response to bacterial lipopeptide or Escherichia coli-derived LPS. |
| 4387 | 12542469 | Infection with the live vaccine strain F. tularensis LVS rendered cells of the murine macrophage-like cell line J774A.1 incapable of secreting TNF-alpha or IL-1beta and mobilizing an antimicrobial activity in response to bacterial lipopeptide or Escherichia coli-derived LPS. |
| 4388 | 12542469 | Also the LPS- or BLP-induced phosphorylation of the mitogen-activated protein kinase p38 and the transcription factor c-Jun was inhibited by F. tularensis LVS but not by the 23 kDa protein mutant. |
| 4389 | 12542469 | Also the LPS- or BLP-induced phosphorylation of the mitogen-activated protein kinase p38 and the transcription factor c-Jun was inhibited by F. tularensis LVS but not by the 23 kDa protein mutant. |
| 4390 | 12542469 | Also the LPS- or BLP-induced phosphorylation of the mitogen-activated protein kinase p38 and the transcription factor c-Jun was inhibited by F. tularensis LVS but not by the 23 kDa protein mutant. |
| 4391 | 12542469 | In conclusion, F. tularensis appears capable of abrogating the TNF-alpha and IL-1 responses of macrophages induced by E. coli LPS or BLP via a mechanism that involves suppression of several intracellular pathways and is dependent on expression of a bacterial 23 kDa protein. |
| 4392 | 12542469 | In conclusion, F. tularensis appears capable of abrogating the TNF-alpha and IL-1 responses of macrophages induced by E. coli LPS or BLP via a mechanism that involves suppression of several intracellular pathways and is dependent on expression of a bacterial 23 kDa protein. |
| 4393 | 12542469 | In conclusion, F. tularensis appears capable of abrogating the TNF-alpha and IL-1 responses of macrophages induced by E. coli LPS or BLP via a mechanism that involves suppression of several intracellular pathways and is dependent on expression of a bacterial 23 kDa protein. |
| 4394 | 12540573 | Vaccine-induced reduction of Helicobacter pylori colonization in mice is interleukin-12 dependent but gamma interferon and inducible nitric oxide synthase independent. |
| 4395 | 12540573 | Elevated levels of mRNA for interleukin-12p40 (IL-12p40), gamma interferon (IFN-gamma), tumor necrosis factor alpha, and inducible nitric oxide synthase (iNOS) were associated with protection in immunized-challenged (I/C) mice, but Th2 cytokine (IL-4, IL-5, IL-10, and IL-13) and chemokine (KC, MIP-2, and MCP-1) expression was not associated with protection. |
| 4396 | 12540573 | Despite the association of IFN-gamma and iNOS message with protection, I/C mice genetically lacking either of these products were able to reduce the bacterial load as well as the wild-type I/C controls. |
| 4397 | 12540573 | We conclude that neither IFN-gamma nor iNOS is essential for vaccine-induced protection from H. pylori infection. |
| 4398 | 12540573 | The p40 subunit of IL-12, which is a component of both IL-12 and IL-23, is necessary for protection in immunized mice. |
| 4399 | 12536236 | The ability of acute myeloid leukaemia (AML) cells to acquire dendritic cell (DC)-like characteristics in vitro with a rapid culture method based either on the phorbol ester PMA or calcium ionophores has been studied in comparison to conventional AML-DC cultures with the cytokines granulocyte-macrophage colony-stimulating factor (GM-CSF), tumour necrosis factor-alpha (TNF-alpha), interleukin-3 (IL-3), SCF, FLT3-L and IL-4. |
| 4400 | 12536236 | The most mature APC were generated by calcium ionophore A23187 plus IL-4, as evidenced by the higher expression of CD40, CD80, CD86 and HLA-DR. |
| 4401 | 12534946 | In addition, CpG DNA was found to activate epidermal Langerhans cells and stimulate the production of TNF-alpha and IL-12 cytokines by epidermal cells, explaining its strong adjuvant activity following epidermal powder immunization. |
| 4402 | 12532177 | Researchers also discussed the role of IL1 gene family and TNF gene polymorphisms in gastric pathology and various immune mechanisms involved in gastric cancer, such as down-regulation of NF kappa B, IL-1 and IL-1RA, cyclooxygenase signalling, and identification of MGAg antibodies. |
| 4403 | 12522051 | Fifteen human cytokines (interleukin 1alpha [IL-1alpha], IL-1beta, IL-2, IL-4, IL-5, IL-6, IL-8, IL-10, IL-12p70, IL-13, IL-15, IL-17, IL-18, gamma interferon, and tumor necrosis factor alpha) were validated with a panel of healthy individuals, rheumatoid arthritis patients, and juvenile idiopathic arthritis patients. |
| 4404 | 12522038 | Destructive arthritis in vaccinated interferon gamma-deficient mice challenged with Borrelia burgdorferi: modulation by tumor necrosis factor alpha. |
| 4405 | 12522038 | Destructive arthritis in vaccinated interferon gamma-deficient mice challenged with Borrelia burgdorferi: modulation by tumor necrosis factor alpha. |
| 4406 | 12522038 | Destructive arthritis in vaccinated interferon gamma-deficient mice challenged with Borrelia burgdorferi: modulation by tumor necrosis factor alpha. |
| 4407 | 12522038 | In contrast, treatment of B. burgdorferi-vaccinated, challenged IFN-gamma(0) mice with recombinant TNF-alpha (rTNF-alpha) inhibited the development of arthritis, including swelling of the hind paws. |
| 4408 | 12522038 | In contrast, treatment of B. burgdorferi-vaccinated, challenged IFN-gamma(0) mice with recombinant TNF-alpha (rTNF-alpha) inhibited the development of arthritis, including swelling of the hind paws. |
| 4409 | 12522038 | In contrast, treatment of B. burgdorferi-vaccinated, challenged IFN-gamma(0) mice with recombinant TNF-alpha (rTNF-alpha) inhibited the development of arthritis, including swelling of the hind paws. |
| 4410 | 12522038 | Moreover, treatment of vaccinated, challenged IFN-gamma(0) mice with anti-TNF-alpha inhibited fourfold the production of an antibody that kills B. burgdorferi, while treatment of vaccinated, challenged IFN-gamma(0) mice with rTNF-alpha slightly elevated the level of the borreliacidal antibody. |
| 4411 | 12522038 | Moreover, treatment of vaccinated, challenged IFN-gamma(0) mice with anti-TNF-alpha inhibited fourfold the production of an antibody that kills B. burgdorferi, while treatment of vaccinated, challenged IFN-gamma(0) mice with rTNF-alpha slightly elevated the level of the borreliacidal antibody. |
| 4412 | 12522038 | Moreover, treatment of vaccinated, challenged IFN-gamma(0) mice with anti-TNF-alpha inhibited fourfold the production of an antibody that kills B. burgdorferi, while treatment of vaccinated, challenged IFN-gamma(0) mice with rTNF-alpha slightly elevated the level of the borreliacidal antibody. |
| 4413 | 12519390 | The addition of TNF-alpha, polyriboinosinic polyribocytidylic acid (Poly(I:C)) and LPS to autologous DCs resulted in the emergence of only a small percentage of CD83+ DCs, IFN-alpha having no demonstrable effect. |
| 4414 | 12519390 | Only the addition of Poly(I:C) to DCs resulted in modestly increased specific cytotoxicity to B-CLL targets, IFN-alpha and LPS having no effect. |
| 4415 | 12513929 | Interferon-alpha (IFN-alpha), tumor necrosis factor (TNF-alpha), interleukin-1 (IL-1), and -6 (IL-6) were determined by bioassay, and IL-8 by a commercial ELISA. |
| 4416 | 12513929 | Interferon-alpha (IFN-alpha), tumor necrosis factor (TNF-alpha), interleukin-1 (IL-1), and -6 (IL-6) were determined by bioassay, and IL-8 by a commercial ELISA. |
| 4417 | 12513929 | Interferon-alpha (IFN-alpha), tumor necrosis factor (TNF-alpha), interleukin-1 (IL-1), and -6 (IL-6) were determined by bioassay, and IL-8 by a commercial ELISA. |
| 4418 | 12513929 | Interferon-alpha (IFN-alpha), tumor necrosis factor (TNF-alpha), interleukin-1 (IL-1), and -6 (IL-6) were determined by bioassay, and IL-8 by a commercial ELISA. |
| 4419 | 12513929 | Interferon-alpha (IFN-alpha), tumor necrosis factor (TNF-alpha), interleukin-1 (IL-1), and -6 (IL-6) were determined by bioassay, and IL-8 by a commercial ELISA. |
| 4420 | 12513929 | Mean levels of IFN-alpha, TNF-alpha, and IL-6, but not IL-1 or IL-8, were lower than in both other groups. |
| 4421 | 12513929 | Mean levels of IFN-alpha, TNF-alpha, and IL-6, but not IL-1 or IL-8, were lower than in both other groups. |
| 4422 | 12513929 | Mean levels of IFN-alpha, TNF-alpha, and IL-6, but not IL-1 or IL-8, were lower than in both other groups. |
| 4423 | 12513929 | Mean levels of IFN-alpha, TNF-alpha, and IL-6, but not IL-1 or IL-8, were lower than in both other groups. |
| 4424 | 12513929 | Mean levels of IFN-alpha, TNF-alpha, and IL-6, but not IL-1 or IL-8, were lower than in both other groups. |
| 4425 | 12513929 | Virus titers in the lungs of individual pigs showed highly significant correlations with IFN-alpha and IL-6, and lower correlations with TNF-alpha and IL-8. |
| 4426 | 12513929 | Virus titers in the lungs of individual pigs showed highly significant correlations with IFN-alpha and IL-6, and lower correlations with TNF-alpha and IL-8. |
| 4427 | 12513929 | Virus titers in the lungs of individual pigs showed highly significant correlations with IFN-alpha and IL-6, and lower correlations with TNF-alpha and IL-8. |
| 4428 | 12513929 | Virus titers in the lungs of individual pigs showed highly significant correlations with IFN-alpha and IL-6, and lower correlations with TNF-alpha and IL-8. |
| 4429 | 12513929 | Virus titers in the lungs of individual pigs showed highly significant correlations with IFN-alpha and IL-6, and lower correlations with TNF-alpha and IL-8. |
| 4430 | 12513929 | Clinical signs were most closely associated with IFN-alpha, IL-6, and TNF-alpha. |
| 4431 | 12513929 | Clinical signs were most closely associated with IFN-alpha, IL-6, and TNF-alpha. |
| 4432 | 12513929 | Clinical signs were most closely associated with IFN-alpha, IL-6, and TNF-alpha. |
| 4433 | 12513929 | Clinical signs were most closely associated with IFN-alpha, IL-6, and TNF-alpha. |
| 4434 | 12513929 | Clinical signs were most closely associated with IFN-alpha, IL-6, and TNF-alpha. |
| 4435 | 12513929 | The relationship between disease and IL-8 or IL-1 was much weaker. |
| 4436 | 12513929 | The relationship between disease and IL-8 or IL-1 was much weaker. |
| 4437 | 12513929 | The relationship between disease and IL-8 or IL-1 was much weaker. |
| 4438 | 12513929 | The relationship between disease and IL-8 or IL-1 was much weaker. |
| 4439 | 12513929 | The relationship between disease and IL-8 or IL-1 was much weaker. |
| 4440 | 12513929 | Our data provide further evidence for a role of IFN-alpha, TNF-alpha, and IL-6 in the pathogenesis of SIV. |
| 4441 | 12513929 | Our data provide further evidence for a role of IFN-alpha, TNF-alpha, and IL-6 in the pathogenesis of SIV. |
| 4442 | 12513929 | Our data provide further evidence for a role of IFN-alpha, TNF-alpha, and IL-6 in the pathogenesis of SIV. |
| 4443 | 12513929 | Our data provide further evidence for a role of IFN-alpha, TNF-alpha, and IL-6 in the pathogenesis of SIV. |
| 4444 | 12513929 | Our data provide further evidence for a role of IFN-alpha, TNF-alpha, and IL-6 in the pathogenesis of SIV. |
| 4445 | 12496150 | We found that neutralization of TNF-alpha at the time of immunization with the protective immunogen (i) reduces the numbers of Langerhans cells, myeloid and lymphoid DC, and activated CD4(+) T cells in DLN and (ii) diminishes the total numbers of cells, the numbers of activated CD4(+) T cells, and amount of gamma interferon at the DTH reaction site. |
| 4446 | 12493553 | T cell telomere length also inversely correlated with serum levels of the proinflammatory cytokine TNFalpha (a clinical marker of disease status), with the proportion of CD8+ T cells lacking expression of the CD28 costimulatory molecule, and with apoptosis. |
| 4447 | 12481940 | Vaccinating mice with DNA encoding the thyrotropin receptor (TSHR), the major autoantigen in Graves' disease, induces memory T cells that secrete interferon-gamma (IFN-gamma) in response to TSHR antigen. |
| 4448 | 12481940 | In initial studies, challenge of splenocytes with TSHR protein induced IFN-gamma and tumor necrosis factor-alpha (TNF-alpha) production in all three strains of mice. |
| 4449 | 12481940 | In summary, we report that TSHR DNA vaccination of BALB/c and NOD.H-2h4 mice, with different major histocompatibility complex (MHC) class II genes (I-Ad and I-Ak, respectively), recognize restricted, nonoverlapping TSHR T-cell epitopes, nearly all in the TSHR A subunit. |
| 4450 | 12477423 | We compared the standard maturation stimulus, autologous monocyte-conditioned medium (MCM), with a synthetic double stranded RNA (poly I:C), soluble CD40 ligand trimer, and a defined cocktail of cytokines (TNF-alpha, IL-1 beta, IL-6) and PGE(2) to promote mature phenotype and function in human monocyte-derived DCs. |
| 4451 | 12477286 | Besides proinflammatory cytokines released from macrophages, such as tumor-necrosis factor-a and interleukin-1beta, and IFN-gamma derived from T-helper 1 lymphocytes, also interleukin-10, a product of T-helper 2 lymphocytes with antiinflammatory properties, seems to be surprisingly involved in the pathogenesis of H. pylori-induced gastritis. |
| 4452 | 12477286 | Besides proinflammatory cytokines released from macrophages, such as tumor-necrosis factor-a and interleukin-1beta, and IFN-gamma derived from T-helper 1 lymphocytes, also interleukin-10, a product of T-helper 2 lymphocytes with antiinflammatory properties, seems to be surprisingly involved in the pathogenesis of H. pylori-induced gastritis. |
| 4453 | 12477286 | In addition, lipopolysaccharide derived from the outher membrane of H. pylori acts as a chemoattractant for monocytes and induces release of free radicals, interleukin-1beta, interleukin-6, interleukin-8 and tumor necrosis factor-alpha. |
| 4454 | 12477286 | In addition, lipopolysaccharide derived from the outher membrane of H. pylori acts as a chemoattractant for monocytes and induces release of free radicals, interleukin-1beta, interleukin-6, interleukin-8 and tumor necrosis factor-alpha. |
| 4455 | 12471131 | In immune-competent animals, CD4(+) T-cell derived cytokines TNF-alpha and IFN-gamma mediate vaccine immunity. |
| 4456 | 12464152 | Imiquimod and its homologues act by activating macrophages and other cells via binding to cell surface receptors, such as Toll receptor 7, thereby inducing secretion of pro-inflammatory cytokines, predominantly interferon (IFN)-alpha, tumour necrosis factor (TNF)-alpha and interleukin (IL)-12. |
| 4457 | 12452837 | We stimulated a whole blood system with heat-inactivated Streptococcus pneumoniae serotype 14 (S14) bacteria, with pneumococcal S14 capsular polysaccharide (PPS S14) and with PPS S14 coated on to latex beads, to compare interleukin 6 (IL-6) and tumour necrosis factor alpha (TNFalpha) production over a six hour period, to ascertain the contribution of PPS to the inflammatory response. |
| 4458 | 12438325 | On the other hand, pretreatment of J774 cells with MTSA-10 markedly reduced NO but not TNF-alpha or interleukin 10 (IL-10) release upon subsequent stimulation with lipopolysaccharide or the cell lysate of M. tuberculosis. |
| 4459 | 12438325 | On the other hand, pretreatment of J774 cells with MTSA-10 markedly reduced NO but not TNF-alpha or interleukin 10 (IL-10) release upon subsequent stimulation with lipopolysaccharide or the cell lysate of M. tuberculosis. |
| 4460 | 12438325 | The activation of protein tyrosine kinases (PTK) and the serine/threonine kinases p38 MAPK and ERK was apparently required for MTSA-10 induction of TNF-alpha and NO release, as revealed by specific kinase inhibitors. |
| 4461 | 12438325 | The activation of protein tyrosine kinases (PTK) and the serine/threonine kinases p38 MAPK and ERK was apparently required for MTSA-10 induction of TNF-alpha and NO release, as revealed by specific kinase inhibitors. |
| 4462 | 12438325 | However, only p38 MAPK activity, not PTK or ERK activity, was partly responsible for MTSA-10-mediated macrophage desensitization. |
| 4463 | 12438325 | However, only p38 MAPK activity, not PTK or ERK activity, was partly responsible for MTSA-10-mediated macrophage desensitization. |
| 4464 | 12430862 | Recent studies indicate that the stealth-like phenotype of leukemia cells can be reversed through transfer of genes encoding recombinant membrane-stabilized proteins of the tumor necrosis factor (TNF) imily, such as the one encoding CD154, the ligand for CD40. |
| 4465 | 12422242 | LPS of E. coli O100 that showed the strongest reactions with both sera was used to stimulate IL-6, TNFalpha and nitric oxide production by the J-774A.1 cell line. |
| 4466 | 12393694 | Comparative analysis of murine marrow-derived dendritic cells generated by Flt3L or GM-CSF/IL-4 and matured with immune stimulatory agents on the in vivo induction of antileukemia responses. |
| 4467 | 12393694 | Comparative analysis of murine marrow-derived dendritic cells generated by Flt3L or GM-CSF/IL-4 and matured with immune stimulatory agents on the in vivo induction of antileukemia responses. |
| 4468 | 12393694 | Comparative analysis of murine marrow-derived dendritic cells generated by Flt3L or GM-CSF/IL-4 and matured with immune stimulatory agents on the in vivo induction of antileukemia responses. |
| 4469 | 12393694 | Bone marrow (BM)-derived dendritic cells (DCs) cultured in granulocyte-macrophage colony-stimulating factor (GM-CSF) and interleukin 4 (IL-4) have been used to generate antitumor immune responses. |
| 4470 | 12393694 | Bone marrow (BM)-derived dendritic cells (DCs) cultured in granulocyte-macrophage colony-stimulating factor (GM-CSF) and interleukin 4 (IL-4) have been used to generate antitumor immune responses. |
| 4471 | 12393694 | Bone marrow (BM)-derived dendritic cells (DCs) cultured in granulocyte-macrophage colony-stimulating factor (GM-CSF) and interleukin 4 (IL-4) have been used to generate antitumor immune responses. |
| 4472 | 12393694 | We investigated whether CpGs would be comparable to TNF-alpha or LPS for the maturation of GM-CSF/IL-4-generated DCs. |
| 4473 | 12393694 | We investigated whether CpGs would be comparable to TNF-alpha or LPS for the maturation of GM-CSF/IL-4-generated DCs. |
| 4474 | 12393694 | We investigated whether CpGs would be comparable to TNF-alpha or LPS for the maturation of GM-CSF/IL-4-generated DCs. |
| 4475 | 12393694 | DCs cultured with GM-CSF/IL-4 and matured with TNF-alpha, LPS, or CpG produced a greater allogeneic T-cell response compared with Flt3L/LPS-generated DCs. |
| 4476 | 12393694 | DCs cultured with GM-CSF/IL-4 and matured with TNF-alpha, LPS, or CpG produced a greater allogeneic T-cell response compared with Flt3L/LPS-generated DCs. |
| 4477 | 12393694 | DCs cultured with GM-CSF/IL-4 and matured with TNF-alpha, LPS, or CpG produced a greater allogeneic T-cell response compared with Flt3L/LPS-generated DCs. |
| 4478 | 12393694 | GM-CSF/IL-4/LPS was superior to Flt3L/LPS for generating anti-AML effects in vivo. |
| 4479 | 12393694 | GM-CSF/IL-4/LPS was superior to Flt3L/LPS for generating anti-AML effects in vivo. |
| 4480 | 12393694 | GM-CSF/IL-4/LPS was superior to Flt3L/LPS for generating anti-AML effects in vivo. |
| 4481 | 12393694 | Whereas TNF-alpha was comparable to LPS in conferring on GM-CSF/IL-4 DCs anti-AML effects in vivo, CpGs were superior to LPS. |
| 4482 | 12393694 | Whereas TNF-alpha was comparable to LPS in conferring on GM-CSF/IL-4 DCs anti-AML effects in vivo, CpGs were superior to LPS. |
| 4483 | 12393694 | Whereas TNF-alpha was comparable to LPS in conferring on GM-CSF/IL-4 DCs anti-AML effects in vivo, CpGs were superior to LPS. |
| 4484 | 12391201 | CD28, TNF receptor, and IL-12 are critical for CD4-independent cross-priming of therapeutic antitumor CD8+ T cells. |
| 4485 | 12391201 | Previously, we have shown that priming of therapeutic CD8(+) T cells in tumor vaccine-draining lymph nodes of mice vaccinated with GM-CSF secreting B16BL6 melanoma cells occurs independent of CD4 T cell help. |
| 4486 | 12391201 | In this study, we examined the contribution of the major costimulatory molecules, CD40 ligand (CD40L), CD80, and CD86, in the priming of CD8(+) T cells. |
| 4487 | 12391201 | Priming of therapeutic CD8(+) T cells by a GM-CSF-transduced tumor vaccine did not require CD40 and CD40L interactions, as therapeutic T cells could be generated from mice injected with anti-CD40L Ab and from CD40L knockout mice. |
| 4488 | 12391201 | However, costimulation via either CD80 or CD86 was required, as therapeutic T cells could be generated from mice injected with either anti-CD80 or anti-CD86 Ab alone, but administration of both Abs completely inhibited the priming of therapeutic T cells. |
| 4489 | 12391201 | Blocking experiments also identified that priming of therapeutic T cells in MHC class II-deficient mice required TNFR and IL-12 signaling, but signaling through CD40, lymphotoxin-betaR, or receptor activator of NF-kappaB was not essential. |
| 4490 | 12391201 | Thus, cross-priming of therapeutic CD8(+) T cells by a tumor vaccine transduced with GM-CSF requires TNFR, IL-12, and CD28 signaling. |
| 4491 | 12391186 | Using monocyte-derived immature DCs and those stimulated with TNF-alpha for maturation, we observed that none of the CD1 isoforms underwent changes in intracellular trafficking that mimicked MHC class II molecules during DC maturation. |
| 4492 | 12391186 | In contrast to the striking increase in surface expression of MHC class II on mature DCs, the surface expression of CD1 molecules was either increased only slightly (for CD1b and CD1c) or decreased (for CD1a). |
| 4493 | 12391186 | Consistent with this, DCs efficiently presented CD1b-restricted lipid Ags to specific T cells similarly in immature and mature DCs. |
| 4494 | 12385032 | In experiments designed to get insights into the interactions between PTX and circulating immune cells, we first observed that addition of PTX to adult whole blood induced the release of IL-12 and TNF-alpha as well as maturation of myeloid dendritic cells (DC). |
| 4495 | 12385032 | Secondly, studies on DC generated in vitro by culturing monocytes with IL-4 and GM-CSF showed that PTX directly stimulates MHC class II and costimulatory molecules up-regulation, cytokine synthesis and NF-kappa B activation. |
| 4496 | 12381575 | In the initial testing of this system, we found that mRNA expression of certain cytokines (interleukin [IL]-1beta, IL-6, IL-12, IL-15, GM-CSF, iNOS, and tumor necrosis factor [TNF]-alpha) is enhanced when monocyte-derived macrophages are stimulated with peptide antigen conjugated with mannan under oxidizing conditions compared to peptide conjugated with reduced mannan. |
| 4497 | 12379697 | These infants also had lower median percentages of lymphocytes spontaneously making interleukin-4 (IL-4) or tumor necrosis factor alpha (TNF-alpha) and lower ratios of T cells spontaneously making IL-4 to T cells making IL-6. |
| 4498 | 12365002 | TNF and IL-10 was increased in response to MCMV infection in mice coimmunised with IFN subtypes and viral gB DNA. |
| 4499 | 12230303 | Some cases of AD are caused by mutations in presenilin-1 (PS1), and it has been shown that PS1 mutations perturb neuronal calcium homeostasis, promote increased production of amyloid beta-peptide (Abeta), and render neurons vulnerable to synaptic dysfunction, excitotoxicity, and apoptosis. |
| 4500 | 12230303 | LPS-induced levels of mRNAs encoding tumor necrosis fctor-alpha (TNFalpha), interleukin (IL)-1alpha, IL-1beta, IL-1 receptor antagonist, and IL-6 are significantly greater in the hippocampus and cerebral cortex of PS1 mutant mice as compared to wild-type mice. |
| 4501 | 12230303 | Studies of cultured microglia from PS1 mutant and wild-type mice reveal that PS1 is expressed in microglia and that the PS1 mutation confers a heightened sensitivity to LPS, as indicated by superinduction of inducible nitric oxide synthase (NOS) and activation of mitogen-activated protein kinase (MAPK). |
| 4502 | 12228279 | CT, LT, dibutyryl-cyclic-3',5'-AMP, and Forskolin also dominantly inhibit interleukin 12 and tumor necrosis factor alpha production by MDDC in the presence of saturating concentrations of lipopolysaccharide. |
| 4503 | 12220808 | FCA augmented IL-4, IL-5 and IL-10 production suggesting a strong Th2 response, while IFN-gamma and IL-12 remained low; poly I:C enhanced IFN-gamma, IL-12 and TNF-alpha eliciting a Th1 response; poly A:U resulted in a IL-10, IL-5, IL-6 and IL-12 secretion; and LPS enhanced the IL-10, IL-6 and TNF-alpha production. |
| 4504 | 12208610 | Spleen cells from immunized mice, after exposure to recombinant MPT SOD (MPT rSOD), produced significant levels of IFNgamma, TNFalpha and IL-6. |
| 4505 | 12208610 | Spleen cells from immunized mice, after exposure to recombinant MPT SOD (MPT rSOD), produced significant levels of IFNgamma, TNFalpha and IL-6. |
| 4506 | 12208610 | IFNgamma and TNFalpha production was increased by the addition of Ribi. |
| 4507 | 12208610 | IFNgamma and TNFalpha production was increased by the addition of Ribi. |
| 4508 | 12208610 | In contrast, low levels of NO, IL-4 and IL-10 were secreted by spleen cells culture from immunized mice. |
| 4509 | 12208610 | In contrast, low levels of NO, IL-4 and IL-10 were secreted by spleen cells culture from immunized mice. |
| 4510 | 12203103 | The role of NF-kappaB in enhancement of TNF-alpha production was confirmed in experiments in which MG132, an inhibitor of NF-kappaB activation, reversed the effect of AdAMP. |
| 4511 | 12203103 | The role of NF-kappaB in enhancement of TNF-alpha production was confirmed in experiments in which MG132, an inhibitor of NF-kappaB activation, reversed the effect of AdAMP. |
| 4512 | 12203103 | AdAMP-induced augmentation of TNF-alpha production by B78/TNF cells was accompanied by morphological changes in the treated cells and a decrease in their adherence to fibrinogen and collagen IV. |
| 4513 | 12203103 | AdAMP-induced augmentation of TNF-alpha production by B78/TNF cells was accompanied by morphological changes in the treated cells and a decrease in their adherence to fibrinogen and collagen IV. |
| 4514 | 12193742 | IFN-gamma-inducible protein 10 (IP-10) is a CXC chemokine that is thought to manifest a proinflammatory role because it stimulates the directional migration of activated T cells, particularly Th1 cells. |
| 4515 | 12193742 | Self-specific Ab to IP-10 developed in protected animals, as well as neutralizing Ab to IP-10 that we have generated in rabbits, could inhibit leukocyte migration, alter the in vivo and in vitro Th1/Th2 balance toward low IFN-gamma, low TNF-alpha, high IL-4-producing T cells, and adoptively transfer disease suppression. |
| 4516 | 12193742 | After all, we did not neutralize the activity of other chemokines that bind CXCR3 (i.e., macrophage-induced gene and IFN-inducible T cell alpha chemoattractant) and yet significantly blocked not only adjuvant-induced arthritis but also the in vivo competence to mount delayed-type hypersensitivity. |
| 4517 | 12193722 | Multiple Chlamydia pneumoniae antigens prime CD8+ Tc1 responses that inhibit intracellular growth of this vacuolar pathogen. |
| 4518 | 12193722 | Eighteen H-2(b) binding peptides representing sequences from 12 Cpn Ags sensitized target cells for MHC class I-restricted lysis by CD8(+) CTL generated from the spleens and lungs of infected mice. |
| 4519 | 12193722 | Peptide-specific IFN-gamma-secreting CD8(+) T cells were present in local and systemic compartments after primary infection, and these cells expanded after pathogen re-exposure. |
| 4520 | 12193722 | CD8(+) T cell lines to the 18 Cpn epitope-bearing peptides were cytotoxic, displayed a memory phenotype, and secreted IFN-gamma and TNF-alpha, but not IL-4. |
| 4521 | 12193722 | Finally, Cpn peptide-specific CD8(+) CTL suppressed chlamydial growth in vitro by direct lysis of infected cells and by secretion of IFN-gamma and other soluble factors. |
| 4522 | 12191514 | We have assessed the optimal conditions in terms of dose and kinetics of those cytokines which are released early (TNF-alpha, IL6 and TGF-beta, IL10) or (interferon [IFN]-gamma and IL5) in WB cultures stimulated with mitogens and mycobacterial antigens. |
| 4523 | 12191514 | Using unpaired Student's t-tests, pulmonary tuberculosis patients (P.TB; n=11), in response to CFP, showed higher monocyte-derived IL6 (p=0.023) and IL10 (p=0.042) compared to endemic controls (EC; n=13), and significantly suppressed T-cell-derived IFN-gamma (p=0.028) and IL5 (p=0.012) secretion but increased IL10 (p=0.047) on day 5, indicating that CFP is a strong stimulus for IL10 secretion in pulmonary TB patients. |
| 4524 | 12191514 | Extrapulmonary TB patients (E.TB; n=6) showed no elevation of early monocyte-derived cytokines to either PPD or CFP, but showed a marked suppression of the T-cell-derived cytokines IFN-gamma (PPD, p=0.015; CFP, p=0.05) and IL5 (PPD, p=0.05; CFP, p=0.015). |
| 4525 | 12189528 | Enhanced HER-2/neu-specific antitumor immunity by cotransduction of mouse dendritic cells with two genes encoding HER-2/neu and alpha tumor necrosis factor. |
| 4526 | 12189528 | Enhanced HER-2/neu-specific antitumor immunity by cotransduction of mouse dendritic cells with two genes encoding HER-2/neu and alpha tumor necrosis factor. |
| 4527 | 12189528 | Enhanced HER-2/neu-specific antitumor immunity by cotransduction of mouse dendritic cells with two genes encoding HER-2/neu and alpha tumor necrosis factor. |
| 4528 | 12189528 | Enhanced HER-2/neu-specific antitumor immunity by cotransduction of mouse dendritic cells with two genes encoding HER-2/neu and alpha tumor necrosis factor. |
| 4529 | 12189528 | Enhanced HER-2/neu-specific antitumor immunity by cotransduction of mouse dendritic cells with two genes encoding HER-2/neu and alpha tumor necrosis factor. |
| 4530 | 12189528 | The infected DCs (DC(HER-2/TNF-alpha)) displayed the expression of both HER-2/neu and TNF-alpha by flow cytometric and ELISA analysis. |
| 4531 | 12189528 | The infected DCs (DC(HER-2/TNF-alpha)) displayed the expression of both HER-2/neu and TNF-alpha by flow cytometric and ELISA analysis. |
| 4532 | 12189528 | The infected DCs (DC(HER-2/TNF-alpha)) displayed the expression of both HER-2/neu and TNF-alpha by flow cytometric and ELISA analysis. |
| 4533 | 12189528 | The infected DCs (DC(HER-2/TNF-alpha)) displayed the expression of both HER-2/neu and TNF-alpha by flow cytometric and ELISA analysis. |
| 4534 | 12189528 | The infected DCs (DC(HER-2/TNF-alpha)) displayed the expression of both HER-2/neu and TNF-alpha by flow cytometric and ELISA analysis. |
| 4535 | 12189528 | We next investigated whether DC(HER-2/TNF-alpha) could induce stronger HER-2/neu-specific immune responses. |
| 4536 | 12189528 | We next investigated whether DC(HER-2/TNF-alpha) could induce stronger HER-2/neu-specific immune responses. |
| 4537 | 12189528 | We next investigated whether DC(HER-2/TNF-alpha) could induce stronger HER-2/neu-specific immune responses. |
| 4538 | 12189528 | We next investigated whether DC(HER-2/TNF-alpha) could induce stronger HER-2/neu-specific immune responses. |
| 4539 | 12189528 | We next investigated whether DC(HER-2/TNF-alpha) could induce stronger HER-2/neu-specific immune responses. |
| 4540 | 12189528 | We found that DC(HER-2/TNF-alpha) displayed up-regulation of immunologically important CD40, CD86, and ICAM-I molecules compared with DC(HER-2), indicating that the former ones are more mature forms of DCs. |
| 4541 | 12189528 | We found that DC(HER-2/TNF-alpha) displayed up-regulation of immunologically important CD40, CD86, and ICAM-I molecules compared with DC(HER-2), indicating that the former ones are more mature forms of DCs. |
| 4542 | 12189528 | We found that DC(HER-2/TNF-alpha) displayed up-regulation of immunologically important CD40, CD86, and ICAM-I molecules compared with DC(HER-2), indicating that the former ones are more mature forms of DCs. |
| 4543 | 12189528 | We found that DC(HER-2/TNF-alpha) displayed up-regulation of immunologically important CD40, CD86, and ICAM-I molecules compared with DC(HER-2), indicating that the former ones are more mature forms of DCs. |
| 4544 | 12189528 | We found that DC(HER-2/TNF-alpha) displayed up-regulation of immunologically important CD40, CD86, and ICAM-I molecules compared with DC(HER-2), indicating that the former ones are more mature forms of DCs. |
| 4545 | 12189528 | Vaccination of DC(HER-2/TNF-alpha) induced stronger allogeneic T-cell proliferation and 36% enhanced HER-2/neu-specific T-cell responses in vitro than DC(HER-2) cells. |
| 4546 | 12189528 | Vaccination of DC(HER-2/TNF-alpha) induced stronger allogeneic T-cell proliferation and 36% enhanced HER-2/neu-specific T-cell responses in vitro than DC(HER-2) cells. |
| 4547 | 12189528 | Vaccination of DC(HER-2/TNF-alpha) induced stronger allogeneic T-cell proliferation and 36% enhanced HER-2/neu-specific T-cell responses in vitro than DC(HER-2) cells. |
| 4548 | 12189528 | Vaccination of DC(HER-2/TNF-alpha) induced stronger allogeneic T-cell proliferation and 36% enhanced HER-2/neu-specific T-cell responses in vitro than DC(HER-2) cells. |
| 4549 | 12189528 | Vaccination of DC(HER-2/TNF-alpha) induced stronger allogeneic T-cell proliferation and 36% enhanced HER-2/neu-specific T-cell responses in vitro than DC(HER-2) cells. |
| 4550 | 12180110 | The frequencies of CD8+ and CD4+ T cells responsive to cytomegalovirus (CMV), varicella zoster virus (VZV), and tetanus in antigen-activated whole blood were determined by flow cytometric analysis of CD69, TNF alpha, IFN gamma and IL-4 expression. |
| 4551 | 12180110 | In spite of a continuously reduced CD4 to CD8 ratio after transplantation, recovery of CD4+ T cells usually occurred prior to CD8+ recovery and often to a higher level. |
| 4552 | 12163272 | IL-6, IL-8 and IL-12 were consistently detected in challenged animals that had been vaccinated. |
| 4553 | 12163272 | Other cytokines--IL-1, IL-2, TNF, TGF and interferons--were not detected. |
| 4554 | 12163272 | Although the IL-6 and IL-8 did not relate to protection, IL-12 production was highest in the protected vaccinated pigs. |
| 4555 | 12163272 | Thus, the induction of monocytic cell activity, demonstrable by the production of IL-6, IL-8 and IL-12, appears to play a critical role in FMDV emergency vaccine induction of the innate immune defences which relate to early protection against FMD. |
| 4556 | 12141048 | In particular, in RS infection the intensive response of macrophages and epithelial cells, accompanied mainly by the synthesis and secretion of tumor necrosis factor and interleukin 8, is observed. |
| 4557 | 12121672 | Treatment of PBMC with either PIII or P24 caused significant decrease in cellular proliferation and granuloma formation induced by S. mansoni antigens, and a significant elevation in IL-10 and TNF-alpha but not in IFN-gamma production. |
| 4558 | 12121672 | Treatment of PBMC with either PIII or P24 caused significant decrease in cellular proliferation and granuloma formation induced by S. mansoni antigens, and a significant elevation in IL-10 and TNF-alpha but not in IFN-gamma production. |
| 4559 | 12121672 | Treatment of PBMC with either PIII or P24 caused significant decrease in cellular proliferation and granuloma formation induced by S. mansoni antigens, and a significant elevation in IL-10 and TNF-alpha but not in IFN-gamma production. |
| 4560 | 12121672 | These findings suggest that, besides inducing protective immunity, PIII and P24 antigens seem to be important in the regulation of in vitro granuloma formation through stimulation of IL-10 and TNF-alpha production in human schistosomiasis. |
| 4561 | 12121672 | These findings suggest that, besides inducing protective immunity, PIII and P24 antigens seem to be important in the regulation of in vitro granuloma formation through stimulation of IL-10 and TNF-alpha production in human schistosomiasis. |
| 4562 | 12121672 | These findings suggest that, besides inducing protective immunity, PIII and P24 antigens seem to be important in the regulation of in vitro granuloma formation through stimulation of IL-10 and TNF-alpha production in human schistosomiasis. |
| 4563 | 12121672 | The more pronounced effect of P24 on reducing the in vitro granulomatous reaction could be associated with a balance between IL-10 and TNF-alpha production. |
| 4564 | 12121672 | The more pronounced effect of P24 on reducing the in vitro granulomatous reaction could be associated with a balance between IL-10 and TNF-alpha production. |
| 4565 | 12121672 | The more pronounced effect of P24 on reducing the in vitro granulomatous reaction could be associated with a balance between IL-10 and TNF-alpha production. |
| 4566 | 12119053 | Infected cells release proinflammatory cytokines and chemokines, including IL-1, tumor necrosis factor-alpha, IL-6, and IL-8. |
| 4567 | 12117942 | Animals were primed with a mixture of DNA plasmids encoding two preerythrocytic-stage proteins and two erythrocytic-stage proteins from P. knowlesi and combinations of the cytokines granulocyte-macrophage colony-stimulating factor, interleukin-4, and tumor necrosis factor alpha and were boosted with a mixture of four recombinant, attenuated vaccinia virus strains encoding the four P. knowlesi antigens. |
| 4568 | 12117936 | Oral immunization of mice with a Salmonella vaccine expressing colonization factor antigen I (CFA/I) from enterotoxigenic Escherichia coli results in the rapid onset of interleukin-4 (IL-4) and IL-5 production, which explains the observed elevations in mucosal immunoglobulin A (IgA) and serum IgG1 antibodies. |
| 4569 | 12117936 | Upon measurement of proinflammatory cytokines, minimal to no tumor necrosis factor alpha (TNF-alpha), IL-1alpha, IL-1beta, or IL-6 was produced by Salmonella-CFA/I-infected RAW 264.7 or peritoneal macrophages, but production was greatly induced in Salmonella vector-infected macrophages. |
| 4570 | 12117936 | Only minute levels of IL-12 p70 were induced by Salmonella vector-infected macrophages, and none was induced by Salmonella-CFA/I-infected macrophages. |
| 4571 | 12117936 | The absence of IL-12 was not due to overt increases in production of either IL-12 p40 or IL-10. |
| 4572 | 12115605 | MyD-1 (SIRPalpha) regulates T cell function in the absence of exogenous danger signals, via a TNFalpha-dependent pathway. |
| 4573 | 12115605 | MyD-1 (SIRPalpha) regulates T cell function in the absence of exogenous danger signals, via a TNFalpha-dependent pathway. |
| 4574 | 12115605 | MyD-1 (SIRPalpha) regulates T cell function in the absence of exogenous danger signals, via a TNFalpha-dependent pathway. |
| 4575 | 12115605 | We observed that the production of TNFalpha, a cytokine that we have earlier identified as important in the mechanism of MyD-1 immune regulation, is inhibited by cross-linking of MyD-1. |
| 4576 | 12115605 | We observed that the production of TNFalpha, a cytokine that we have earlier identified as important in the mechanism of MyD-1 immune regulation, is inhibited by cross-linking of MyD-1. |
| 4577 | 12115605 | We observed that the production of TNFalpha, a cytokine that we have earlier identified as important in the mechanism of MyD-1 immune regulation, is inhibited by cross-linking of MyD-1. |
| 4578 | 12115605 | We further show that TNFalpha is critically important in the regulation of T cell responses in the absence of danger signals, and indeed addition of TNFalpha can overcome the inhibitory effects of anti-MyD-1 antibody. |
| 4579 | 12115605 | We further show that TNFalpha is critically important in the regulation of T cell responses in the absence of danger signals, and indeed addition of TNFalpha can overcome the inhibitory effects of anti-MyD-1 antibody. |
| 4580 | 12115605 | We further show that TNFalpha is critically important in the regulation of T cell responses in the absence of danger signals, and indeed addition of TNFalpha can overcome the inhibitory effects of anti-MyD-1 antibody. |
| 4581 | 12114290 | In vitro cellular and humoral immune responses were measured to detect functional abnormalities in antigen presenting cells (autologous mixed leukocyte reactions and expression of interleukin (IL)-1beta, IL-6, IL-10, and tumor necrosis factor-alpha); T cells (lymphocyte proliferation using the polyclonal T-cell activators phytohemagglutinin and Concanavalin A; primary immune responses in allogeneic mixed leukocyte reactions; secondary immune response using the recall antigens tetanus toxoid, Candida albicans, and anthrax vaccine; and soluble IL-2 receptor expression); type-1 T-helper cells (gamma interferon expression); type-2 T-helper cells (IL-4 and IL-10 expression); and B cells (polyclonal B-cell activator pokeweed mitogen-induced immunoglobulin production). |
| 4582 | 12091878 | Hyporesponsiveness to vaccination with Borrelia burgdorferi OspA in humans and in TLR1- and TLR2-deficient mice. |
| 4583 | 12091878 | The macrophages of low responders produced less tumor necrosis factor-alpha and interleukin-6 after OspA stimulation and had lower cell-surface expression of Toll-like receptor (TLR) 1 as compared to normal cells, but normal expression of TLR2. |
| 4584 | 12091878 | After OspA immunization, mice genetically deficient in either TLR2 (TLR2(-/-)) or TLR1 (TLR1(-/-)) produced low titers of antibodies against OspA. |
| 4585 | 12091878 | Notably, macrophages from TLR2(-/-) mice were unresponsive to OspA and PGN, whereas those from TLR1(-/-) mice responded normally to PGN but not to OspA. |
| 4586 | 12091878 | These data indicate that TLR1 and TLR2 are required for lipoprotein recognition and that defects in the TLR1/2 signaling pathway may account for human hyporesponsiveness to OspA vaccination. |
| 4587 | 12085313 | To study the effect of preexisting T cell responses to DV on the severity of secondary virus infection, peripheral blood mononuclear cells (PBMC) from 10 subsequently hospitalized and 12 nonhospitalized Thai schoolchildren were stimulated with inactivated dengue antigens, and proliferation of interferon (IFN)-gamma or tumor necrosis factor (TNF)-alpha responses of the preinfection PBMC were measured. |
| 4588 | 12082305 | Bacterial DNA with unmethylated CpG-DNA stimulates vertebrate immature immune cells to induce maturation and to produce TNF-alpha as well as Th1-type cytokines, IL-12 and IFN-gamma. |
| 4589 | 12079558 | Using synthetic RNA standards, we quantified mRNAs of IL-2, IL-4, IL-6, IL-10, IL-12 p40, interferon gamma (IFN-gamma), tumor necrosis factor alpha (TNF-alpha), RANTES, macrophage inflammatory protein 1 alpha (MIP-1 alpha), and MIP-1 beta in unstimulated peripheral blood mononuclear cells (PBMCs) and lymph nodes from macaques chronically infected with SIV or SHIV. |
| 4590 | 12079558 | Viremic monkeys with decreased CD4(+) T cell counts (<500 cells/microl) had significantly higher IL-10 mRNA expression than uninfected controls, which parallels the findings in HIV-1-infected humans. |
| 4591 | 12079558 | In addition, MIP-1 alpha, MIP-1 beta, and RANTES mRNA expression increased in viremic monkeys with decreased CD4(+) T cell counts; gene expression was inversely correlated with CD4(+) T cell counts, but not viral load. |
| 4592 | 12078857 | Interaction of disease-related antigen-reactive T-cell lines from multiple sclerosis patients with type IV collagen: role of integrin VLA-1 and effects of irradiation. |
| 4593 | 12078857 | Vaccination with T-cell lines reactive with myelin basic protein (MBP) and myelin oligodendrocytic glycoprotein (MOG) epitopes, expanded with interleukin-2 (IL-2), and attenuated by ionizing radiation is currently being evaluated as a therapeutic modality for this disease. |
| 4594 | 12078857 | Seven of 7 autoantigen-responsive T-cell lines from MS patients adhered to collagen IV, the major collagenous constituent of BMs. |
| 4595 | 12078857 | T-cell lines from healthy donors adhered more variably to collagen IV. |
| 4596 | 12078857 | Furthermore, patient derived T cells actively transmigrated through a collagen IV gel toward medium containing TNF-a, in a process that was inhibited by MAbs to VLA-1. |
| 4597 | 12078857 | Ionizing radiation at the dose used in vaccine preparation, inhibited morphological polarization associated with migratory capability, induced integrin clustering on the cell membrane, and abrogated adhesion to collagen IV. |
| 4598 | 12065488 | Mice were immunized by priming with DNA vaccine plasmids encoding the Plasmodium yoelii circumsporozoite protein (PyCSP) and murine granulocyte-macrophage colony-stimulating factor and boosting with recombinant vaccinia encoding PyCSP. |
| 4599 | 12065488 | The antigen (Ag)-specific effector CD8(+)-T-cell population present 2 weeks after boosting had ex vivo Ag-specific cytolytic activity, expressed both gamma interferon (IFN-gamma) and tumor necrosis factor alpha, and constituted 12 to 20% of splenic CD8(+) T cells. |
| 4600 | 12065488 | In contrast, the memory CD8(+)-Ag-specific-cell population at 28 weeks lacked cytolytic activity and constituted only 6% of splenic CD8(+) T cells, but at the single-cell level it produced significantly higher levels of IFN-gamma than the effectors. |
| 4601 | 12050371 | A comparison of intrahepatic cytokine levels in Ch1552 and Ch1605 showed greater and earlier gamma interferon (IFN-gamma) and tumor necrosis factor alpha responses in the previously infected animal, responses that were 30-fold greater than baseline responses at week 4 p.i. for IFN-gamma in Ch1552 compared to 12-fold in Ch1605 at week 10 p.i. |
| 4602 | 12047757 | Macrophages showed a rapid inflammatory response in which the expression of interleukin-1beta (IL-1beta), major histocompatibility complex class II (MHC II), inducible cyclo-oxygenase (Cox-2), and inducible nitric oxide synthase (iNOS) was enhanced, but tumour necrosis factor-alpha (TNF-alpha) expression was greatly reduced initially and then increased. |
| 4603 | 12047757 | Macrophages showed a rapid inflammatory response in which the expression of interleukin-1beta (IL-1beta), major histocompatibility complex class II (MHC II), inducible cyclo-oxygenase (Cox-2), and inducible nitric oxide synthase (iNOS) was enhanced, but tumour necrosis factor-alpha (TNF-alpha) expression was greatly reduced initially and then increased. |
| 4604 | 12047757 | Macrophages showed a rapid inflammatory response in which the expression of interleukin-1beta (IL-1beta), major histocompatibility complex class II (MHC II), inducible cyclo-oxygenase (Cox-2), and inducible nitric oxide synthase (iNOS) was enhanced, but tumour necrosis factor-alpha (TNF-alpha) expression was greatly reduced initially and then increased. |
| 4605 | 12047757 | Macrophages showed a rapid inflammatory response in which the expression of interleukin-1beta (IL-1beta), major histocompatibility complex class II (MHC II), inducible cyclo-oxygenase (Cox-2), and inducible nitric oxide synthase (iNOS) was enhanced, but tumour necrosis factor-alpha (TNF-alpha) expression was greatly reduced initially and then increased. |
| 4606 | 12047757 | Macrophages showed a rapid inflammatory response in which the expression of interleukin-1beta (IL-1beta), major histocompatibility complex class II (MHC II), inducible cyclo-oxygenase (Cox-2), and inducible nitric oxide synthase (iNOS) was enhanced, but tumour necrosis factor-alpha (TNF-alpha) expression was greatly reduced initially and then increased. |
| 4607 | 12047757 | After 5 days, except for TNF-alpha and MHC II, expression returned to levels approaching those of uninfected macrophages. |
| 4608 | 12047757 | After 5 days, except for TNF-alpha and MHC II, expression returned to levels approaching those of uninfected macrophages. |
| 4609 | 12047757 | After 5 days, except for TNF-alpha and MHC II, expression returned to levels approaching those of uninfected macrophages. |
| 4610 | 12047757 | After 5 days, except for TNF-alpha and MHC II, expression returned to levels approaching those of uninfected macrophages. |
| 4611 | 12047757 | After 5 days, except for TNF-alpha and MHC II, expression returned to levels approaching those of uninfected macrophages. |
| 4612 | 12047757 | We found that msa reduced the expression of IL-1beta, Cox-2, and MHC II but stimulated TNF-alpha while hly, rsh and grp stimulated MHC II but down-regulated TNF-alpha. |
| 4613 | 12047757 | We found that msa reduced the expression of IL-1beta, Cox-2, and MHC II but stimulated TNF-alpha while hly, rsh and grp stimulated MHC II but down-regulated TNF-alpha. |
| 4614 | 12047757 | We found that msa reduced the expression of IL-1beta, Cox-2, and MHC II but stimulated TNF-alpha while hly, rsh and grp stimulated MHC II but down-regulated TNF-alpha. |
| 4615 | 12047757 | We found that msa reduced the expression of IL-1beta, Cox-2, and MHC II but stimulated TNF-alpha while hly, rsh and grp stimulated MHC II but down-regulated TNF-alpha. |
| 4616 | 12047757 | We found that msa reduced the expression of IL-1beta, Cox-2, and MHC II but stimulated TNF-alpha while hly, rsh and grp stimulated MHC II but down-regulated TNF-alpha. |
| 4617 | 12047757 | Constructs expressing hly or lysB stimulated iNOS expression and additionally, lysB stimulated TNF-alpha. |
| 4618 | 12047757 | Constructs expressing hly or lysB stimulated iNOS expression and additionally, lysB stimulated TNF-alpha. |
| 4619 | 12047757 | Constructs expressing hly or lysB stimulated iNOS expression and additionally, lysB stimulated TNF-alpha. |
| 4620 | 12047757 | Constructs expressing hly or lysB stimulated iNOS expression and additionally, lysB stimulated TNF-alpha. |
| 4621 | 12047757 | Constructs expressing hly or lysB stimulated iNOS expression and additionally, lysB stimulated TNF-alpha. |
| 4622 | 12047757 | The results show how p57 suppresses the host immune system and suggest that the immune mechanisms for the containment of R. salmoninarum infections rely on MHC II- and TNF-alpha-dependent pathways. |
| 4623 | 12047757 | The results show how p57 suppresses the host immune system and suggest that the immune mechanisms for the containment of R. salmoninarum infections rely on MHC II- and TNF-alpha-dependent pathways. |
| 4624 | 12047757 | The results show how p57 suppresses the host immune system and suggest that the immune mechanisms for the containment of R. salmoninarum infections rely on MHC II- and TNF-alpha-dependent pathways. |
| 4625 | 12047757 | The results show how p57 suppresses the host immune system and suggest that the immune mechanisms for the containment of R. salmoninarum infections rely on MHC II- and TNF-alpha-dependent pathways. |
| 4626 | 12047757 | The results show how p57 suppresses the host immune system and suggest that the immune mechanisms for the containment of R. salmoninarum infections rely on MHC II- and TNF-alpha-dependent pathways. |
| 4627 | 12042449 | This study was designed to test whether breast-feeding attenuates reductions in energy intake associated with a mild immunologic stimulus and to assess poststimulus relationships among putative reductions in energy intake and serum interleukin (IL)-1beta, tumor necrosis factor (TNF)-alpha and leptin concentrations. |
| 4628 | 12042449 | Increases in leptin are associated with reductions in energy consumption in the postimmunization period in FF infants and postimmunization changes in IL-1beta concentrations likely are related to reductions in energy intake in response to immunologic stimuli. |
| 4629 | 12009571 | Specifically, recombinant strains expressing IL-2 (known as GIDIL2) or TNF-alpha (GIDTNF) were compared with the parental, non-cytokine-secreting, strain (BRD509) for their ability to induce a variety of immune responses in susceptible BALB/c mice. |
| 4630 | 11994440 | IFN-alpha beta promote priming of antigen-specific CD8+ and CD4+ T lymphocytes by immunostimulatory DNA-based vaccines. |
| 4631 | 11994440 | Immunostimulatory sequence (ISS) DNA containing unmethylated CpG dinucleotides stimulate NK and APC to secrete proinflammatory cytokines, including IFN-alphabeta and -gamma, TNF-alpha, and IL-6 and -12, and to express costimulatory surface molecules such as CD40, B7-1, and B7-2. |
| 4632 | 11994440 | This investigation examines the mechanisms by which ISS DNA primes CD8(+) and CD4(+) lymphocyte activities. |
| 4633 | 11994440 | Coordinated regulation of B7 costimulation and TAP-dependent cross-presentation results in priming of Ag-specific CD8(+) CTL, whereas CD40, B7, and IL-12 costimulation is required for priming of CD4(+) Th cells by ISS-based vaccines. |
| 4634 | 11991987 | Among the proinflammatory cytokines and their mRNAs measured (IL-6, IL-1 beta, IL-8, and tumor necrosis factor alpha), IL-8 showed the greatest change following D2V infection. |
| 4635 | 11991987 | Nuclear factor kappa B (NF-kappa B) and nuclear factor IL-6 (NFIL-6) are primary mediators of IL-8 expression. |
| 4636 | 11991987 | We studied the transcriptional regulation of IL-8 in the ECV304 and 293T cell lines and found that the induction of IL-8 gene expression involved the activation of NF-kappa B (P = 0.001) and, to a lesser extent, the activation of NFIL-6 in ECV304 cells only. |
| 4637 | 11991987 | IL-8 produced by infected monocytes and also IL-8 that may be produced by endothelial or other epithelial cells is associated with the hyperacetylation of histones bound to the IL-8 promoter in addition to the activation of transcription by NF-kappa B. |
| 4638 | 11986269 | Vitamin A-deficient children (<20 microg/dl) were more likely than non-vitamin A-deficient children to have higher proportions of natural killer (NK) cells (median, 8.3 and 5.2%, respectively) and lower ratios of interleukin-10-producing monocytes to tumor necrosis factor alpha-producing monocytes after induction (median, 1.0 and 2.3, respectively). |
| 4639 | 11983250 | The stimulation of Vgamma9Vdelta2 T cells with phosphocarbohydrates induces the production of cytokines (IFNgamma and TNFalpha) and the release of chemokines with suppressive activity on HIV replication. |
| 4640 | 11983250 | Th1 cytokines (IL-12 and IL-15) positively regulate cytokine production by Vgamma9Vdelta2 T cells but they are inefficient in restoring normal functions in patients' gammadelta T cells. |
| 4641 | 11982590 | BCG stimulated thioglycollate-elicited murine peritoneal exudate cells (PEC) to induce cytotoxic activity and to produce cytokines such as interferon (IFN)-gamma, tumour necrosis factor (TNF)-alpha and PGE2. |
| 4642 | 11982590 | BCG stimulated thioglycollate-elicited murine peritoneal exudate cells (PEC) to induce cytotoxic activity and to produce cytokines such as interferon (IFN)-gamma, tumour necrosis factor (TNF)-alpha and PGE2. |
| 4643 | 11982590 | BCG stimulated thioglycollate-elicited murine peritoneal exudate cells (PEC) to induce cytotoxic activity and to produce cytokines such as interferon (IFN)-gamma, tumour necrosis factor (TNF)-alpha and PGE2. |
| 4644 | 11982590 | BCG stimulated thioglycollate-elicited murine peritoneal exudate cells (PEC) to induce cytotoxic activity and to produce cytokines such as interferon (IFN)-gamma, tumour necrosis factor (TNF)-alpha and PGE2. |
| 4645 | 11982590 | NS398, a specific COX-2 inhibitor, and indomethacin (IM), a COX-1 and COX-2 inhibitor, enhanced viable BCG-induced cytotoxic activity and IFN-gamma and TNF-alpha production of PEC. |
| 4646 | 11982590 | NS398, a specific COX-2 inhibitor, and indomethacin (IM), a COX-1 and COX-2 inhibitor, enhanced viable BCG-induced cytotoxic activity and IFN-gamma and TNF-alpha production of PEC. |
| 4647 | 11982590 | NS398, a specific COX-2 inhibitor, and indomethacin (IM), a COX-1 and COX-2 inhibitor, enhanced viable BCG-induced cytotoxic activity and IFN-gamma and TNF-alpha production of PEC. |
| 4648 | 11982590 | NS398, a specific COX-2 inhibitor, and indomethacin (IM), a COX-1 and COX-2 inhibitor, enhanced viable BCG-induced cytotoxic activity and IFN-gamma and TNF-alpha production of PEC. |
| 4649 | 11982590 | Enhanced cytotoxicity was mediated by increased amounts of IFN-gamma and TNF-alpha. |
| 4650 | 11982590 | Enhanced cytotoxicity was mediated by increased amounts of IFN-gamma and TNF-alpha. |
| 4651 | 11982590 | Enhanced cytotoxicity was mediated by increased amounts of IFN-gamma and TNF-alpha. |
| 4652 | 11982590 | Enhanced cytotoxicity was mediated by increased amounts of IFN-gamma and TNF-alpha. |
| 4653 | 11982590 | Exogenous PGE2 reduced cytotoxic activity and IFN-gamma and TNF-alpha production of PEC. |
| 4654 | 11982590 | Exogenous PGE2 reduced cytotoxic activity and IFN-gamma and TNF-alpha production of PEC. |
| 4655 | 11982590 | Exogenous PGE2 reduced cytotoxic activity and IFN-gamma and TNF-alpha production of PEC. |
| 4656 | 11982590 | Exogenous PGE2 reduced cytotoxic activity and IFN-gamma and TNF-alpha production of PEC. |
| 4657 | 11972976 | Splenocyte stimulation by T. gondii antigen produced lymphoproliferative response and cytokine profile (IL-10, IL-12, IFN-gamma and TNF-alpha) similar to those produced by chronic natural infection. |
| 4658 | 11962727 | Peritoneal cells collected from mice intraperitoneally injected with a 100 microg/dose of Lactoferrin demonstrated modest, but significant, production of TNF-alpha, IL-12 and MIP-1alpha when cultured in vitro, compared to saline-injected controls. |
| 4659 | 11962727 | Peritoneal cells collected from mice intraperitoneally injected with a 100 microg/dose of Lactoferrin demonstrated modest, but significant, production of TNF-alpha, IL-12 and MIP-1alpha when cultured in vitro, compared to saline-injected controls. |
| 4660 | 11962727 | J774A.1 murine macrophages stimulated with Lactoferrin resulted in increased TNF-alpha protein production, and upregulated IL-12 and IL-15 mRNA. |
| 4661 | 11962727 | J774A.1 murine macrophages stimulated with Lactoferrin resulted in increased TNF-alpha protein production, and upregulated IL-12 and IL-15 mRNA. |
| 4662 | 11962727 | Levels of message for chemokines MIP-1alpha and MIP-2 were also increased in a dose-dependent way. |
| 4663 | 11962727 | Levels of message for chemokines MIP-1alpha and MIP-2 were also increased in a dose-dependent way. |
| 4664 | 11947931 | In this study we provide evidence that a prolonged increase in the plasma levels of IL-2, but not IL-1beta, IL-4, IL-10, IL-2R or TNF-alpha occured in patients affected by bladder cancer following effective BCG treatment. |
| 4665 | 11941455 | In this study we have used the methylcholanthrene (MC)-induced sarcomas MC57S and MC57X, previously shown to express individually distinct MHC-I associated peptides recognized by tumor necrosis factor-alpha (TNF-alpha) producing CD8(+) T cells. |
| 4666 | 11941455 | In this study we have used the methylcholanthrene (MC)-induced sarcomas MC57S and MC57X, previously shown to express individually distinct MHC-I associated peptides recognized by tumor necrosis factor-alpha (TNF-alpha) producing CD8(+) T cells. |
| 4667 | 11941455 | In vitro, T cell lines from mice immunized with tumor-derived hsp70 could recognize tumor cells from the same MC57 tumor as that used for the hsp70 purification, resulting in TNF-alpha production. |
| 4668 | 11941455 | In vitro, T cell lines from mice immunized with tumor-derived hsp70 could recognize tumor cells from the same MC57 tumor as that used for the hsp70 purification, resulting in TNF-alpha production. |
| 4669 | 11927652 | Stimulation of DC with IFN-gamma increased the release of interleukin (IL)-12 and tumor necrosis factor-alpha and inhibited the production of IL-10. |
| 4670 | 11927652 | Moreover, IFN-gamma-treated DC up-regulated the release of CXCL10 (IP-10) markedly and reduced the secretion of CCL17 TARC significantly, attracting preferentially T-helper (Th)1 and Th2 cells, respectively. |
| 4671 | 11927652 | Compared with DC pulsed with soluble Tat, DC incubated with RBC-Tat elicited specific CD4+ and CD8+ T-cell responses at a much lower antigen dose. |
| 4672 | 11927652 | Finally, immature and mature DC exposed to IFN-gamma were better stimulators of allogeneic T cells and induced a higher IFN-gamma production from Tat-specific CD4+ and CD8+ T lymphocytes. |
| 4673 | 11927632 | Using tumor necrosis factor (TNF)-RI knockout- and Fas-deficient mice, we demonstrate that the depletion of parasite-specific CD4(+) T cells is not via TNF or Fas pathways. |
| 4674 | 11927632 | Taken together, these data suggest that long-term immunity to malaria infection may be affected by an IFN-gamma-mediated depletion of parasite-specific CD4(+) T cells during infection. |
| 4675 | 11920816 | Tumor necrosis factor-alpha (TNF-alpha) and TNF-beta expression was detected in all samples by PCR and in < 50% of samples by immunostaining. |
| 4676 | 11920816 | Tumor necrosis factor-alpha (TNF-alpha) and TNF-beta expression was detected in all samples by PCR and in < 50% of samples by immunostaining. |
| 4677 | 11920816 | Interleukin-2 (IL-2) and IL-4 expression was detected in a few samples by immunostaining but was not detectable by PCR. |
| 4678 | 11920816 | Interleukin-2 (IL-2) and IL-4 expression was detected in a few samples by immunostaining but was not detectable by PCR. |
| 4679 | 11920816 | We found greater expression of TNF-alpha and IL-4 in DHF than in dengue fever or other (non-dengue) febrile illnesses. |
| 4680 | 11920816 | We found greater expression of TNF-alpha and IL-4 in DHF than in dengue fever or other (non-dengue) febrile illnesses. |
| 4681 | 11916244 | Brain tumor-bearing mice were treated with cytokine (IL -4, IL-6, IL-7, GM-CSF, TNF-alpha, LIF, LT) producing vaccines made by in vitro transduction of GI261 cells with the corresponding adenoviral vectors. |
| 4682 | 11916244 | Vaccines producing either IL-4 or GM-CSF cured 20-40% of mice. |
| 4683 | 11916244 | Brain tumors were heavily infiltrated by CD4+ lymphocytes after treatment with IL-4- or GM-CSF-secreting cells. |
| 4684 | 11916244 | GM-CSF vaccination induced moderate CD8+ infiltration, as well. |
| 4685 | 11916244 | Depleting either CD4+ or CD8+ lymphocyte subsets abolished the anticancer effect of GM-CSF-expressing cells. |
| 4686 | 11916244 | Strong synergism was observed by combining cytokine vaccination (GM-CSF, IL-4, IL-12) with local tumor irradiation: about 80-100% of the glioma-bearing mice was cured. |
| 4687 | 11907108 | Reduced functional capacity of CD8+ T cells expanded by post-exposure vaccination of gamma-herpesvirus-infected CD4-deficient mice. |
| 4688 | 11907108 | More CD69(high)CD8(+) D(b)p56(+) T cells were found in the CD4-deficient mice, an effect that might be thought to reflect higher Ag load. |
| 4689 | 11907108 | By contrast, the mean fluorescence intensity of staining for the CD44 glycoprotein was diminished on CD8(+)D(b)p56(+) T cells from the I-A(b-/-) group, the level of CTL activity was lower on a per cell basis, and the relative prevalence of IFN-gamma(+)TNF-alpha(+) T cells detected after in vitro stimulation with the p56 peptide was decreased. |
| 4690 | 11907108 | Given that this experimental system provides an accessible model for evaluating postexposure vaccination protocols that might be used in diseases like HIV/AIDS, the further need is to clarify the underlying molecular mechanisms and the relative significance of lack of CD4(+) T help vs higher Ag load for these expanded CD8(+) effector populations. |
| 4691 | 11904734 | The authors performed a clinical study of a vaccine using autologous dendritic cells (DCs) pulsed with CEA652 and adjuvant cytokines, natural human interferon alpha (nhuIFN-alpha), and natural human tumor necrosis factor alpha (nhuTNF-alpha), for the treatment of patients with CEA-expressing advanced metastatic malignancies. |
| 4692 | 11904734 | DCs were generated from plastic adherent monocytes of granulocyte colony-stimulating factor (G-CSF)-mobilized peripheral blood mononuclear cells (PBMCs) in the presence of granulocyte/macrophage colony-stimulating factor (GM-CSF) and interleukin 4 (IL-4). |
| 4693 | 11899386 | Expansion of HER2/neu-specific T cells ex vivo following immunization with a HER2/neu peptide-based vaccine. |
| 4694 | 11899386 | Transgenic mice overexpressing rat neu in mammary tissue develop malignancy, histologically similar to human HER2/neu-overexpressing breast cancer. |
| 4695 | 11899386 | In addition, cytokines, such as interleukin-12, when added during ex vivo culturing along with interleukin-2 can selectively expand antigen-specific T-cells. |
| 4696 | 11899386 | Interleukin-12 also enhances antigen-specific functional measurements such as interferon-gamma and tumor necrosis factor-alpha release. |
| 4697 | 11899386 | Refinements in ex vivo expansion techniques may greatly improve the feasibility of tumor-antigen T-cell-based therapy for the treatment of advanced-stage HER2/neu-overexpressing breast malignancy. |
| 4698 | 11895976 | Similarly, additional mycobacterial antigen delivered directly to the lungs by aerosol infection with viable M. tuberculosis mixed with heat-killed Mycobacterium tuberculosis (1:1) also did not reduce the bacillary load but caused increased expression of tumor necrosis factor alpha (TNF-alpha) and interleukin 6 (IL-6), which was associated with larger granulomas in the lungs. |
| 4699 | 11895976 | Similarly, additional mycobacterial antigen delivered directly to the lungs by aerosol infection with viable M. tuberculosis mixed with heat-killed Mycobacterium tuberculosis (1:1) also did not reduce the bacillary load but caused increased expression of tumor necrosis factor alpha (TNF-alpha) and interleukin 6 (IL-6), which was associated with larger granulomas in the lungs. |
| 4700 | 11895976 | When M. tuberculosis-infected mice were treated with recombinant BCG that secreted cytokines shown to reduce disease in a preinfection vaccine model, the BCG secreting TNF-alpha, and to a lesser extent, IL-2 and gamma interferon (IFN-gamma), caused a significant increase in granuloma size in the lungs. |
| 4701 | 11895976 | When M. tuberculosis-infected mice were treated with recombinant BCG that secreted cytokines shown to reduce disease in a preinfection vaccine model, the BCG secreting TNF-alpha, and to a lesser extent, IL-2 and gamma interferon (IFN-gamma), caused a significant increase in granuloma size in the lungs. |
| 4702 | 11895951 | To understand the mechanism(s) implicated in the regulation of the synthesis and release of IL-10 during early infection, we investigated the autocrine effects of IL-6, IL-12, tumor necrosis factor alpha (TNF-alpha), and IL-10 itself, as well as the exocrine effect of IFN-gamma on the production of macrophage-derived IL-10 with lipoprotein as a stimulant. |
| 4703 | 11895951 | To understand the mechanism(s) implicated in the regulation of the synthesis and release of IL-10 during early infection, we investigated the autocrine effects of IL-6, IL-12, tumor necrosis factor alpha (TNF-alpha), and IL-10 itself, as well as the exocrine effect of IFN-gamma on the production of macrophage-derived IL-10 with lipoprotein as a stimulant. |
| 4704 | 11895951 | TNF-alpha increased the production of IL-10, as elicited by lipoproteins. |
| 4705 | 11895951 | TNF-alpha increased the production of IL-10, as elicited by lipoproteins. |
| 4706 | 11895951 | The production of IL-10 by THP-1 cells stimulated with L-OspA was autoregulated by a negative feedback mechanism involving the IL-10 receptor (IL-10R). |
| 4707 | 11895951 | The production of IL-10 by THP-1 cells stimulated with L-OspA was autoregulated by a negative feedback mechanism involving the IL-10 receptor (IL-10R). |
| 4708 | 11895951 | Exogenous IFN-gamma significantly inhibited the production of IL-10. |
| 4709 | 11895951 | Exogenous IFN-gamma significantly inhibited the production of IL-10. |
| 4710 | 11895951 | Both autocrine (IL-10) and exocrine (IFN-gamma) inhibition of IL-10 production resulted in an increase in the production of the proinflammatory cytokines IL-6 and IL-12. |
| 4711 | 11895951 | Both autocrine (IL-10) and exocrine (IFN-gamma) inhibition of IL-10 production resulted in an increase in the production of the proinflammatory cytokines IL-6 and IL-12. |
| 4712 | 11884558 | (i) VV-NP118 induced potent and long-lasting CD8 and CD4 T-cell responses to the vector; at the peak of the response (approximately 1 week), there were approximately 10(7) VV-specific CD8 T cells (25% of the CD8 T cells) and approximately 10(6) VV-specific CD4 T cells (approximately 5% of the CD4 T cells) in the spleen. |
| 4713 | 11884558 | These numbers decreased to approximately 5 x 10(5) CD8 T cells (approximately 5% frequency) and approximately 10(5) CD4 T cells (approximately 0.5% frequency), respectively, by day 30 and were then stably maintained at these levels for >300 days. |
| 4714 | 11884558 | (ii) VV-specific CD8 and CD4 T cells were capable of producing gamma interferon (IFN-gamma), tumor necrosis factor alpha (TNF-alpha), and interleukin-2; all cells were able to make IFN-gamma, a subset produced both IFN-gamma and TNF-alpha, and another subset produced all three cytokines. |
| 4715 | 11881495 | In the course of the vaccinal process the restoration of the initially inhibited characteristics (the production of TNF-alpha and IL-2) to normal values were shown to occur, which was indicative of the fact that the reserve capacities of immunocompetent cells were retained in these patients. |
| 4716 | 11867164 | We have examined T cell responses against recombinant analogues of the surface-exposed C. ruminantium major antigen 1 (MAP1) a 28.8 kDa protein and MAP2 (21 kDa) antigen in cattle immunised by infection and treatment. |
| 4717 | 11867164 | We have examined T cell responses against recombinant analogues of the surface-exposed C. ruminantium major antigen 1 (MAP1) a 28.8 kDa protein and MAP2 (21 kDa) antigen in cattle immunised by infection and treatment. |
| 4718 | 11867164 | MAP1-specific responses were predominantly restricted to cluster of differentiation four antigen positive T cells (CD4+ T cells). |
| 4719 | 11867164 | MAP1-specific responses were predominantly restricted to cluster of differentiation four antigen positive T cells (CD4+ T cells). |
| 4720 | 11867164 | Reverse transcription polymerase chain reaction (RT-PCR) analysis of cytokine expression by T cell lines derived from this population revealed strong expression of interferon gamma (IFN-gamma), interferon alpha (IFN-alpha), tumour necrosis factor alpha (TNF-alpha), tumour necrosis factor beta (TNF-beta), interleukin-2 receptor alpha (IL-2Ralpha) transcripts, and weak expression of IL-2 and IL-4. |
| 4721 | 11867164 | Reverse transcription polymerase chain reaction (RT-PCR) analysis of cytokine expression by T cell lines derived from this population revealed strong expression of interferon gamma (IFN-gamma), interferon alpha (IFN-alpha), tumour necrosis factor alpha (TNF-alpha), tumour necrosis factor beta (TNF-beta), interleukin-2 receptor alpha (IL-2Ralpha) transcripts, and weak expression of IL-2 and IL-4. |
| 4722 | 11867164 | CD4+ T cell clones specific for MAP1 were generated. |
| 4723 | 11867164 | CD4+ T cell clones specific for MAP1 were generated. |
| 4724 | 11867164 | RT-PCR analysis of cytokine expression by T cell lines which were dominated by gammadelta T cells revealed expression of IFN-gamma, TNF-alpha, TNF-beta, IL-2Ralpha transcripts. |
| 4725 | 11867164 | RT-PCR analysis of cytokine expression by T cell lines which were dominated by gammadelta T cells revealed expression of IFN-gamma, TNF-alpha, TNF-beta, IL-2Ralpha transcripts. |
| 4726 | 11867164 | Our findings indicate that immunisation of cattle by infection with C. ruminantium results in generation of MAP1- and MAP2-specific T cell responses that may play a role in protection against the pathogen. |
| 4727 | 11867164 | Our findings indicate that immunisation of cattle by infection with C. ruminantium results in generation of MAP1- and MAP2-specific T cell responses that may play a role in protection against the pathogen. |
| 4728 | 11848512 | It was followed by a transient elevation of the serum levels of pro-inflammatory cytokines: TNF-alpha IL-6. |
| 4729 | 11846424 | In vaccines produced in eukaryote cells as well as in commercial medical preparations of leukocyte interferon a number of cytokines such as IL-1beta, IL-6 and TNF-alpha have been detected. |
| 4730 | 11846424 | In vaccines produced in eukaryote cells as well as in commercial medical preparations of leukocyte interferon a number of cytokines such as IL-1beta, IL-6 and TNF-alpha have been detected. |
| 4731 | 11846424 | Among the vaccines examined in this study the highest level of IL-1beta was demonstrated in inactivated hepatitis A vaccine prepared in the green monkey kidney cell line 4647, that of IL-6 in inactivated rabies vaccine produced in Syrian hamster kidney (SHK) cell culture, and that of TNF-alpha in live poliomyelitis vaccine manufactured in VERO cells. |
| 4732 | 11846424 | Among the vaccines examined in this study the highest level of IL-1beta was demonstrated in inactivated hepatitis A vaccine prepared in the green monkey kidney cell line 4647, that of IL-6 in inactivated rabies vaccine produced in Syrian hamster kidney (SHK) cell culture, and that of TNF-alpha in live poliomyelitis vaccine manufactured in VERO cells. |
| 4733 | 11840267 | Leukaemia cells derived from 42 patients with AML were cultured in vitro with cytokines GM-CSF, IL-4 and TNFalpha/CD40L. |
| 4734 | 11836673 | Systems studied have included lysis by interleukin-2 (IL-2)-activated lymphokine-activated killer (LAK) cells, tumor necrosis factor-alpha (TNF-alpha), a p16-expressing adenovirus vector, suicide gene therapy using the herpes simplex virus-tyrosine kinase (HSV-tk) followed by ganciclovir, and immunomodulatory gene therapy with IL-2, IL-4, interferon-gamma (IFN-gamma), IFN-alpha, TNF-alpha, granulocyte-macrophage colony-stimulating factor (GM-CSF), IL-6, and IL-1beta transfected into tumors. |
| 4735 | 11836673 | Since platelet-derived growth factor (PDGF) is thought to be an autocrine growth factor for mesothelioma STI-571 (Gleevec; Novartis, Basel, Switzerland), a highly selective inhibitor of the PDGF receptor tyrosine kinase, is being tested in a phase II trial. |
| 4736 | 11805229 | These compounds showed intrinsic agonistic properties when tested for their ability to stimulate tumor necrosis factor-alpha in human whole blood and interleukin-6 in U373 human glioblastoma cells without added LPS coreceptor CD14. |
| 4737 | 11792391 | Characteristic immunophenotypic and functional DC maturation induced by standard monocyte conditioned medium (MCM) was compared to the activation induced by a panel of stimuli including soluble CD40L, LPS, Poly I:C, PGE(2)/TNFalpha, and a cocktail mixture of PGE(2)/TNFalpha/IL-1beta/IL-6. |
| 4738 | 11792391 | Immunophenotypic analysis confirmed that all stimuli induced stable up-regulation of CD25, CD40, CD80, CD83, CD86, HLA-DR, DC-LAMP (CD208), and DEC-205 (CD205). |
| 4739 | 11775545 | Co-modification of IL-2-TNF alpha fusion gene and B7.1 gene to murine breast tumor cells leads to improved tumor rejection and vaccine effect. |
| 4740 | 11751978 | CTL from monkeys infected with nonpathogenic isolates of simian and simian-human immunodeficiency virus expressed high levels of IFN-gamma, TNF-alpha, and IL-2 after in vitro exposure to a nonspecific mitogen or the optimal peptide representing a dominant virus-specific CTL epitope. |
| 4741 | 11751978 | CTL from monkeys infected with nonpathogenic isolates of simian and simian-human immunodeficiency virus expressed high levels of IFN-gamma, TNF-alpha, and IL-2 after in vitro exposure to a nonspecific mitogen or the optimal peptide representing a dominant virus-specific CTL epitope. |
| 4742 | 11751978 | CTL from monkeys infected with nonpathogenic isolates of simian and simian-human immunodeficiency virus expressed high levels of IFN-gamma, TNF-alpha, and IL-2 after in vitro exposure to a nonspecific mitogen or the optimal peptide representing a dominant virus-specific CTL epitope. |
| 4743 | 11751978 | However, similarly performed studies assessing these capabilities in CTL from monkeys infected with pathogenic immunodeficiency virus isolates demonstrated a significant dysfunction in the ability of the CTL to produce IL-2 and TNF-alpha. |
| 4744 | 11751978 | However, similarly performed studies assessing these capabilities in CTL from monkeys infected with pathogenic immunodeficiency virus isolates demonstrated a significant dysfunction in the ability of the CTL to produce IL-2 and TNF-alpha. |
| 4745 | 11751978 | However, similarly performed studies assessing these capabilities in CTL from monkeys infected with pathogenic immunodeficiency virus isolates demonstrated a significant dysfunction in the ability of the CTL to produce IL-2 and TNF-alpha. |
| 4746 | 11751978 | Moreover, an AIDS vaccine that confers protection against clinical disease evolution in this experimental model also preserves the functional capacity of these CTL to produce both IL-2 and TNF-alpha. |
| 4747 | 11751978 | Moreover, an AIDS vaccine that confers protection against clinical disease evolution in this experimental model also preserves the functional capacity of these CTL to produce both IL-2 and TNF-alpha. |
| 4748 | 11751978 | Moreover, an AIDS vaccine that confers protection against clinical disease evolution in this experimental model also preserves the functional capacity of these CTL to produce both IL-2 and TNF-alpha. |
| 4749 | 11745487 | In contrast, established RM11psa tumors ranging in size from 500 to 1,000 mm(3) were efficiently eliminated if Ad5-PSA priming was followed 7 days later by intratumoral injection of recombinant canarypox viruses (ALVAC) encoding interleukin-12 (IL-12), IL-2, and tumor necrosis factor-alpha. |
| 4750 | 11744830 | Interferon (IFN)-gamma-producing CD8(+) T cells were quantified in an enzyme-linked immunosorbent assay. |
| 4751 | 11744830 | Results showed that M-stimulated production of interleukin (IL)-10 and tumor necrosis factor (TNF)-alpha increases in CD4(+) and CD8(+) cells of African infected patients and uninfected study subject; and that env-stimulated IL-10 and TNF-alpha production is increased in CD8(+) T lymphocytes of African HIV-infected patients. |
| 4752 | 11744830 | M- and env-stimulated IFN-gamma-producing CD8(+) T cells were reduced in African participants and not increased by preincubation with alpha IL-10 monoclonal antibody. |
| 4753 | 11739712 | Here we show that infection of cynomolgus macaques by wild-type Puumala hantavirus resulted in typical signs of HFRS including lethargy, anorexia, proteinuria, and/or hematuria, in addition to cytokine (interleukin 6 [IL-6], IL-10, and tumor necrosis factor alpha), C-reactive protein, creatinine, and nitric oxide responses. |
| 4754 | 11739538 | These responses were associated with Ag-specific IFN-gamma and/or TNF-alpha secretion, but not IL-4, consistent with induction of Th1 immunity. |
| 4755 | 11726219 | Generation of CD4(+) and CD8(+) T lymphocyte responses by dendritic cells armed with PSA/anti-PSA (antigen/antibody) complexes. |
| 4756 | 11726219 | We compared the capacity of DC to generate CD4(+) and CD8(+) T cell responses after exposure to prostate-specific antigen (PSA) alone, PSA targeted to the mannose receptor (mannosylated PSA (PSA-m)), or PSA targeted to Fc receptors by combining PSA with an anti-PSA antibody (AR47.47). |
| 4757 | 11726219 | Autologous CD3(+) T cells were added to monocyte-derived immature DC that had been cultured with GM-CSF/IL-4 for 4 days, exposed to antigen, and matured with CD40L or TNFalpha/IFN-alpha. |
| 4758 | 11726219 | Both CD4(+) and CD8(+) T cell responses were observed after stimulation with DC exposed to the PSA/anti-PSA complexes, whereas CD4(+) predominated over CD8(+) T cell responses after stimulation with PSA-armed DC or PSA-m. |
| 4759 | 11726219 | These CD8(+) T cells responded when rechallenged with DC pulsed with HLA allele-restricted PSA peptides. |
| 4760 | 11726136 | Standardized generation of fully mature p70 IL-12 secreting monocyte-derived dendritic cells for clinical use. |
| 4761 | 11726136 | Only a combination of TNFalpha + Poly (I:C), or a previously described cytokine cocktail of TNFalpha + IL-1beta + IL-6 + prostaglandin E2, induced the complete activation of the whole DC population, as assessed by the cell surface expression of CD83 and costimulatory molecules. |
| 4762 | 11726134 | Transduction of human dendritic cells with a recombinant modified vaccinia Ankara virus encoding MUC1 and IL-2. |
| 4763 | 11726134 | In this study we have characterized the transduction of monocyte-derived DC with a highly attenuated vaccinia virus vector [modified vaccinia Ankara (MVA)] encoding human MUC1 and the immunostimulatory cytokine IL-2. |
| 4764 | 11726134 | Analysis of transduced DC cultures generated from a number of donors revealed MUC1 expression in the range of 27-54% of the cells and a co-regulated secretion of bioactive IL-2. |
| 4765 | 11726134 | As shown by FACS analysis with MUCI-specific antibodies, the MVA-MUC1/IL-2-transduced DC predominantly expressed the fully processed glycoform of MUC1, typical of that displayed by normal epithelia. |
| 4766 | 11726134 | The MVA-MUC1/IL-2 vector effectively transduced both immature and TNF-alpha-matured DC. |
| 4767 | 11712808 | Serial urinary IL-2, IL-6, IL-8, TNFalpha, UBC, CYFRA 21-1 and NMP22 during follow-up of patients with bladder cancer receiving intravesical BCG. |
| 4768 | 11705920 | IFN-gamma production was proportional to tumor necrosis factor alpha and interleukin 10 (IL-10) levels but did not correlate with IL-5 production. |
| 4769 | 11705920 | In high IFN-gamma producers there was an increased frequency of activated CD8(+) T cells both in vitro and in vivo compared to the frequency in low producers, and such cells were positive for IFN-gamma as determined by intracellular staining. |
| 4770 | 11703320 | We have analysed the functional capability of DC generated in vitro from blood CD14(+) cells of chronic lymphocytic leukaemia (CLL) patients and healthy donors by culturing for 10 d with granulocyte-macrophage colony-stimulating factor (GM-CSF), interleukin 4 (IL-4) and tumour necrosis factor-alpha (TNF-alpha). |
| 4771 | 11703320 | We have analysed the functional capability of DC generated in vitro from blood CD14(+) cells of chronic lymphocytic leukaemia (CLL) patients and healthy donors by culturing for 10 d with granulocyte-macrophage colony-stimulating factor (GM-CSF), interleukin 4 (IL-4) and tumour necrosis factor-alpha (TNF-alpha). |
| 4772 | 11703320 | Most of the DC generated from both patients and controls exhibited a mature phenotype indicated by CD83 and major histocompatibility complex (MHC) class II expression, as well as by a characteristic morphology. |
| 4773 | 11703320 | Most of the DC generated from both patients and controls exhibited a mature phenotype indicated by CD83 and major histocompatibility complex (MHC) class II expression, as well as by a characteristic morphology. |
| 4774 | 11703320 | CLL DC had a similar expression of accessory molecules (CD54, CD80 and CD86) as control DC. |
| 4775 | 11703320 | CLL DC had a similar expression of accessory molecules (CD54, CD80 and CD86) as control DC. |
| 4776 | 11703320 | The mean fluorescence intensity of CD80 and MHC class I molecules was significantly higher on CLL DC than on control DC (P < 0.05). |
| 4777 | 11703320 | The mean fluorescence intensity of CD80 and MHC class I molecules was significantly higher on CLL DC than on control DC (P < 0.05). |
| 4778 | 11703320 | The expression of IL-4 and TNF-alpha was similar to that of control DC. |
| 4779 | 11703320 | The expression of IL-4 and TNF-alpha was similar to that of control DC. |
| 4780 | 11691814 | Here we describe a novel RCC vaccine strategy that allows for the concomitant delivery of dual immune activators: G250, a widely expressed RCC associated antigen; and granulocyte/macrophage-colony stimulating factor (GM-CSF), an immunomodulatory factor for antigen-presenting cells. |
| 4781 | 11691814 | When combined with interleukin 4 (IL-4; 1000 units/ml), FP (0.34 microg/ml) induces differentiation of monocytes (CD14+) into dendritic cells (DCs) expressing surface markers characteristic for antigen-presenting cells. |
| 4782 | 11691814 | Up-regulation of mature DCs (CD83+CD19-; 17% versus 6%) with enhanced expression of HLA class I and class II antigens was detected in FP-cultured DCs as compared with DCs cultured with recombinant GM-CSF. |
| 4783 | 11691814 | Treatment of peripheral blood mononuclear cells (PBMCs) with FP alone (2.7 microg/10(7) cells) augments both T-cell helper 1 (Th1) and Th2 cytokine mRNA expression (IL-2, IL-4, GM-CSF, IFN-gamma, and tumor necrosis factor-alpha). |
| 4784 | 11691814 | Comparison of various immune manipulation strategies in parallel, bulk PBMCs treated with FP (0.34 microg/ml) plus IL-4 (1000 units/ml) for 1 week and restimulated weekly with FP plus IL-2 (20 IU/ml) induced maximal growth expansion of active T cells expressing the T-cell receptor and specific anti-RCC cytotoxicity, which could be blocked by the addition of anti-HLA class I, anti-CD3, or anti-CD8 antibodies. |
| 4785 | 11691814 | These results suggest that GM-CSF-G250 FP is a potent immunostimulant with the capacity for activating immunomodulatory DCs and inducing a T-helper cell-supported, G250-targeted, and CD8+-mediated antitumor response. |
| 4786 | 11675375 | Here, in the course of trying to understand the mechanism for synergy between IL-12 and TNF-alpha in up-regulating IFN-gamma production, we find that when the stimulus through the TCR is too weak to induce cell proliferation, which would be needed for selection, IL-12 and TNF-alpha synergize to up-regulate not only IFN-gamma, but also the IL-12Rbeta2 chain, which triggers IFN-gamma production. |
| 4787 | 11672919 | It was shown that only Ticovac, which contains no albumin as a stabilizer, can induce relative high amounts of TNF-alpha (P < or = 0.0001) and lower amounts of IL-1 beta (P < or = 0.05). |
| 4788 | 11592071 | Previously, we have shown ADAC in CD8+ populations to be Fas independent, TNF-alpha receptor 2 (TNFR2) mediated, caspase dependent, and accompanied by a decrease in Bcl-2. |
| 4789 | 11592071 | Individual CTL undergoing apoptosis exhibit a dramatic and concurrent: (1) positive staining with Annexin V and propidium iodide; (2) transformation to a smaller cell size characteristic of apoptosis; and (3) a nearly complete loss of Bcl-2, c-IAP1, and TRAF2. |
| 4790 | 11585920 | Human T-cell lymphotropic virus type 1 Tax represses c-Myb-dependent transcription through activation of the NF-kappaB pathway and modulation of coactivator usage. |
| 4791 | 11585920 | Here we demonstrate that activation of the NF-kappaB pathway by the HTLV-1 Tax protein leads to transcriptional inactivation of c-Myb. |
| 4792 | 11585920 | This conclusion was supported by the fact that Tax mutants unable to stimulate the NF-kappaB pathway could not inhibit c-Myb transactivating functions. |
| 4793 | 11585920 | In addition, inhibition of Tax-mediated NF-kappaB activation by coexpression of IkappaBalpha restored c-Myb transcription, and Tax was unable to block c-Myb transcription in a NEMO knockout cell line. |
| 4794 | 11585920 | Importantly, physiological stimuli, such as signaling with the cellular cytokines tumor necrosis factor alpha, interleukin 1 beta (IL-1beta), and lipopolysaccharide, also inhibited c-Myb transcription. |
| 4795 | 11585920 | Interestingly, an amino-terminal deletion form of p300 lacking the C/H1 and KIX domains and unable to bind RelA retained the ability to stimulate c-Myb transcription and prevented NF-kappaB-mediated repression. |
| 4796 | 11585761 | Using HSVtk suicide gene therapy, we showed that macrophages can distinguish between tumor cells dying through classical apoptosis and tumor cells engineered to die through nonapoptotic mechanisms, resulting in secretion of either immunosuppressive cytokines (interleukin 10 and transforming growth factor beta) or inflammatory cytokines (tumor necrosis factor alpha or interleukin 1beta), respectively. |
| 4797 | 11577995 | Tumor necrosis factor-alpha/interleukin-10 balance in normal and cystic fibrosis children. |
| 4798 | 11576883 | The in vivo response to standard hepatitis B booster vaccine and in vitro proliferation and release of interleukin-2 (IL-2), IL-6, tumor necrosis factor-alpha, and interferon-gamma from stimulated lymphocytes were not different between the groups. |
| 4799 | 11576883 | In contrast to clinical immune effects, paricalcitol increased serum calcium levels and decreased PTH and bone alkaline phosphatase levels (all P < 0.05). |
| 4800 | 11559797 | Compared to VacE7, VacSigE7LAMP-1 and VacLLOE7 resulted in increased numbers of H2-D(b)-specific tetramer-positive CD8(+) T cells in mouse spleens that produced gamma interferon and tumor necrosis factor alpha upon stimulation with RAHYNIVTF peptide. |
| 4801 | 11558546 | Reverse transcriptase polymerase chain reaction (RT-PCR) analysis revealed that T cell lines derived from each animal expressed relatively high levels of interferon (IFN)-gamma mRNA, low levels of interleukin (IL)-2, IL-10, and tumor necrosis factor (TNF)-alpha mRNAs, but no detectable level of IL-4 mRNA. |
| 4802 | 11549417 | Tumour necrosis factor (TNF)-alpha, interleukin (IL)-1 and IL-6 are the first set of cytokines produced upon such an encounter, which have roles both in protective immunity and immunopathogenesis evident with respiratory syncytial virus (RSV). |
| 4803 | 11549417 | Tumour necrosis factor (TNF)-alpha, interleukin (IL)-1 and IL-6 are the first set of cytokines produced upon such an encounter, which have roles both in protective immunity and immunopathogenesis evident with respiratory syncytial virus (RSV). |
| 4804 | 11549417 | Tumour necrosis factor (TNF)-alpha, interleukin (IL)-1 and IL-6 are the first set of cytokines produced upon such an encounter, which have roles both in protective immunity and immunopathogenesis evident with respiratory syncytial virus (RSV). |
| 4805 | 11549417 | Tumour necrosis factor (TNF)-alpha, interleukin (IL)-1 and IL-6 are the first set of cytokines produced upon such an encounter, which have roles both in protective immunity and immunopathogenesis evident with respiratory syncytial virus (RSV). |
| 4806 | 11549417 | Live virus and LPS induced higher levels of IL-6 and TNF-alpha than ISCOM and so did non-adjuvanted UV-inactivated RSV but only at high doses. |
| 4807 | 11549417 | Live virus and LPS induced higher levels of IL-6 and TNF-alpha than ISCOM and so did non-adjuvanted UV-inactivated RSV but only at high doses. |
| 4808 | 11549417 | Live virus and LPS induced higher levels of IL-6 and TNF-alpha than ISCOM and so did non-adjuvanted UV-inactivated RSV but only at high doses. |
| 4809 | 11549417 | Live virus and LPS induced higher levels of IL-6 and TNF-alpha than ISCOM and so did non-adjuvanted UV-inactivated RSV but only at high doses. |
| 4810 | 11549417 | Kinetic studies showed that ISCOM induced cytokine production first detected at hours 1, 2, 4 for TNF-alpha, IL-6 and IL-1alpha respectively, which was earlier than for the other antigen formulations containing corresponding doses of antigen and/or Quillaja adjuvant. |
| 4811 | 11549417 | Kinetic studies showed that ISCOM induced cytokine production first detected at hours 1, 2, 4 for TNF-alpha, IL-6 and IL-1alpha respectively, which was earlier than for the other antigen formulations containing corresponding doses of antigen and/or Quillaja adjuvant. |
| 4812 | 11549417 | Kinetic studies showed that ISCOM induced cytokine production first detected at hours 1, 2, 4 for TNF-alpha, IL-6 and IL-1alpha respectively, which was earlier than for the other antigen formulations containing corresponding doses of antigen and/or Quillaja adjuvant. |
| 4813 | 11549417 | Kinetic studies showed that ISCOM induced cytokine production first detected at hours 1, 2, 4 for TNF-alpha, IL-6 and IL-1alpha respectively, which was earlier than for the other antigen formulations containing corresponding doses of antigen and/or Quillaja adjuvant. |
| 4814 | 11549417 | Peak values for production of TNF-alpha and IL-6 were at 8 h and for IL-1alpha at 72 h following stimulation with ISCOM. |
| 4815 | 11549417 | Peak values for production of TNF-alpha and IL-6 were at 8 h and for IL-1alpha at 72 h following stimulation with ISCOM. |
| 4816 | 11549417 | Peak values for production of TNF-alpha and IL-6 were at 8 h and for IL-1alpha at 72 h following stimulation with ISCOM. |
| 4817 | 11549417 | Peak values for production of TNF-alpha and IL-6 were at 8 h and for IL-1alpha at 72 h following stimulation with ISCOM. |
| 4818 | 11531955 | Influence of the IL-1Ra gene polymorphism on in vivo synthesis of IL-1Ra and IL-1beta after live yellow fever vaccination. |
| 4819 | 11531955 | Influence of the IL-1Ra gene polymorphism on in vivo synthesis of IL-1Ra and IL-1beta after live yellow fever vaccination. |
| 4820 | 11531955 | The IL-1 complex contains polymorphic genes coding for IL-1alpha, IL-1beta and IL-1Ra. |
| 4821 | 11531955 | The IL-1 complex contains polymorphic genes coding for IL-1alpha, IL-1beta and IL-1Ra. |
| 4822 | 11531955 | The IL-1Ra (variable number of tanden repeat) VNTR polymorphism has been shown to influence the capacity to produce IL-1beta and IL-1Ra after in vitro stimulation. |
| 4823 | 11531955 | The IL-1Ra (variable number of tanden repeat) VNTR polymorphism has been shown to influence the capacity to produce IL-1beta and IL-1Ra after in vitro stimulation. |
| 4824 | 11531955 | After administration of the RKI vaccine (34 volunteers), plasma TNF-alpha concentration increased from 13.4 +/- 0.9 pg/ml to 23.3 +/- 1.1 pg/ml (P < 0.001), and plasma IL-1Ra concentration increased from 308 +/- 25 pg/ml to 1019 +/- 111 pg/ml (P < 0.001), on day 2. |
| 4825 | 11531955 | After administration of the RKI vaccine (34 volunteers), plasma TNF-alpha concentration increased from 13.4 +/- 0.9 pg/ml to 23.3 +/- 1.1 pg/ml (P < 0.001), and plasma IL-1Ra concentration increased from 308 +/- 25 pg/ml to 1019 +/- 111 pg/ml (P < 0.001), on day 2. |
| 4826 | 11531955 | Using Stamaril vaccine, no increase in the plasma concentrations of either TNF-alpha or IL-1Ra could be detected (n = 17). |
| 4827 | 11531955 | Using Stamaril vaccine, no increase in the plasma concentrations of either TNF-alpha or IL-1Ra could be detected (n = 17). |
| 4828 | 11531955 | Carriers of allele 2 of the IL-1Ra polymorphism had increased baseline concentrations of IL-1Ra (350 +/- 32 pg/ml) compared with non-carriers (222 +/- 18 pg/ml, P < 0.001), and decreased concentrations of IL-1beta (0.9 +/- 0.2 pg/ml for carriers versus 2.8 +/- 0.7 pg/ml for non-carriers, P = 0.017). |
| 4829 | 11531955 | Carriers of allele 2 of the IL-1Ra polymorphism had increased baseline concentrations of IL-1Ra (350 +/- 32 pg/ml) compared with non-carriers (222 +/- 18 pg/ml, P < 0.001), and decreased concentrations of IL-1beta (0.9 +/- 0.2 pg/ml for carriers versus 2.8 +/- 0.7 pg/ml for non-carriers, P = 0.017). |
| 4830 | 11531955 | This is the first study to examine the influence of this genetic polymorphism on in vivo-induced human IL-1beta and IL-1Ra synthesis. |
| 4831 | 11531955 | This is the first study to examine the influence of this genetic polymorphism on in vivo-induced human IL-1beta and IL-1Ra synthesis. |
| 4832 | 11531955 | Baseline concentrations of IL-1Ra and IL-1beta were significantly influenced by the IL-1Ra polymorphism. |
| 4833 | 11531955 | Baseline concentrations of IL-1Ra and IL-1beta were significantly influenced by the IL-1Ra polymorphism. |
| 4834 | 11531955 | No influence of the IL-1Ra polymorphism on the in vivo-induced production of IL-1Ra and IL-1beta could be detected. |
| 4835 | 11531955 | No influence of the IL-1Ra polymorphism on the in vivo-induced production of IL-1Ra and IL-1beta could be detected. |
| 4836 | 11524916 | Recent work has emphasized the role of genetic polymorphisms in various systems to explain the most severe cases: anti-inflammatory cytokine profile IL-10/TNF-alpha, elevated levels of plasminogen activator inhibitor type-1, variants of the gene for mannose-binding lectin complement pathway. |
| 4837 | 11507070 | We demonstrate that a mouse-human chimeric anti-ganglioside GD2-interleukin (IL)-2 fusion protein (ch14.18-IL2) substantially amplifies tumor-protective immunity against murine melanoma induced by an autologous oral DNA vaccine containing the murine ubiquitin gene fused to murine melanoma peptide epitopes gp100(25-35) and TRP-2(181-188). |
| 4838 | 11507070 | The tumor-protective immunity was mediated by MHC class I antigen- restricted CD8(+) T cells together with CD4(+) T cell help, which was required only for tumor cell killing in the effector phase of the immune response. |
| 4839 | 11507070 | The immunological mechanisms involved in this antitumor effect were suggested by a decisively increased secretion of tumor necrosis factor alpha TNFTnTNa and IFN-gamma from CD4(+) and CD8(+) T cells and a markedly up-regulated expression on CD8(+) T cells of high-affinity IL-2 receptor alpha chain (CD25), costimulatory molecule CD28, and adhesion molecule lymphocyte function-associated antigen-2 (LFA-2/CD2). |
| 4840 | 11500399 | In addition, high levels of interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-alpha), IL-12, IL-10, gamma interferon (IFN-gamma), and IL-4 production were detected in lung cells, and nitric oxide (NO) production was high in culture supernatants of bronchoalveolar lavage cells. |
| 4841 | 11500399 | In addition, high levels of interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-alpha), IL-12, IL-10, gamma interferon (IFN-gamma), and IL-4 production were detected in lung cells, and nitric oxide (NO) production was high in culture supernatants of bronchoalveolar lavage cells. |
| 4842 | 11500399 | High levels of IFN-gamma, IL-6, TNF-alpha, IL-12, IL-10, and NO were detected in the culture supernatants. |
| 4843 | 11500399 | High levels of IFN-gamma, IL-6, TNF-alpha, IL-12, IL-10, and NO were detected in the culture supernatants. |
| 4844 | 11490008 | The efficacy of the Vbeta6+ clone was associated with elevated production of IFN-gamma, TNF-alpha, and GM-CSF compared with that of the Vbeta14+ clone. |
| 4845 | 11489935 | A comparison of Ab responses against the self (TNF-alpha) and foreign components of the fusion protein showed that VLP conjugation abrogated the ability of the humoral immune system to distinguish between self and foreign. |
| 4846 | 11483274 | Post-challenge levels of interferon-alpha and tumor necrosis factor-alpha in bronchoalveolar lavage fluids were reduced in the vaccinates, while levels of interleukin-1 and neutrophils were less consistent. |
| 4847 | 11477558 | Our data showed that phagocytosis of apoptotic/necrotic tumor cells resulted in maturation of DCs with up-regulated expression of proinflammatory cytokines [interleukin (IL)-1beta, IL-6, tumor necrosis factor-alpha, interferon-gamma and granulocyte-macrophage colony-stimulating factor], chemokines (MIP-1alpha, MIP-1beta and MIP-2), the CC chemokine receptor CCR7 and the cell surface molecules (MHC class II, CD11b, CD40 and CD86), and down-regulated expression of the CC chemokine receptors CCR2 and CCR5. |
| 4848 | 11448026 | While cell surface expression of apoptosis-related molecules such as TNF-related apoptosis-inducing ligand (TRAIL), TRAIL-receptors, CD95(Fas) and Fas-ligand, and plasma interferon-gamma were increased for measles patients, they remained unchanged after vaccination. |
| 4849 | 11435492 | Immunostimulatory CpG-modified plasmid DNA enhances IL-12, TNF-alpha, and NO production by bovine macrophages. |
| 4850 | 11435492 | Immunostimulatory CpG-modified plasmid DNA enhances IL-12, TNF-alpha, and NO production by bovine macrophages. |
| 4851 | 11435492 | Macrophages activated with CpG-modified pDNA secreted significantly more interleukin-12, tumor necrosis factor-alpha, and nitric oxide than macrophages stimulated with unmodified pDNA or modified pDNA that contained nucleotides scrambled to remove CpG motifs. |
| 4852 | 11435492 | Macrophages activated with CpG-modified pDNA secreted significantly more interleukin-12, tumor necrosis factor-alpha, and nitric oxide than macrophages stimulated with unmodified pDNA or modified pDNA that contained nucleotides scrambled to remove CpG motifs. |
| 4853 | 11431420 | The ability of cytokines to steer CD4(+) T(h) cell responses toward a T(h)1 or T(h)2 phenotype and enhance the magnitude of both CD8(+) cytotoxic T lymphocytes (CTL) and antibody responses has clearly been demonstrated by our lab and others, but the influence of cytokines on protective immune responses is much less clear. |
| 4854 | 11431420 | The ability of cytokines to steer CD4(+) T(h) cell responses toward a T(h)1 or T(h)2 phenotype and enhance the magnitude of both CD8(+) cytotoxic T lymphocytes (CTL) and antibody responses has clearly been demonstrated by our lab and others, but the influence of cytokines on protective immune responses is much less clear. |
| 4855 | 11431420 | The ability of cytokines to steer CD4(+) T(h) cell responses toward a T(h)1 or T(h)2 phenotype and enhance the magnitude of both CD8(+) cytotoxic T lymphocytes (CTL) and antibody responses has clearly been demonstrated by our lab and others, but the influence of cytokines on protective immune responses is much less clear. |
| 4856 | 11431420 | The ability of cytokines to steer CD4(+) T(h) cell responses toward a T(h)1 or T(h)2 phenotype and enhance the magnitude of both CD8(+) cytotoxic T lymphocytes (CTL) and antibody responses has clearly been demonstrated by our lab and others, but the influence of cytokines on protective immune responses is much less clear. |
| 4857 | 11431420 | Here we show an essential role for CD4(+) T(h)1 helper cell induction and IFN-gamma production in protection from viral challenge with a recombinant vaccinia virus expressing HIV-1MN viral envelope glycoprotein gp160. |
| 4858 | 11431420 | Here we show an essential role for CD4(+) T(h)1 helper cell induction and IFN-gamma production in protection from viral challenge with a recombinant vaccinia virus expressing HIV-1MN viral envelope glycoprotein gp160. |
| 4859 | 11431420 | Here we show an essential role for CD4(+) T(h)1 helper cell induction and IFN-gamma production in protection from viral challenge with a recombinant vaccinia virus expressing HIV-1MN viral envelope glycoprotein gp160. |
| 4860 | 11431420 | Here we show an essential role for CD4(+) T(h)1 helper cell induction and IFN-gamma production in protection from viral challenge with a recombinant vaccinia virus expressing HIV-1MN viral envelope glycoprotein gp160. |
| 4861 | 11431420 | Complete protection from viral challenge is achieved only when the triple combination of exogenous cytokines granulocyte macrophage colony stimulating factor (GM-CSF), IL-12 and tumor necrosis factor (TNF)-alpha are co-administered with the peptide vaccine. |
| 4862 | 11431420 | Complete protection from viral challenge is achieved only when the triple combination of exogenous cytokines granulocyte macrophage colony stimulating factor (GM-CSF), IL-12 and tumor necrosis factor (TNF)-alpha are co-administered with the peptide vaccine. |
| 4863 | 11431420 | Complete protection from viral challenge is achieved only when the triple combination of exogenous cytokines granulocyte macrophage colony stimulating factor (GM-CSF), IL-12 and tumor necrosis factor (TNF)-alpha are co-administered with the peptide vaccine. |
| 4864 | 11431420 | Complete protection from viral challenge is achieved only when the triple combination of exogenous cytokines granulocyte macrophage colony stimulating factor (GM-CSF), IL-12 and tumor necrosis factor (TNF)-alpha are co-administered with the peptide vaccine. |
| 4865 | 11431420 | In vivo depletion of CD4(+) cells or immunization of IFN-gamma-deficient mice abrogates protection. |
| 4866 | 11431420 | In vivo depletion of CD4(+) cells or immunization of IFN-gamma-deficient mice abrogates protection. |
| 4867 | 11431420 | In vivo depletion of CD4(+) cells or immunization of IFN-gamma-deficient mice abrogates protection. |
| 4868 | 11431420 | In vivo depletion of CD4(+) cells or immunization of IFN-gamma-deficient mice abrogates protection. |
| 4869 | 11431420 | GM-CSF, IL-12 and TNF-alpha also synergize for the enhanced induction of CTL; however, adoptive transfer of a CD8(+) CTL line afforded only partial protection in this viral challenge model. |
| 4870 | 11431420 | GM-CSF, IL-12 and TNF-alpha also synergize for the enhanced induction of CTL; however, adoptive transfer of a CD8(+) CTL line afforded only partial protection in this viral challenge model. |
| 4871 | 11431420 | GM-CSF, IL-12 and TNF-alpha also synergize for the enhanced induction of CTL; however, adoptive transfer of a CD8(+) CTL line afforded only partial protection in this viral challenge model. |
| 4872 | 11431420 | GM-CSF, IL-12 and TNF-alpha also synergize for the enhanced induction of CTL; however, adoptive transfer of a CD8(+) CTL line afforded only partial protection in this viral challenge model. |
| 4873 | 11431420 | We further demonstrate synergy between IL-12 and the proinflammatory cytokine TNF-alpha in driving IFN-gamma production. |
| 4874 | 11431420 | We further demonstrate synergy between IL-12 and the proinflammatory cytokine TNF-alpha in driving IFN-gamma production. |
| 4875 | 11431420 | We further demonstrate synergy between IL-12 and the proinflammatory cytokine TNF-alpha in driving IFN-gamma production. |
| 4876 | 11431420 | We further demonstrate synergy between IL-12 and the proinflammatory cytokine TNF-alpha in driving IFN-gamma production. |
| 4877 | 11431420 | Thus, a combination of IL-12 and TNF-alpha is essential for the optimal development of T(h)1 responses and help for CTL induction in BALB/c mice, and is complemented by a third cytokine, GM-CSF, which enhances antigen presentation. |
| 4878 | 11431420 | Thus, a combination of IL-12 and TNF-alpha is essential for the optimal development of T(h)1 responses and help for CTL induction in BALB/c mice, and is complemented by a third cytokine, GM-CSF, which enhances antigen presentation. |
| 4879 | 11431420 | Thus, a combination of IL-12 and TNF-alpha is essential for the optimal development of T(h)1 responses and help for CTL induction in BALB/c mice, and is complemented by a third cytokine, GM-CSF, which enhances antigen presentation. |
| 4880 | 11431420 | Thus, a combination of IL-12 and TNF-alpha is essential for the optimal development of T(h)1 responses and help for CTL induction in BALB/c mice, and is complemented by a third cytokine, GM-CSF, which enhances antigen presentation. |
| 4881 | 11401973 | Both the parent and lpxA strains induced production of tumor necrosis factor alpha (TNF-alpha), interleukin-1alpha (IL-1alpha), and IL-6 in DCs, although the parent was the more potent stimulus. |
| 4882 | 11401973 | Both the parent and lpxA strains induced production of tumor necrosis factor alpha (TNF-alpha), interleukin-1alpha (IL-1alpha), and IL-6 in DCs, although the parent was the more potent stimulus. |
| 4883 | 11401973 | Compared to intact bacteria, purified LPS was a very poor inducer of IL-1alpha, IL-6, and TNF-alpha production and induced no detectable IL-12. |
| 4884 | 11401973 | Compared to intact bacteria, purified LPS was a very poor inducer of IL-1alpha, IL-6, and TNF-alpha production and induced no detectable IL-12. |
| 4885 | 11395208 | We evaluated antibody, cytokine (IFN-gamma, IL-5, TNF-alpha), and cytotoxic T lymphocyte (CTL) responses in chimpanzees immunized with monovalent or quadrivalent (HPV-6, -11, -16, -18) L1 virus-like particle (VLP) vaccines administered i.m. on aluminum hydroxyphosphate (alum) at weeks 0, 8 and 24. |
| 4886 | 11359441 | Cytokine gene expression of Th1 related cytokines (IL-12, IFNgamma and TNFalpha) in adult PBMC was more evident to live than to heat killed promastigotes. |
| 4887 | 11352664 | Monocyte-derived human macrophages and peripheral blood mononuclear cells infected with ebola virus secrete MIP-1alpha and TNF-alpha and inhibit poly-IC-induced IFN-alpha in vitro. |
| 4888 | 11352664 | Monocyte-derived human macrophages and peripheral blood mononuclear cells infected with ebola virus secrete MIP-1alpha and TNF-alpha and inhibit poly-IC-induced IFN-alpha in vitro. |
| 4889 | 11352664 | Monocyte-derived human macrophages and peripheral blood mononuclear cells infected with ebola virus secrete MIP-1alpha and TNF-alpha and inhibit poly-IC-induced IFN-alpha in vitro. |
| 4890 | 11352664 | We demonstrate that direct infection of human PBMC results in the induction of MCP-1, MIP-1alpha, RANTES, and TNF-alpha as early as 24 h p.i. in response to live virus. |
| 4891 | 11352664 | We demonstrate that direct infection of human PBMC results in the induction of MCP-1, MIP-1alpha, RANTES, and TNF-alpha as early as 24 h p.i. in response to live virus. |
| 4892 | 11352664 | We demonstrate that direct infection of human PBMC results in the induction of MCP-1, MIP-1alpha, RANTES, and TNF-alpha as early as 24 h p.i. in response to live virus. |
| 4893 | 11352664 | Monocyte-derived macrophages infected with live Ebola-virus secreted MIP-1alpha and TNF-alpha specifically while RANTES and MCP-1 were secreted by with both live or inactivated virus stimulation and do not require viral replication. |
| 4894 | 11352664 | Monocyte-derived macrophages infected with live Ebola-virus secreted MIP-1alpha and TNF-alpha specifically while RANTES and MCP-1 were secreted by with both live or inactivated virus stimulation and do not require viral replication. |
| 4895 | 11352664 | Monocyte-derived macrophages infected with live Ebola-virus secreted MIP-1alpha and TNF-alpha specifically while RANTES and MCP-1 were secreted by with both live or inactivated virus stimulation and do not require viral replication. |
| 4896 | 11352664 | Type I interferons (IFN-alpha and -beta), IL-1beta and IL-10, were not induced by Ebola virus. |
| 4897 | 11352664 | Type I interferons (IFN-alpha and -beta), IL-1beta and IL-10, were not induced by Ebola virus. |
| 4898 | 11352664 | Type I interferons (IFN-alpha and -beta), IL-1beta and IL-10, were not induced by Ebola virus. |
| 4899 | 11349067 | Influence of vector-encoded cytokines on anti-Salmonella immunity: divergent effects of interleukin-2 and tumor necrosis factor alpha. |
| 4900 | 11349067 | Influence of vector-encoded cytokines on anti-Salmonella immunity: divergent effects of interleukin-2 and tumor necrosis factor alpha. |
| 4901 | 11349067 | In the present study, interleukin-2 (IL-2)-expressing (GIDIL2) or tumor necrosis factor alpha (TNF-alpha)-expressing (GIDTNF) strains were compared with the parent strain (BRD509) for the effect of cytokines on anti-Salmonella immunity. |
| 4902 | 11349067 | In the present study, interleukin-2 (IL-2)-expressing (GIDIL2) or tumor necrosis factor alpha (TNF-alpha)-expressing (GIDTNF) strains were compared with the parent strain (BRD509) for the effect of cytokines on anti-Salmonella immunity. |
| 4903 | 11325600 | Influenza A virus infection results in the production of chemotactic (RANTES, MIP-1 alpha, MCP-1, MCP-3, and IP-10), pro-inflammatory (IL-1 beta, IL-6, IL-18, and TNF-alpha), and antiviral (IFN-alpha/beta) cytokines. |
| 4904 | 11325600 | Cytokine gene expression is associated with the activation of NF-kappa B, AP-1, STAT and IRF signal transducing molecules in influenza A virus-infected cells. |
| 4905 | 11325600 | IFN-alpha/beta also prolongs T cell survival, upregulates IL-12 and IL-18 receptor gene expression and together with IL-18 stimulates NK and T cell IFN-gamma production and the development of Th1-type immune response. |
| 4906 | 11319616 | Administration of subtumor regression dosage of TNF-alpha to mice with pre-existing parental tumors augments the vaccination effect of TNF gene-modified tumor through the induction of MHC class I molecule. |
| 4907 | 11313370 | DCs that had incorporated HPV16 VLPs produced proinflammatory cytokines IL-6 and TNF-alpha; however, the release of these cytokines was delayed relative to LPS activation. |
| 4908 | 11313269 | In this study, blasts from 40 patients with acute myeloid leukemia (AML) were cultured with combinations of granulocyte-macrophage colony-stimulating factor, interleukin 4, and tumor necrosis factor alpha, and development to DCs was assessed. |
| 4909 | 11313269 | After culture, cells from 24 samples exhibited morphological and immunophenotypic features of DCs, including expression of major histocompatibility complex class II, CD1a, CD83, and CD86, and were potent stimulators in an allogeneic mixed lymphocyte reaction (MLR). |
| 4910 | 11310844 | Although all strains stimulated secretion of TNF-alpha and IL-12 strongly, PhoPc induced significantly less IL-10 than the other three strains and as much as 10 times less IL-10 than heat-killed PhoPc, suggesting that this mutant suppressed the secretion of IL-10 by the DC. |
| 4911 | 11300490 | For CFC, whole blood was incubated overnight with antigen in the presence of costimulatory antibodies to CD28 and CD49d. |
| 4912 | 11300490 | For CFC, whole blood was incubated overnight with antigen in the presence of costimulatory antibodies to CD28 and CD49d. |
| 4913 | 11300490 | The blood was then treated with EDTA, erythrocytes were lysed, and leukocytes were fixed, permeabilized, and stained for intracellular cytokines [tumor necrosis factor-alpha (TNF-alpha) or IFN-gamma], CD4, and CD69. |
| 4914 | 11300490 | The blood was then treated with EDTA, erythrocytes were lysed, and leukocytes were fixed, permeabilized, and stained for intracellular cytokines [tumor necrosis factor-alpha (TNF-alpha) or IFN-gamma], CD4, and CD69. |
| 4915 | 11300490 | Most responses were detected with both TNF-alpha and IFN-gamma, but one patient's KLH response was detected only with TNF-alpha. |
| 4916 | 11300490 | Most responses were detected with both TNF-alpha and IFN-gamma, but one patient's KLH response was detected only with TNF-alpha. |
| 4917 | 11290810 | Targeting antigen in mature dendritic cells for simultaneous stimulation of CD4+ and CD8+ T cells. |
| 4918 | 11290810 | Immature DC (DCimm) capture, process, and present Ags to CD4(+) lymphocytes, which reciprocally activate DCimm through CD40, and the resulting mature DC (DCmat) loose phagocytic capacity, but acquire the ability to efficiently stimulate CD8(+) lymphocytes. |
| 4919 | 11290810 | Recombinant vaccinia viruses (rVV) provide a rapid, easy, and efficient method to introduce Ags into DC, but we observed that rVV infection of DCimm results in blockade of DC maturation in response to all activation signals, including CD40L, monocyte-conditioned medium, LPS, TNF-alpha, and poly(I:C), and failure to induce a CD8(+) response. |
| 4920 | 11290810 | These results demonstrate that despite rVV interference with DCimm maturation, a single targeting vector can deliver Ags to DCmat for the effective simultaneous stimulation of both CD4(+) and CD8(+) cells. |
| 4921 | 11265775 | In mice, MUCI conjugated to oxidized mannan (MUC1-mannan fusion protein [M-FP]) targets the mannose receptor and induces a high frequency of cytotoxic T lymphocytes and anti-tumor responses. |
| 4922 | 11265775 | Cellular responses (proliferation, cytotoxic T cells, or CD8 T cells secreting tumor necrosis factor-alpha alphand interferon-gamma in response to MUC1 stimulation in vitro) were found in 28% of the patients, which was similar to that seen without cyclophosphamide. |
| 4923 | 11264339 | Exposure to live dengue virus led to maturation and activation of both the infected and surrounding, uninfected DCs and stimulated production of tumor necrosis factor alpha (TNF-alpha) and alpha interferon (IFN-alpha). |
| 4924 | 11264339 | Activation of the dengue virus-infected DCs was blunted compared to the surrounding, uninfected DCs, and dengue virus infection induced low-level release of interleukin-12 p70 (IL-12 p70), a key cytokine in the development of cell-mediated immunity (CMI). |
| 4925 | 11264339 | Upon the addition of IFN-gamma, there was enhanced activation of dengue virus-infected DCs and enhanced dengue virus-induced IL-12 p70 release. |
| 4926 | 11257392 | We have demonstrated the ability of these organotypic cultures to be manipulated by altering the epithelial stratification with cytokines (interferon-gamma and tumor necrosis factor-alpha) and by integrating activated lymphocytes or dendritic cells into the in vitro formed epithelial sheet. |
| 4927 | 11243685 | The increased resistance that develops after primary infection/ vaccination requires T-cells cytokines such as IFNgamma TNFalpha and IL12 in addition to opsonising antibody. |
| 4928 | 11238615 | Oligodeoxynucleotides containing CpG motifs induce low levels of TNF-alpha in human B lymphocytes: possible adjuvants for Th1 responses. |
| 4929 | 11238615 | Oligodeoxynucleotides containing CpG motifs induce low levels of TNF-alpha in human B lymphocytes: possible adjuvants for Th1 responses. |
| 4930 | 11238615 | Oligodeoxynucleotides containing CpG motifs induce low levels of TNF-alpha in human B lymphocytes: possible adjuvants for Th1 responses. |
| 4931 | 11238615 | The goal of the present study was to evaluate the release of TNF-alpha in human cells by a CpG-ODN proven to induce Th1 immune responses in cells from atopic individuals and in mice. |
| 4932 | 11238615 | The goal of the present study was to evaluate the release of TNF-alpha in human cells by a CpG-ODN proven to induce Th1 immune responses in cells from atopic individuals and in mice. |
| 4933 | 11238615 | The goal of the present study was to evaluate the release of TNF-alpha in human cells by a CpG-ODN proven to induce Th1 immune responses in cells from atopic individuals and in mice. |
| 4934 | 11238615 | TNF-alpha contributed to the CpG-ODN-augmented proliferation and Ig synthesis in PBMC, but was not involved in IFN-gamma synthesis. |
| 4935 | 11238615 | TNF-alpha contributed to the CpG-ODN-augmented proliferation and Ig synthesis in PBMC, but was not involved in IFN-gamma synthesis. |
| 4936 | 11238615 | TNF-alpha contributed to the CpG-ODN-augmented proliferation and Ig synthesis in PBMC, but was not involved in IFN-gamma synthesis. |
| 4937 | 11237281 | TNFalpha antibodies correlated positively with viral load, (P = 0.013, r = 0.282), and CD8+ cell count (P = 0.03, r = 0.258), and inversely with CD4+ cell count (P = 0.003, r = - 0.246), percent CD4+ cells (P = 0.008, r = -0.306), and CD4 :CD8 ratio (P = 0.033, r = - 0.251). |
| 4938 | 11237281 | TNFalpha antibodies correlated positively with viral load, (P = 0.013, r = 0.282), and CD8+ cell count (P = 0.03, r = 0.258), and inversely with CD4+ cell count (P = 0.003, r = - 0.246), percent CD4+ cells (P = 0.008, r = -0.306), and CD4 :CD8 ratio (P = 0.033, r = - 0.251). |
| 4939 | 11237281 | TNFalpha antibodies also correlated positively with antibodies to peptides corresponding to the CD4 binding site of gp160 (P = 0.001, r = 0.384), the CD4 identity region (P = 0.016, r = 0.29), the V3 loop (P = 0.005, r = 0.34), and the amino terminus of Tat (P = 0.001, r = 0.395); TNFalpha antibodies also correlated positively with antibodies to Nef protein (P = 0.008, r = 0.302). |
| 4940 | 11237281 | TNFalpha antibodies also correlated positively with antibodies to peptides corresponding to the CD4 binding site of gp160 (P = 0.001, r = 0.384), the CD4 identity region (P = 0.016, r = 0.29), the V3 loop (P = 0.005, r = 0.34), and the amino terminus of Tat (P = 0.001, r = 0.395); TNFalpha antibodies also correlated positively with antibodies to Nef protein (P = 0.008, r = 0.302). |
| 4941 | 11228537 | Antitumor effects of the combination therapy with TNF-alpha gene-modified tumor cells and interleukin 12 in a melanoma model in mice. |
| 4942 | 11228537 | Antitumor effects of the combination therapy with TNF-alpha gene-modified tumor cells and interleukin 12 in a melanoma model in mice. |
| 4943 | 11228537 | Antitumor effects of the combination therapy with TNF-alpha gene-modified tumor cells and interleukin 12 in a melanoma model in mice. |
| 4944 | 11228537 | FACS analysis of parental B78 melanoma cells and its B78/TNF genetically modified variant showed that a proportion of cells of both cell lines expressed 87-1 (CD80) costimulatory molecule and that the expression of this molecule was increased during incubation with IFN-gamma. |
| 4945 | 11228537 | FACS analysis of parental B78 melanoma cells and its B78/TNF genetically modified variant showed that a proportion of cells of both cell lines expressed 87-1 (CD80) costimulatory molecule and that the expression of this molecule was increased during incubation with IFN-gamma. |
| 4946 | 11228537 | FACS analysis of parental B78 melanoma cells and its B78/TNF genetically modified variant showed that a proportion of cells of both cell lines expressed 87-1 (CD80) costimulatory molecule and that the expression of this molecule was increased during incubation with IFN-gamma. |
| 4947 | 11228537 | Moreover, IFN-gamma markedly augmented expression of major histocompatibility class (MHC) class I and II molecules on B78/TNF cells that were primarily MHC class I and II negative with no substantial effect on MHC-negative parental B78 melanoma. |
| 4948 | 11228537 | Moreover, IFN-gamma markedly augmented expression of major histocompatibility class (MHC) class I and II molecules on B78/TNF cells that were primarily MHC class I and II negative with no substantial effect on MHC-negative parental B78 melanoma. |
| 4949 | 11228537 | Moreover, IFN-gamma markedly augmented expression of major histocompatibility class (MHC) class I and II molecules on B78/TNF cells that were primarily MHC class I and II negative with no substantial effect on MHC-negative parental B78 melanoma. |
| 4950 | 11228537 | IFN-gamma also synergized in cytostatic/cytotoxic effects with TNF-alpha against B78 melanoma in vitro. |
| 4951 | 11228537 | IFN-gamma also synergized in cytostatic/cytotoxic effects with TNF-alpha against B78 melanoma in vitro. |
| 4952 | 11228537 | IFN-gamma also synergized in cytostatic/cytotoxic effects with TNF-alpha against B78 melanoma in vitro. |
| 4953 | 11228537 | The results suggest that, when used therapeutically, IL-12 and a vaccine containing TNF-alpha gene-transduced tumor cells may reciprocally augment their overall antitumor effectiveness by facilitating development of systemic antitumor immunity and by stimulating local effector mechanisms of the tumor destruction. |
| 4954 | 11228537 | The results suggest that, when used therapeutically, IL-12 and a vaccine containing TNF-alpha gene-transduced tumor cells may reciprocally augment their overall antitumor effectiveness by facilitating development of systemic antitumor immunity and by stimulating local effector mechanisms of the tumor destruction. |
| 4955 | 11228537 | The results suggest that, when used therapeutically, IL-12 and a vaccine containing TNF-alpha gene-transduced tumor cells may reciprocally augment their overall antitumor effectiveness by facilitating development of systemic antitumor immunity and by stimulating local effector mechanisms of the tumor destruction. |
| 4956 | 11228534 | IL-12 DNA administration induces long-lasting systemic IFN -gamma production, whereas IL-4 and TNF-alpha levels remained undetectable. |
| 4957 | 11220980 | The importance of gamma-interferon, tumor necrosis factor alpha, interleukin 12 and other mediators in ensuring the differentiation of (CD4(+) T-cells into Th1-helpers and cytotoxic T-lymphocytes in animals infected with L. monocytogenes is described in detail. |
| 4958 | 11182501 | Results show that pigs respond to CpG ODN by proliferating and secreting IL-6, IL-12 and TNF-alpha. |
| 4959 | 11179309 | Infection resulted in reduced production of tumor necrosis factor alpha (TNF-alpha) (P < 0.01), interleukin-12 (IL-12) (P < 0.05), IL-6 (P < 0.05), and IL-10 (P < 0.05), compared to infection with M. smegmatis vector (M. smegV). |
| 4960 | 11179309 | Infection resulted in reduced production of tumor necrosis factor alpha (TNF-alpha) (P < 0.01), interleukin-12 (IL-12) (P < 0.05), IL-6 (P < 0.05), and IL-10 (P < 0.05), compared to infection with M. smegmatis vector (M. smegV). |
| 4961 | 11179309 | Infection resulted in reduced production of tumor necrosis factor alpha (TNF-alpha) (P < 0.01), interleukin-12 (IL-12) (P < 0.05), IL-6 (P < 0.05), and IL-10 (P < 0.05), compared to infection with M. smegmatis vector (M. smegV). |
| 4962 | 11179309 | When MDM were infected with M. smegmatis expressing mutated forms of the 19-kDa lipoprotein, including non-O-glycosylated (M. smeg19NOG), nonsecreted (M. smeg19NS), and nonacylated (M. smeg19NA) variants, the reduced production of TNF-alpha or IL-12 was not observed. |
| 4963 | 11179309 | When MDM were infected with M. smegmatis expressing mutated forms of the 19-kDa lipoprotein, including non-O-glycosylated (M. smeg19NOG), nonsecreted (M. smeg19NS), and nonacylated (M. smeg19NA) variants, the reduced production of TNF-alpha or IL-12 was not observed. |
| 4964 | 11179309 | When MDM were infected with M. smegmatis expressing mutated forms of the 19-kDa lipoprotein, including non-O-glycosylated (M. smeg19NOG), nonsecreted (M. smeg19NS), and nonacylated (M. smeg19NA) variants, the reduced production of TNF-alpha or IL-12 was not observed. |
| 4965 | 11179309 | These results suggest that the diminished protection against challenge with M. tuberculosis seen in mice vaccinated with M. smegmatis expressing the 19-kDa lipoprotein is the result of reduced TNF-alpha and IL-12 production, possibly leading to reduced induction of T-cell activation. |
| 4966 | 11179309 | These results suggest that the diminished protection against challenge with M. tuberculosis seen in mice vaccinated with M. smegmatis expressing the 19-kDa lipoprotein is the result of reduced TNF-alpha and IL-12 production, possibly leading to reduced induction of T-cell activation. |
| 4967 | 11179309 | These results suggest that the diminished protection against challenge with M. tuberculosis seen in mice vaccinated with M. smegmatis expressing the 19-kDa lipoprotein is the result of reduced TNF-alpha and IL-12 production, possibly leading to reduced induction of T-cell activation. |
| 4968 | 11178547 | Endotoxins from gram negative bacteria are known to be potent inducers for the synthesis and the release of cytokines such as tumour necrosis factor (TNF) and interleukin 6 (IL-6). |
| 4969 | 11178547 | Endotoxins from gram negative bacteria are known to be potent inducers for the synthesis and the release of cytokines such as tumour necrosis factor (TNF) and interleukin 6 (IL-6). |
| 4970 | 11178547 | Endotoxins from gram negative bacteria are known to be potent inducers for the synthesis and the release of cytokines such as tumour necrosis factor (TNF) and interleukin 6 (IL-6). |
| 4971 | 11178547 | In connection with regular testing of vaccine lots we determine the release and the kinetic of TNF and IL-6 in piglets after immunisation with different vaccines containing endotoxin. |
| 4972 | 11178547 | In connection with regular testing of vaccine lots we determine the release and the kinetic of TNF and IL-6 in piglets after immunisation with different vaccines containing endotoxin. |
| 4973 | 11178547 | In connection with regular testing of vaccine lots we determine the release and the kinetic of TNF and IL-6 in piglets after immunisation with different vaccines containing endotoxin. |
| 4974 | 11178547 | TNF peaked in plasma after one hour, IL-6 peaked between two and four hours p.appl. |
| 4975 | 11178547 | TNF peaked in plasma after one hour, IL-6 peaked between two and four hours p.appl. |
| 4976 | 11178547 | TNF peaked in plasma after one hour, IL-6 peaked between two and four hours p.appl. |
| 4977 | 11166900 | The effect of aluminum-containing adjuvants on the systemic response of Sprague-Dawley rats to a 15 microg/kg subcutaneous dose of endotoxin was determined by measuring the serum concentration of tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6). |
| 4978 | 11166900 | The effect of aluminum-containing adjuvants on the systemic response of Sprague-Dawley rats to a 15 microg/kg subcutaneous dose of endotoxin was determined by measuring the serum concentration of tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6). |
| 4979 | 11166900 | The effect of aluminum-containing adjuvants on the systemic response of Sprague-Dawley rats to a 15 microg/kg subcutaneous dose of endotoxin was determined by measuring the serum concentration of tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6). |
| 4980 | 11166900 | TNF-alpha and IL-6 were observed in the group which received an endotoxin solution or endotoxin and aluminum phosphate adjuvant. |
| 4981 | 11166900 | TNF-alpha and IL-6 were observed in the group which received an endotoxin solution or endotoxin and aluminum phosphate adjuvant. |
| 4982 | 11166900 | TNF-alpha and IL-6 were observed in the group which received an endotoxin solution or endotoxin and aluminum phosphate adjuvant. |
| 4983 | 11166900 | No TNF-alpha or IL-6 was detected in the group that received endotoxin and aluminum hydroxide adjuvant. |
| 4984 | 11166900 | No TNF-alpha or IL-6 was detected in the group that received endotoxin and aluminum hydroxide adjuvant. |
| 4985 | 11166900 | No TNF-alpha or IL-6 was detected in the group that received endotoxin and aluminum hydroxide adjuvant. |
| 4986 | 11163460 | Influenza A virus-infected respiratory epithelial cells produce limited amounts of chemokines (RANTES, MCP-1, IL-8) and IFN-alpha/beta, whereas monocytes/macrophages readily produce chemokines such as RANTES, MIP-1alpha, MCP-1, MCP-3, IP-10 and cytokines TNF-alpha, IL-1beta, IL-6, IL-18 and IFN-alpha/beta. |
| 4987 | 11150544 | We demonstrated significant correlations of cytokine mRNA and protein expression for TNF alpha, IL10, and IFN gamma. |
| 4988 | 11150544 | Expression of IL2 mRNA at 16 h was correlated with proliferation indices at 96 h whereas IL4 mRNA levels were negatively correlated. |
| 4989 | 11145848 | We have studied the ability of this OMV vaccine preparation to induce secretion of pro-inflammatory cytokines, tumour necrosis factor alpha (TNF-alpha), interleukin 1beta (IL-1beta), interleukin 6 (IL-6), interleukin 8 (IL-8) and anti-inflammatory cytokines, interleukin 4 (IL-4), interleukin 10 (IL-10) and interleukin 13 (IL-13) in a human whole blood model. |
| 4990 | 11145848 | We have studied the ability of this OMV vaccine preparation to induce secretion of pro-inflammatory cytokines, tumour necrosis factor alpha (TNF-alpha), interleukin 1beta (IL-1beta), interleukin 6 (IL-6), interleukin 8 (IL-8) and anti-inflammatory cytokines, interleukin 4 (IL-4), interleukin 10 (IL-10) and interleukin 13 (IL-13) in a human whole blood model. |
| 4991 | 11145848 | Plasma levels of TNF-alpha, IL-1beta, IL-6 and IL-8 were massively increased; mean peak levels of TNF-alpha 44 696+/-7764, IL-1beta 38 043+/-5411, IL-6 10 057+/-1619 and IL-8 30 449+/-5397 pg/ml were obtained with an OMV-LPS concentration of 1 microg/ml; corresponding levels in control plasmas were below the detection limit of the assay. |
| 4992 | 11145848 | Plasma levels of TNF-alpha, IL-1beta, IL-6 and IL-8 were massively increased; mean peak levels of TNF-alpha 44 696+/-7764, IL-1beta 38 043+/-5411, IL-6 10 057+/-1619 and IL-8 30 449+/-5397 pg/ml were obtained with an OMV-LPS concentration of 1 microg/ml; corresponding levels in control plasmas were below the detection limit of the assay. |
| 4993 | 11145848 | OMV-LPS did not induce release of IL-4 and IL-13 in doses from 0.001-10 microg/ml. |
| 4994 | 11145848 | OMV-LPS did not induce release of IL-4 and IL-13 in doses from 0.001-10 microg/ml. |
| 4995 | 11145691 | M2(82-90)-specific CD8(+) T cells were detected by IFN-gamma enzyme-linked immunospot and (51)Cr release assay in local and systemic lymph nodes, and their induction was dependent on the use of a mucosal adjuvant. |
| 4996 | 11145691 | Depletion of IFN-gamma did, however, reduce the concentration of TNF detected in lung homogenates of challenged mice and largely prevented the weight loss associated with CTL-mediated viral clearance. |
| 4997 | 11128522 | Culture supernatants of splenocytes from immune DBA/2 mice, which were stimulated with crude C. ruminantium antigens or recombinant major antigenic proteins 1 or 2, contained significant levels of interferon (IFN)-gamma and interleukin (IL)-6, but insignificant levels of IL-1alpha, IL-2, IL-4, IL-5, IL-10, IL-12, tumor necrosis factor-alpha (TNF), and nitric oxide. |
| 4998 | 11123429 | Synergistic suppressive effect of double transfection of tumor necrosis factor-alpha and interleukin 12 genes on tumorigenicity of Meth-A cells. |
| 4999 | 11123429 | Synergistic suppressive effect of double transfection of tumor necrosis factor-alpha and interleukin 12 genes on tumorigenicity of Meth-A cells. |
| 5000 | 11123429 | Synergistic suppressive effect of double transfection of tumor necrosis factor-alpha and interleukin 12 genes on tumorigenicity of Meth-A cells. |
| 5001 | 11123429 | Tumor necrosis factor-alpha (TNF-alpha) and interleukin 12 (IL-12), both potent antitumor cytokines, are known to be involved in the host's antitumor immune surveillance in tumor bearers, via different mechanisms. |
| 5002 | 11123429 | Tumor necrosis factor-alpha (TNF-alpha) and interleukin 12 (IL-12), both potent antitumor cytokines, are known to be involved in the host's antitumor immune surveillance in tumor bearers, via different mechanisms. |
| 5003 | 11123429 | Tumor necrosis factor-alpha (TNF-alpha) and interleukin 12 (IL-12), both potent antitumor cytokines, are known to be involved in the host's antitumor immune surveillance in tumor bearers, via different mechanisms. |
| 5004 | 11123429 | Thus, double transfection of TNF-alpha and IL-12 genes was considered to bring about synergistic suppressive effects on the tumorigenicity of transfectants through the activation of killer cells by produced cytokines and the enhancement of expression of MHC class I, II and B7.1 molecules. |
| 5005 | 11123429 | Thus, double transfection of TNF-alpha and IL-12 genes was considered to bring about synergistic suppressive effects on the tumorigenicity of transfectants through the activation of killer cells by produced cytokines and the enhancement of expression of MHC class I, II and B7.1 molecules. |
| 5006 | 11123429 | Thus, double transfection of TNF-alpha and IL-12 genes was considered to bring about synergistic suppressive effects on the tumorigenicity of transfectants through the activation of killer cells by produced cytokines and the enhancement of expression of MHC class I, II and B7.1 molecules. |
| 5007 | 11122234 | Tumour necrosis factor-alpha (TNF-alpha), IL-1alpha and IL-6 production by human monocytes in response to a clinical strain of the Gram-negative encapsulated bacteria Neisseria meningitidis and an isogenic lpxA- strain deficient in LPS was investigated. |
| 5008 | 11122109 | In these five patients, detection of cytokines by real-time reverse transcription polymerase chain reaction (RT-PCR) revealed that granulocyte-macrophage colony-stimulating factor (GM-CSF) was the most abundant cytokine gene expressed by the T cells that recognized the autologous tumour B cells. |
| 5009 | 11122109 | Other activated cytokine genes were gamma-interferon (IFN), interleukin (IL)-2 and tumour necrosis factor (TNF)-alpha, but not IL-4. |
| 5010 | 11122109 | CD80 and CD54 were relatively downregulated on the native tumour B cells compared with control normal B cells. |
| 5011 | 11122109 | CD80 and CD54 monoclonal antibodies inhibited the specific T-cell DNA synthesis proliferation. |
| 5012 | 11122109 | The specific cytokine gene expression could be found in isolated CD4, as well as CD8, T-cell subsets. |
| 5013 | 11122109 | This study demonstrated the presence of a potential natural specific CD4, as well as a CD8 type 1 T-cell immunity against the leukaemic CLL tumour B cells in CLL. |
| 5014 | 11106231 | Induction of cytolytic activity at priming was enhanced in responders by tumor necrosis factor-alpha and interleukin 12 but not in the nonresponders. |
| 5015 | 11086086 | Identification of major epitopes of Mycobacterium tuberculosis AG85B that are recognized by HLA-A*0201-restricted CD8+ T cells in HLA-transgenic mice and humans. |
| 5016 | 11086086 | Although several nonprotein ligands have been identified for CD1-restricted CD8(+) CTLs, epitopes for classical MHC class I-restricted CD8(+) T cells, which most likely represent a majority among CD8(+) T cells, have remained ill defined. |
| 5017 | 11086086 | In this study, we demonstrate the presence of HLA class I-restricted, CD8(+) T cells against Ag85B of M. tuberculosis in HLA-A2/K(b) transgenic mice and HLA-A*0201(+) humans. |
| 5018 | 11086086 | Moreover, two immunodominant Ag85 peptide epitopes for HLA-A*0201-restricted, M. tuberculosis-reactive CD8(+) CTLs were identified. |
| 5019 | 11086086 | These CD8(+) T cells produced IFN-gamma and TNF-alpha and recognized Ag-pulsed or bacillus Calmette-Guérin-infected, HLA-A*0201-positive, but not HLA-A*0201-negative or uninfected human macrophages. |
| 5020 | 11086086 | Using fluorescent peptide/HLA-A*0201 tetramers, Ag85-specific CD8(+) T cells could be visualized in bacillus Calmette-Guérin-responsive, HLA-A*0201(+) individuals. |
| 5021 | 11086086 | Collectively, our results demonstrate the presence of HLA class I-restricted CD8(+) CTL against a major Ag of M. tuberculosis and identify Ag85B epitopes that are strongly recognized by HLA-A*0201-restricted CD8(+) T cells in humans and mice. |
| 5022 | 11083779 | To understand the mechanism(s) of IL-10 action during early infection, when innate immunity expressed chiefly by skin macrophages is key, we investigated the effect of exogenous and endogenous IL-10 on the production of the macrophage-derived cytokines IL-6, IL-1beta, IL-12, and tumor necrosis factor alpha (TNF-alpha). |
| 5023 | 11083779 | To understand the mechanism(s) of IL-10 action during early infection, when innate immunity expressed chiefly by skin macrophages is key, we investigated the effect of exogenous and endogenous IL-10 on the production of the macrophage-derived cytokines IL-6, IL-1beta, IL-12, and tumor necrosis factor alpha (TNF-alpha). |
| 5024 | 11083779 | To understand the mechanism(s) of IL-10 action during early infection, when innate immunity expressed chiefly by skin macrophages is key, we investigated the effect of exogenous and endogenous IL-10 on the production of the macrophage-derived cytokines IL-6, IL-1beta, IL-12, and tumor necrosis factor alpha (TNF-alpha). |
| 5025 | 11083779 | The inhibition of endogenous IL-10 function by anti-IL-10 antibody reduced the production of IL-12 and IL-6 but not that of IL-1beta and TNF-alpha. |
| 5026 | 11083779 | The inhibition of endogenous IL-10 function by anti-IL-10 antibody reduced the production of IL-12 and IL-6 but not that of IL-1beta and TNF-alpha. |
| 5027 | 11083779 | The inhibition of endogenous IL-10 function by anti-IL-10 antibody reduced the production of IL-12 and IL-6 but not that of IL-1beta and TNF-alpha. |
| 5028 | 11083779 | TNF-alpha was produced prior to, and IL-beta was produced at the same time as, IL-10, whereas IL-6 and IL-12 were produced later. |
| 5029 | 11083779 | TNF-alpha was produced prior to, and IL-beta was produced at the same time as, IL-10, whereas IL-6 and IL-12 were produced later. |
| 5030 | 11083779 | TNF-alpha was produced prior to, and IL-beta was produced at the same time as, IL-10, whereas IL-6 and IL-12 were produced later. |
| 5031 | 11075550 | Expression of interleukin-1 (IL-1), IL-6, IL-12 and tumour necrosis factor-alpha (TNF-alpha), but not of IL-10, was detected in INMD-stimulated alveolar macrophages. |
| 5032 | 11075550 | Stimulated PBMC expressed IL-1, IL-2, IL-4, IL-6, IL-10 and IL-12 and secreted interferon-gamma (IFN-gamma). |
| 5033 | 11042280 | We generated monocyte-derived DC from leukapheresis products by using GM-CSF and IL-4 and showed that amongst several known maturation stimuli the cocktail consisting of TNF-alpha+IL-1 beta+IL-6+PGE(2) achieved the highest survival of mature DC. |
| 5034 | 11042280 | The addition of CD40L or TRANCE/RANKL further improved DC survival. |
| 5035 | 11034366 | However, the conjugation of consecutive deoxyriboguanosine residues, called a dG run, at the 3' terminus of phosphodiester CpG ODNs significantly enhanced TNF-alpha and IL-12 production from mouse splenic dendritic cells (DCs). |
| 5036 | 11029527 | The growth rates of both vaccines in murine macrophages were the same, however, Onco-BCG induced stronger and longer-lasting secretion of TNF-alpha, IL-6 and nitric oxide. |
| 5037 | 11029527 | Onco-vaccine was also more potent in inducing NF-kappaB p65/p50 DNA-binding activity whilst in ID-BCG-infected cells the activity was transient and then gradually replaced by the transcriptionally inactive homodimer p50/p50. |
| 5038 | 11015437 | B lymphocyte stimulator (BLyS) is a newly identified monocyte-specific TNF family cytokine. |
| 5039 | 11015437 | BLyS acts on primary splenic B cells autonomously, and directly cooperates with CD40 ligand (CD40L) in B cell activation in vitro by protecting replicating B cells from apoptosis. |
| 5040 | 11015437 | Attenuation of apoptosis by BLyS correlates with changes in the ratios between Bcl-2 family proteins in favor of cell survival, predominantly by reducing the proapoptotic Bak and increasing its prosurvival partners, Bcl-2 and Bcl-xL. |
| 5041 | 11015437 | In either resting or CD40L-activated B cells, the NF-kappaB transcription factors RelB and p50 are specifically activated, suggesting that they may mediate BLyS signals for B cell survival. |
| 5042 | 11015437 | The ability of BLyS to increase B cell survival indiscriminately, at either a resting or activated state, and to cooperate with CD40L, further suggests that attenuation of apoptosis underlies BLyS enhancement of polyclonal autoimmunity as well as the physiologic humoral immune response. |
| 5043 | 11012616 | It has been detected in rheumatoid arthritis (RA) synovial membrane and found to stimulate the production of the proinflammatory cytokines IL-6, IL-8, tumour necrosis factor-alpha (TNF-alpha) and granulocyte-macrophage colony-stimulating factor (GM-CSF) in vitro. |
| 5044 | 11012616 | It has been detected in rheumatoid arthritis (RA) synovial membrane and found to stimulate the production of the proinflammatory cytokines IL-6, IL-8, tumour necrosis factor-alpha (TNF-alpha) and granulocyte-macrophage colony-stimulating factor (GM-CSF) in vitro. |
| 5045 | 11012616 | It has been detected in rheumatoid arthritis (RA) synovial membrane and found to stimulate the production of the proinflammatory cytokines IL-6, IL-8, tumour necrosis factor-alpha (TNF-alpha) and granulocyte-macrophage colony-stimulating factor (GM-CSF) in vitro. |
| 5046 | 11012616 | We therefore investigated the in vitro IL-17 response to a variety of mitogens and antigens, and compared the IL-17 response to interferon-gamma (IFN-gamma), IL-4, IL-10 and TNF-alpha. |
| 5047 | 11012616 | We therefore investigated the in vitro IL-17 response to a variety of mitogens and antigens, and compared the IL-17 response to interferon-gamma (IFN-gamma), IL-4, IL-10 and TNF-alpha. |
| 5048 | 11012616 | We therefore investigated the in vitro IL-17 response to a variety of mitogens and antigens, and compared the IL-17 response to interferon-gamma (IFN-gamma), IL-4, IL-10 and TNF-alpha. |
| 5049 | 11012616 | The antigens TT and PPD significantly increased IL-17 mRNA expression over time, but failed to have such an effect at the protein level. |
| 5050 | 11012616 | The antigens TT and PPD significantly increased IL-17 mRNA expression over time, but failed to have such an effect at the protein level. |
| 5051 | 11012616 | The antigens TT and PPD significantly increased IL-17 mRNA expression over time, but failed to have such an effect at the protein level. |
| 5052 | 11012616 | IL-17 production did not correlate with either the type-1 cytokine IFN-gamma or TNF-alpha or the type-2 cytokine IL-4 or IL-10 at either the mRNA or protein level. |
| 5053 | 11012616 | IL-17 production did not correlate with either the type-1 cytokine IFN-gamma or TNF-alpha or the type-2 cytokine IL-4 or IL-10 at either the mRNA or protein level. |
| 5054 | 11012616 | IL-17 production did not correlate with either the type-1 cytokine IFN-gamma or TNF-alpha or the type-2 cytokine IL-4 or IL-10 at either the mRNA or protein level. |
| 5055 | 11006019 | R-848 and imiquimod belong to a class of immune response modifiers that are potent inducers of cytokines, including IFN-alpha, TNF-alpha, IL-12, and IFN-gamma. |
| 5056 | 11006019 | R-848 and imiquimod belong to a class of immune response modifiers that are potent inducers of cytokines, including IFN-alpha, TNF-alpha, IL-12, and IFN-gamma. |
| 5057 | 11006019 | The mechanism of R-848's adjuvant activity is linked to cytokine production, where increases in IgG2a levels are associated with IFN-alpha, TNF-alpha, IL-12, and IFN-gamma induction, and decreases in IgE levels are associated with IFN-alpha and TNF-alpha. |
| 5058 | 11006019 | The mechanism of R-848's adjuvant activity is linked to cytokine production, where increases in IgG2a levels are associated with IFN-alpha, TNF-alpha, IL-12, and IFN-gamma induction, and decreases in IgE levels are associated with IFN-alpha and TNF-alpha. |
| 5059 | 10975678 | Systemic IL-3 vaccine treatment increased intratumoral levels of intercellular adhesion molecule-1, Mac-1, EB22/5.3, tumor necrosis factor-alpha, and IL-1 mRNA in irradiated tumors, indicating that cellular infiltration was part of the response. |
| 5060 | 10974020 | This study used naked DNA vaccination to induce breakdown of tolerance to self and thus elicit immunological memory to native, membrane-bound Fas ligand (FasL). |
| 5061 | 10974020 | FasL-specific autoantibodies isolated from protected animals differentially downregulated the in vitro production of TNF-alpha, but not IFN-gamma, by cultured T cells. |
| 5062 | 10959433 | Several cytokines, including interleukin- (IL-) 1 beta, IL-6, IL-8, tumour necrosis factor- (TNF-) alpha and interferon- (IFN-) gamma are known to be important to elicit the acute phase response and allow the accumulation of leukocytes at the site of infection. |
| 5063 | 10953979 | Upon culture with granulocyte-macrophage colony-stimulating factor (GM-CSF) plus interleukin-4 (IL-4) plus tumor necrosis factor alpha (TNFalpha), CMML cells develop DC morphology and acquire the phenotypic characteristics of DCs. |
| 5064 | 10950804 | Reduced interleukin-12 and transforming growth factor-beta1 in severe childhood malaria: relationship of cytokine balance with disease severity. |
| 5065 | 10950804 | Reduced interleukin-12 and transforming growth factor-beta1 in severe childhood malaria: relationship of cytokine balance with disease severity. |
| 5066 | 10950804 | Reduced interleukin-12 and transforming growth factor-beta1 in severe childhood malaria: relationship of cytokine balance with disease severity. |
| 5067 | 10950804 | IL-12 and TGF-beta1 were significantly lower, whereas tumor necrosis factor (TNF)-alpha and IL-10 were significantly higher in children with severe malaria. |
| 5068 | 10950804 | IL-12 and TGF-beta1 were significantly lower, whereas tumor necrosis factor (TNF)-alpha and IL-10 were significantly higher in children with severe malaria. |
| 5069 | 10950804 | IL-12 and TGF-beta1 were significantly lower, whereas tumor necrosis factor (TNF)-alpha and IL-10 were significantly higher in children with severe malaria. |
| 5070 | 10950804 | The ratios of TGF-beta1/IL-12 and IL-10/IL-12 were significantly higher in the severe, compared with the mild, malaria group. |
| 5071 | 10950804 | The ratios of TGF-beta1/IL-12 and IL-10/IL-12 were significantly higher in the severe, compared with the mild, malaria group. |
| 5072 | 10950804 | The ratios of TGF-beta1/IL-12 and IL-10/IL-12 were significantly higher in the severe, compared with the mild, malaria group. |
| 5073 | 10950804 | In contrast, ratios of TGF-beta1/TNF-alpha and IL-10/TNF-alpha were significantly lower in the severe malaria group. |
| 5074 | 10950804 | In contrast, ratios of TGF-beta1/TNF-alpha and IL-10/TNF-alpha were significantly lower in the severe malaria group. |
| 5075 | 10950804 | In contrast, ratios of TGF-beta1/TNF-alpha and IL-10/TNF-alpha were significantly lower in the severe malaria group. |
| 5076 | 10950804 | These results suggest that the inflammatory cascade in severe malaria is characterized by suppression of the protective effects of TGF-beta1 and IL-12, and that overproduction of TNF-alpha may promote deleterious effects, such as severe anemia. |
| 5077 | 10950804 | These results suggest that the inflammatory cascade in severe malaria is characterized by suppression of the protective effects of TGF-beta1 and IL-12, and that overproduction of TNF-alpha may promote deleterious effects, such as severe anemia. |
| 5078 | 10950804 | These results suggest that the inflammatory cascade in severe malaria is characterized by suppression of the protective effects of TGF-beta1 and IL-12, and that overproduction of TNF-alpha may promote deleterious effects, such as severe anemia. |
| 5079 | 10950786 | Restricted mycobacterial growth was associated with significantly higher production of tumor necrosis factor (TNF)-alpha and interferon (IFN)-gamma (P=.01 and.004, respectively). |
| 5080 | 10950786 | Restricted mycobacterial growth was associated with significantly higher production of tumor necrosis factor (TNF)-alpha and interferon (IFN)-gamma (P=.01 and.004, respectively). |
| 5081 | 10950786 | Inhibition of the TNF-alpha and IFN-gamma response pathways by neutralizing monoclonal antibodies increased mycobacterial growth in whole blood. |
| 5082 | 10950786 | Inhibition of the TNF-alpha and IFN-gamma response pathways by neutralizing monoclonal antibodies increased mycobacterial growth in whole blood. |
| 5083 | 10948159 | Consistent with the latter finding, non-ADP-ribosylating exotoxins, including an oligonucleotide DNA sequence, as well as several cytokines (interleukin-1beta [IL-1beta] fragment, IL-2, IL-12, and tumor necrosis factor alpha) and lipopolysaccharide also elicited detectable anti-DTx immunoglobulin G titers in the immunized mice. |
| 5084 | 10947856 | The interaction between IFN-gamma-secreting CD4+ T cells and macrophages has long been established as integral in the protective immune response against tuberculosis. |
| 5085 | 10947856 | CD8+ T cells can produce the protective cytokines IFN-gamma and TNF-alpha in addition to their classical cytolytic functions. |
| 5086 | 10930689 | The most dramatic immune responses occurred in draining lymph nodes 24 h following vaccination with increased levels of activated B cells and T cells of both CD4(+) and CD8(+) subtypes. |
| 5087 | 10930689 | Cytokine mRNA was quantified by RT-PCR and revealed production of the Th1 cytokine IFN-gamma and the inflammatory cytokine TNF-alpha, whereas the Th2 cytokine IL4 was not detected above control levels at any of the time points studied. |
| 5088 | 10929063 | In BALB/c mice infected via the trachea with Mycobacterium tuberculosis H37Rv there is an initial phase of partial resistance dominated by type 1 cytokines plus tumour necrosis factor-alpha (TNF-alpha) and interleukin-1 (IL-1), followed by a phase of progressive disease. |
| 5089 | 10929063 | In BALB/c mice infected via the trachea with Mycobacterium tuberculosis H37Rv there is an initial phase of partial resistance dominated by type 1 cytokines plus tumour necrosis factor-alpha (TNF-alpha) and interleukin-1 (IL-1), followed by a phase of progressive disease. |
| 5090 | 10929063 | This progressive phase is accompanied by increasing expression of IL-4, and diminished expression of IL-1 and TNF-alpha. |
| 5091 | 10929063 | This progressive phase is accompanied by increasing expression of IL-4, and diminished expression of IL-1 and TNF-alpha. |
| 5092 | 10926544 | Surfactant-associated protein A (SP-A) is involved in surfactant homeostasis and host defense in the lung. |
| 5093 | 10926544 | TNF-alpha and nitric oxide production induced by BCG were enhanced by SP-A. |
| 5094 | 10926544 | In addition, SP-A enhanced the BCG-induced increase in the level of inducible nitric oxide synthase protein. |
| 5095 | 10926544 | Addition of antibodies directed against SPR210, a specific macrophage SP-A receptor, inhibited the SP-A-enhanced mediator production. |
| 5096 | 10909420 | We recently used a modification of gene therapy (naked DNA vaccination) to induce immunological memory against self-pro-inflammatory chemokines such as macrophage inflammatory protein-1 alpha or monocyte chemoattractant protein-1, and against the pro-inflammatory cytokine tumor necrosis factor-alpha. |
| 5097 | 10899844 | Adaptive immunity against Listeria monocytogenes in the absence of type I tumor necrosis factor receptor p55. |
| 5098 | 10899844 | Tumor necrosis factor (TNF) and the type I TNF receptor (TNFRI), p55, are critical for resistance against primary infections with the intracellular bacterial pathogen Listeria monocytogenes. |
| 5099 | 10889508 | Involvement of the apoptosis-mediating CD95/CD95 ligand system in MS has been demonstrated. |
| 5100 | 10889508 | Here, we report that (auto)antigen-specific human T cells are not killed in vitro by soluble TNF-related apoptosis-inducing ligand (TRAIL) although expressing death-inducing receptors, TRAIL receptor 1 (TRAIL-R1) and TRAIL-R2. |
| 5101 | 10889508 | The (auto)antigen-specific T cells were also resistant to specific TRAIL-R1/TRAIL-R2-directed induction of apoptosis, indicating that coexpression of the truncated TRAIL-R3 and TRAIL-R4 in these T cells is not responsible for the observed resistance. |
| 5102 | 10889508 | In contrast to CD95, the role of TRAIL receptors in MS might not involve regulation of T cell vulnerability. |
| 5103 | 10881678 | At the onset of rash, remarkable lymphopenia had already occurred in all measles cases with reduction in cell numbers of CD4+ T cells, CD8+ T cells, B cells, neutrophils, and monocytes. |
| 5104 | 10881678 | Apoptosis-associated molecules such as CD95(Fas) and TNF-related apoptosis-inducing ligand-receptor (TRAIL-R) were highly expressed on the cell surface of most surviving non-infected lymphocytes, and DNA fragmentation was also observed upon incubation in vitro. |
| 5105 | 10873778 | In this study, cytokine flow cytometry (CFC) was used to quantify SIV-specific CD8+ antigen-reactive T cells in macaques infected with SIV. |
| 5106 | 10873778 | We found a strong correlation (r = 0.96, P < 0.001) between CD8+ antigen-reactive T cells stained with the Mamu-A*01 p11C, C-M tetramer and production of intracellular TNF-alpha in the CFC assay. |
| 5107 | 10866836 | It has been proposed that the more aggressive liver disease observed in individuals infected with HAV in addition to chronic HBV/HCV is a result of the induction of interferon (IFN)-alpha during acute HAV infection. |
| 5108 | 10866836 | Alternatively, HAV may indirectly stimulate the T helper 1 (Th1)-type cytokine responses, such as interleukin (IL)-2, IFN-gamma and tumour necrosis factor (TNF)-alpha, which directly promote the antiviral CTL response. |
| 5109 | 10845721 | Chimeric forms of IL-4 with the type I transmembrane protein CD4 or type II transmembrane protein TNF were designed to express IL-4 in opposite orientations on the tumor cell surface. |
| 5110 | 10845721 | Chimeric forms of IL-4 with the type I transmembrane protein CD4 or type II transmembrane protein TNF were designed to express IL-4 in opposite orientations on the tumor cell surface. |
| 5111 | 10845721 | Expression of the IL-4/TNF chimeric protein on MethA cells elicited antitumor immunity and protected from MethA tumor challenge. |
| 5112 | 10845721 | Expression of the IL-4/TNF chimeric protein on MethA cells elicited antitumor immunity and protected from MethA tumor challenge. |
| 5113 | 10849370 | CD4+ T cells of schistosomiasis naturally resistant individuals living in an endemic area produce interferon-gamma and tumour necrosis factor-alpha in response to the recombinant 14KDA Schistosoma mansoni fatty acid-binding protein. |
| 5114 | 10849370 | CD4+ T cells of schistosomiasis naturally resistant individuals living in an endemic area produce interferon-gamma and tumour necrosis factor-alpha in response to the recombinant 14KDA Schistosoma mansoni fatty acid-binding protein. |
| 5115 | 10849370 | CD4+ T cells of schistosomiasis naturally resistant individuals living in an endemic area produce interferon-gamma and tumour necrosis factor-alpha in response to the recombinant 14KDA Schistosoma mansoni fatty acid-binding protein. |
| 5116 | 10849370 | Regarding the cytokines produced, the levels of interleukin (IL)-5 and IL-10, known as Th2 cytokines, were not statistically different among all groups studied. |
| 5117 | 10849370 | Regarding the cytokines produced, the levels of interleukin (IL)-5 and IL-10, known as Th2 cytokines, were not statistically different among all groups studied. |
| 5118 | 10849370 | Regarding the cytokines produced, the levels of interleukin (IL)-5 and IL-10, known as Th2 cytokines, were not statistically different among all groups studied. |
| 5119 | 10849370 | In contrast, interferon (IFN)-gamma and tumour necrosis factor (TNF)-alpha were produced in significantly higher amounts by PBMC of EN individuals following rSm14 stimulation. |
| 5120 | 10849370 | In contrast, interferon (IFN)-gamma and tumour necrosis factor (TNF)-alpha were produced in significantly higher amounts by PBMC of EN individuals following rSm14 stimulation. |
| 5121 | 10849370 | In contrast, interferon (IFN)-gamma and tumour necrosis factor (TNF)-alpha were produced in significantly higher amounts by PBMC of EN individuals following rSm14 stimulation. |
| 5122 | 10849370 | Additionally, we have determined by flow cytometry that CD4+ T cells from these individuals are the main lymphocyte subpopulation producing IFN-gamma and TNF-alpha. |
| 5123 | 10849370 | Additionally, we have determined by flow cytometry that CD4+ T cells from these individuals are the main lymphocyte subpopulation producing IFN-gamma and TNF-alpha. |
| 5124 | 10849370 | Additionally, we have determined by flow cytometry that CD4+ T cells from these individuals are the main lymphocyte subpopulation producing IFN-gamma and TNF-alpha. |
| 5125 | 10849370 | Exogenous IL-10 suppressed T-cell proliferation and neutralization of endogenous IL-10 restored lymphocyte activation and enhanced IFN-gamma and TNF-alpha production in chronically infected patients. |
| 5126 | 10849370 | Exogenous IL-10 suppressed T-cell proliferation and neutralization of endogenous IL-10 restored lymphocyte activation and enhanced IFN-gamma and TNF-alpha production in chronically infected patients. |
| 5127 | 10849370 | Exogenous IL-10 suppressed T-cell proliferation and neutralization of endogenous IL-10 restored lymphocyte activation and enhanced IFN-gamma and TNF-alpha production in chronically infected patients. |
| 5128 | 10849370 | This study demonstrated that IL-10 is an important cytokine down-regulating T-cell responses in chronic schistosomiasis, whereas lymphocyte proliferation in the uninfected resistant group is dependent on IFN-gamma. |
| 5129 | 10849370 | This study demonstrated that IL-10 is an important cytokine down-regulating T-cell responses in chronic schistosomiasis, whereas lymphocyte proliferation in the uninfected resistant group is dependent on IFN-gamma. |
| 5130 | 10849370 | This study demonstrated that IL-10 is an important cytokine down-regulating T-cell responses in chronic schistosomiasis, whereas lymphocyte proliferation in the uninfected resistant group is dependent on IFN-gamma. |
| 5131 | 10841077 | For example, coadministration of costimulatory molecules (CD80 and CD86), proinflammatory cytokines (interleukin-1alpha [IL-1alpha], tumor necrosis factor-alpha [TNF-alpha, and TNF-beta), Th1 cytokines (interleukin-2 [IL-2], IL-12, IL-15, and IL-18), Th2 cytokines (IL-4, IL-5, and IL-10), and granulocytes-macrophage colony-stimulating factor (GM-CSF) with DNA vaccine constructs leads to modulation of the magnitude and direction (humoral or cellular) of the immune responses. |
| 5132 | 10841077 | To further engineer the immune response in vivo, we compared the induction and regulation of immune responses from the codelivery of chemokine (IL-8, interferon-gamma-inducible protein-10 [gammaIP-10], macrophage inhibitory protein-1alpha [MIP-1alpha], and RANTES) genes with codelivery of cytokine genes. |
| 5133 | 10841077 | We observed that coimmunization with IL-8, gammaIP-10, and MIP-1alpha genes increased the antibody response. |
| 5134 | 10841077 | We also found that coinjection with IL-8, gammaIP-10, and RANTES resulted in a dramatic enhancement of T helper (Th) proliferation response. |
| 5135 | 10841077 | This enhancement of CTL responses observed from the coinjection with RANTES was CD8+ T cell dependent. |
| 5136 | 10835499 | L-NMMA enhanced BCG-induced cytotoxic activity of PEC, as well as interferon (IFN)-gamma and tumor necrosis factor (TNF)-alpha production. |
| 5137 | 10835499 | L-NMMA enhanced BCG-induced cytotoxic activity of PEC, as well as interferon (IFN)-gamma and tumor necrosis factor (TNF)-alpha production. |
| 5138 | 10835499 | L-NMMA enhanced BCG-induced cytotoxic activity of PEC, as well as interferon (IFN)-gamma and tumor necrosis factor (TNF)-alpha production. |
| 5139 | 10835499 | The L-NMMA-induced enhancement was due to the prolonged survival of BCG in macrophages, because no enhancement of cytotoxicity was observed and neither IFN-gamma nor TNF-alpha production was significantly enhanced by killed BCG. |
| 5140 | 10835499 | The L-NMMA-induced enhancement was due to the prolonged survival of BCG in macrophages, because no enhancement of cytotoxicity was observed and neither IFN-gamma nor TNF-alpha production was significantly enhanced by killed BCG. |
| 5141 | 10835499 | The L-NMMA-induced enhancement was due to the prolonged survival of BCG in macrophages, because no enhancement of cytotoxicity was observed and neither IFN-gamma nor TNF-alpha production was significantly enhanced by killed BCG. |
| 5142 | 10835499 | The depletion of T cells from PEC reduced the production of both IFN-gamma and TNF-alpha, as well as the enhancement of cytotoxicity induced by viable BCG plus L-NMMA. |
| 5143 | 10835499 | The depletion of T cells from PEC reduced the production of both IFN-gamma and TNF-alpha, as well as the enhancement of cytotoxicity induced by viable BCG plus L-NMMA. |
| 5144 | 10835499 | The depletion of T cells from PEC reduced the production of both IFN-gamma and TNF-alpha, as well as the enhancement of cytotoxicity induced by viable BCG plus L-NMMA. |
| 5145 | 10823854 | Since gamma interferon (IFN-gamma) stimulates cytotoxic cells, including antigen-specific CTL which may control virus replication by secretion of antiviral cytokines such as tumor necrosis factor alpha and IFN-gamma, we have investigated the mechanism of HSI by analyzing the role of IFN-gamma for HSI in IFN-gamma gene-deleted (IFN-gamma(-/-)) mice. |
| 5146 | 10820273 | CD40 ligand (CD154) enhances the Th1 and antibody responses to respiratory syncytial virus in the BALB/c mouse. |
| 5147 | 10820273 | CD40 ligand (CD40L) is a cell surface costimulatory molecule expressed mainly by activated T cells. |
| 5148 | 10820273 | CD40L expression promotes Th1 cytokine responses to protein Ags and is responsible for Ig isotype switching in B cells. |
| 5149 | 10820273 | These studies show that coincident expression of CD40L enhances the Th1 (IL-2 and IFN-gamma) cytokine responses, increases the expression of TNF-alpha and NO, accelerates virus clearance, and increases the anti-F and anti-G Ab responses. |
| 5150 | 10820246 | These bovine insulin-primed CTL displayed a type 0 CTL phenotype, producing IL-4, IL-5, IL-10, low levels of IFN-gamma, but no TNF-alpha. |
| 5151 | 10820246 | These bovine insulin-primed CTL displayed a type 0 CTL phenotype, producing IL-4, IL-5, IL-10, low levels of IFN-gamma, but no TNF-alpha. |
| 5152 | 10820246 | By contrast, CTL generated from C57BL/6 mice primed with OVA in CFA produced IFN-gamma and TNF-alpha but no IL-4, IL-5, or IL-10 and therefore were classified as type 1 CTL. |
| 5153 | 10820246 | By contrast, CTL generated from C57BL/6 mice primed with OVA in CFA produced IFN-gamma and TNF-alpha but no IL-4, IL-5, or IL-10 and therefore were classified as type 1 CTL. |
| 5154 | 10820246 | Although both types of CTL express many of the same cell-surface Ags, OVA-specific CTL but not bovine insulin-primed CTL expressed CT-1, a carbohydrate epitope of CD45, and bovine insulin-primed CTL but not OVA-specific CTL expressed Fas constitutively. |
| 5155 | 10820246 | Although both types of CTL express many of the same cell-surface Ags, OVA-specific CTL but not bovine insulin-primed CTL expressed CT-1, a carbohydrate epitope of CD45, and bovine insulin-primed CTL but not OVA-specific CTL expressed Fas constitutively. |
| 5156 | 10820246 | Neither endogenous IL-4 nor the dose of priming Ag altered the CTL phenotypes, but the antigenic peptides of OVA and bovine insulin were key to determining the differentiation of either type 1 or type 0 CTL. |
| 5157 | 10820246 | Neither endogenous IL-4 nor the dose of priming Ag altered the CTL phenotypes, but the antigenic peptides of OVA and bovine insulin were key to determining the differentiation of either type 1 or type 0 CTL. |
| 5158 | 10816614 | Il-1, EGF, and HGF suppress the antiviral activity of interferon in primary monkey hepatic parenchymal cells. |
| 5159 | 10816614 | Interleukin-1 alpha, EGF, and HGF showed suppressive effects on the antiviral activity of IFN-alpha, -beta in primary monkey hepatic cells when examined by the yield reduction method using vesicular stomatitis virus (VSV). |
| 5160 | 10816614 | In contrast, 50 ng/ml of TNF and IL-6 had no suppressive effect on the IFN-induced antiviral state in the hepatic cells. |
| 5161 | 10811870 | Here, we have investigated the effects of type I IFNs on freshly isolated granulocyte/macrophage colony-stimulating factor (GM-CSF)-treated human monocytes in terms of dendritic cell (DC) differentiation and activity in vitro and in severe combined immunodeficiency mice reconstituted with human peripheral blood leukocytes (hu-PBL-SCID) mice. |
| 5162 | 10811870 | Type I IFNs induced a surprisingly rapid maturation of monocytes into short-lived tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL)-expressing DCs endowed with potent functional activities, superior with respect to the interleukin (IL)-4/GM-CSF treatment, as shown by FACS((R)) analyses, mixed leukocyte reaction assays with allogeneic PBLs, and lymphocyte proliferation responses to HIV-1-pulsed autologous DCs. |
| 5163 | 10811870 | Type I IFN induced IL-15 production and strongly promoted a T helper cell type 1 response. |
| 5164 | 10811863 | In contrast, vaccination with granulocyte/macrophage colony-stimulating factor (GM-CSF)-transduced tumor cells, previously shown to induce potent antitumor immunity in standard tumor challenge assays, led to a decreased therapeutic effect in the metastasis model and no effect in the subcutaneous tumor model. |
| 5165 | 10811863 | Further engineering of DCs to express either GM-CSF, tumor necrosis factor alpha, or CD40 ligand via retroviral-mediated gene transfer, led to a significantly increased therapeutic effect in the subcutaneous tumor model. |
| 5166 | 10811863 | The immunological mechanism, as shown for GM-CSF-transduced DCs, involves MAGE-1-specific CD4(+) and CD8(+) T cells. |
| 5167 | 10790422 | We also show that HP-NAP is chemotactic for human leukocytes and that it activates their NADPH oxidase to produce reactive oxygen intermediates, as demonstrated by the translocation of its cytosolic subunits to the plasma membrane, and by the lack of activity on chronic granulomatous disease leukocytes. |
| 5168 | 10790422 | This stimulating effect is strongly potentiated by tumor necrosis factor alpha and interferon gamma and is mediated by a rapid increase of the cytosolic calcium concentration. |
| 5169 | 10777144 | Subjects in this study exhibited significant increases (p < 0.05) in the frequency of helper T memory cells expressing interferon gamma (IFN-gamma) and tumor necrosis factor alpha (TNF-alpha) in response to HIV-1 antigens in vitro. |
| 5170 | 10775795 | Immunohistochemical analysis of cytokine-producing cells in the gut villi showed no significant induction of the cytokines IL-1alpha, IFN-gamma, IL-4 or IL-10 after oral administration of wild type Lactobacillus strains. |
| 5171 | 10775795 | In contrast, oral administration of L. reuteri and L. brevis induced expression of the proinflammatory/Th1 cytokines TNF-alpha, IL-2 and/or IL-1beta. |
| 5172 | 10770625 | Enhanced antitumoral effect of adenovirus-mediated cytosine deaminase gene therapy by induction of antigen-presenting cells through stem cell factor/granulocyte-macrophage colony-stimulating factor gene transfer. |
| 5173 | 10770625 | We preinjected the mice with murine stem cell factor (SCF)-encoding adenovirus (AdSCF) and murine granulocyte-macrophage colony-stimulating factor (GM-CSF)-encoding adenovirus (AdGM-CSF); after 7 days, the mice were inoculated with CT26 colon adenocarcinoma. |
| 5174 | 10770625 | Cytotoxic T-lymphocyte activity was induced efficiently after the combined therapy, and mRNA of tumor necrosis factor-alpha, interleukin-4, interferon-gamma, and interleukin-2 was present in the tumor mass after combined therapy, suggesting that a more potent antitumoral response was induced by enhanced APCs. |
| 5175 | 10768975 | The evaluation of the cytokine profile (interleukin 5 [IL-5], IL-10, gamma interferon [IFN-gamma], and tumor necrosis factor alpha) in response to these antigens showed inverse correlations between the degree of infection and IFN-gamma levels in PBMC supernatants stimulated with paramyosin (P < 0.05) and IrV-5 (P < 0.01). |
| 5176 | 10741704 | The detection of tumor-specific T cells in immunized cancer patients usually relies on lengthy and difficult CTL assays; we now report on flow cytometry to detect the intracellular cytokines interleukin 2 (IL-2), IL-4, IFN-gamma, and tumor necrosis factor alpha (TNF-alpha) produced by CD4+CD69+ and CD8+CD69+ activated T cells after MUC1 antigen stimulation. |
| 5177 | 10741704 | The detection of tumor-specific T cells in immunized cancer patients usually relies on lengthy and difficult CTL assays; we now report on flow cytometry to detect the intracellular cytokines interleukin 2 (IL-2), IL-4, IFN-gamma, and tumor necrosis factor alpha (TNF-alpha) produced by CD4+CD69+ and CD8+CD69+ activated T cells after MUC1 antigen stimulation. |
| 5178 | 10741704 | The detection of tumor-specific T cells in immunized cancer patients usually relies on lengthy and difficult CTL assays; we now report on flow cytometry to detect the intracellular cytokines interleukin 2 (IL-2), IL-4, IFN-gamma, and tumor necrosis factor alpha (TNF-alpha) produced by CD4+CD69+ and CD8+CD69+ activated T cells after MUC1 antigen stimulation. |
| 5179 | 10741704 | The detection of tumor-specific T cells in immunized cancer patients usually relies on lengthy and difficult CTL assays; we now report on flow cytometry to detect the intracellular cytokines interleukin 2 (IL-2), IL-4, IFN-gamma, and tumor necrosis factor alpha (TNF-alpha) produced by CD4+CD69+ and CD8+CD69+ activated T cells after MUC1 antigen stimulation. |
| 5180 | 10741704 | After stimulation in vitro with MUC1-variable number of tandem repeats peptides, CD8+CD69+ T cells from all immunized patients generated 3-9 times higher levels of TNF-alpha(P < 0.038) and IFN-gamma (P <0.010) than did cells from 12 normal subjects; minor increases in IL-4 occurred. |
| 5181 | 10741704 | After stimulation in vitro with MUC1-variable number of tandem repeats peptides, CD8+CD69+ T cells from all immunized patients generated 3-9 times higher levels of TNF-alpha(P < 0.038) and IFN-gamma (P <0.010) than did cells from 12 normal subjects; minor increases in IL-4 occurred. |
| 5182 | 10741704 | After stimulation in vitro with MUC1-variable number of tandem repeats peptides, CD8+CD69+ T cells from all immunized patients generated 3-9 times higher levels of TNF-alpha(P < 0.038) and IFN-gamma (P <0.010) than did cells from 12 normal subjects; minor increases in IL-4 occurred. |
| 5183 | 10741704 | After stimulation in vitro with MUC1-variable number of tandem repeats peptides, CD8+CD69+ T cells from all immunized patients generated 3-9 times higher levels of TNF-alpha(P < 0.038) and IFN-gamma (P <0.010) than did cells from 12 normal subjects; minor increases in IL-4 occurred. |
| 5184 | 10741704 | By contrast, CD4+CD69+ cells showed no overall alteration in TNF-alpha and IFN-gamma cytokine production, although in some patients, their measurement was informative; the measurement of IL-2 was not useful in either CD4+CD69+ or CD8+CD69+ cells. |
| 5185 | 10741704 | By contrast, CD4+CD69+ cells showed no overall alteration in TNF-alpha and IFN-gamma cytokine production, although in some patients, their measurement was informative; the measurement of IL-2 was not useful in either CD4+CD69+ or CD8+CD69+ cells. |
| 5186 | 10741704 | By contrast, CD4+CD69+ cells showed no overall alteration in TNF-alpha and IFN-gamma cytokine production, although in some patients, their measurement was informative; the measurement of IL-2 was not useful in either CD4+CD69+ or CD8+CD69+ cells. |
| 5187 | 10741704 | By contrast, CD4+CD69+ cells showed no overall alteration in TNF-alpha and IFN-gamma cytokine production, although in some patients, their measurement was informative; the measurement of IL-2 was not useful in either CD4+CD69+ or CD8+CD69+ cells. |
| 5188 | 10741704 | We conclude that in MUC1-immunized patients, the measurement of TNF-alpha and IFN-gamma in activated CD69+CD8+ T cells may be indicative of their immune status. |
| 5189 | 10741704 | We conclude that in MUC1-immunized patients, the measurement of TNF-alpha and IFN-gamma in activated CD69+CD8+ T cells may be indicative of their immune status. |
| 5190 | 10741704 | We conclude that in MUC1-immunized patients, the measurement of TNF-alpha and IFN-gamma in activated CD69+CD8+ T cells may be indicative of their immune status. |
| 5191 | 10741704 | We conclude that in MUC1-immunized patients, the measurement of TNF-alpha and IFN-gamma in activated CD69+CD8+ T cells may be indicative of their immune status. |
| 5192 | 10736116 | The in vitro production of interferon (IFN)-gamma, interleukin (IL)-5, tumour necrosis factor (TNF)-alpha and IL-10 by blood mononuclear cells in response to whole Mycobacterium leprae and polyclonal stimulii of 23 individuals, representing a variety of conditions in relation to exposure/susceptibility to M. leprae, was assayed. |
| 5193 | 10736116 | The in vitro production of interferon (IFN)-gamma, interleukin (IL)-5, tumour necrosis factor (TNF)-alpha and IL-10 by blood mononuclear cells in response to whole Mycobacterium leprae and polyclonal stimulii of 23 individuals, representing a variety of conditions in relation to exposure/susceptibility to M. leprae, was assayed. |
| 5194 | 10736116 | The in vitro production of interferon (IFN)-gamma, interleukin (IL)-5, tumour necrosis factor (TNF)-alpha and IL-10 by blood mononuclear cells in response to whole Mycobacterium leprae and polyclonal stimulii of 23 individuals, representing a variety of conditions in relation to exposure/susceptibility to M. leprae, was assayed. |
| 5195 | 10736116 | The in vitro production of interferon (IFN)-gamma, interleukin (IL)-5, tumour necrosis factor (TNF)-alpha and IL-10 by blood mononuclear cells in response to whole Mycobacterium leprae and polyclonal stimulii of 23 individuals, representing a variety of conditions in relation to exposure/susceptibility to M. leprae, was assayed. |
| 5196 | 10736116 | The in vitro production of interferon (IFN)-gamma, interleukin (IL)-5, tumour necrosis factor (TNF)-alpha and IL-10 by blood mononuclear cells in response to whole Mycobacterium leprae and polyclonal stimulii of 23 individuals, representing a variety of conditions in relation to exposure/susceptibility to M. leprae, was assayed. |
| 5197 | 10736116 | In most cases, healthy household contacts of newly diagnosed multibacillary leprosy patients, designated exposed household contacts (EC), showed low-to-undetectable in vitro IFN-gamma production in addition to substantial TNF-alpha production in response to M. leprae. |
| 5198 | 10736116 | In most cases, healthy household contacts of newly diagnosed multibacillary leprosy patients, designated exposed household contacts (EC), showed low-to-undetectable in vitro IFN-gamma production in addition to substantial TNF-alpha production in response to M. leprae. |
| 5199 | 10736116 | In most cases, healthy household contacts of newly diagnosed multibacillary leprosy patients, designated exposed household contacts (EC), showed low-to-undetectable in vitro IFN-gamma production in addition to substantial TNF-alpha production in response to M. leprae. |
| 5200 | 10736116 | In most cases, healthy household contacts of newly diagnosed multibacillary leprosy patients, designated exposed household contacts (EC), showed low-to-undetectable in vitro IFN-gamma production in addition to substantial TNF-alpha production in response to M. leprae. |
| 5201 | 10736116 | In most cases, healthy household contacts of newly diagnosed multibacillary leprosy patients, designated exposed household contacts (EC), showed low-to-undetectable in vitro IFN-gamma production in addition to substantial TNF-alpha production in response to M. leprae. |
| 5202 | 10736116 | TNF-alpha/IL-10 ratios in response to M. leprae and Concanavalin A were significantly higher in EC than in R contacts suggesting a role for the TNF-alpha/IL-10 ratio in restraining mycobacteria proliferation and spreading early in infection. |
| 5203 | 10736116 | TNF-alpha/IL-10 ratios in response to M. leprae and Concanavalin A were significantly higher in EC than in R contacts suggesting a role for the TNF-alpha/IL-10 ratio in restraining mycobacteria proliferation and spreading early in infection. |
| 5204 | 10736116 | TNF-alpha/IL-10 ratios in response to M. leprae and Concanavalin A were significantly higher in EC than in R contacts suggesting a role for the TNF-alpha/IL-10 ratio in restraining mycobacteria proliferation and spreading early in infection. |
| 5205 | 10736116 | TNF-alpha/IL-10 ratios in response to M. leprae and Concanavalin A were significantly higher in EC than in R contacts suggesting a role for the TNF-alpha/IL-10 ratio in restraining mycobacteria proliferation and spreading early in infection. |
| 5206 | 10736116 | TNF-alpha/IL-10 ratios in response to M. leprae and Concanavalin A were significantly higher in EC than in R contacts suggesting a role for the TNF-alpha/IL-10 ratio in restraining mycobacteria proliferation and spreading early in infection. |
| 5207 | 10736116 | Post-treatment lepromatous leprosy patients secreted relatively high levels of IL-10 in response to M. leprae, whereas one self-cured tuberculoid leprosy patient produced simultaneously high levels of IFN-gamma and TNF-alpha. |
| 5208 | 10736116 | Post-treatment lepromatous leprosy patients secreted relatively high levels of IL-10 in response to M. leprae, whereas one self-cured tuberculoid leprosy patient produced simultaneously high levels of IFN-gamma and TNF-alpha. |
| 5209 | 10736116 | Post-treatment lepromatous leprosy patients secreted relatively high levels of IL-10 in response to M. leprae, whereas one self-cured tuberculoid leprosy patient produced simultaneously high levels of IFN-gamma and TNF-alpha. |
| 5210 | 10736116 | Post-treatment lepromatous leprosy patients secreted relatively high levels of IL-10 in response to M. leprae, whereas one self-cured tuberculoid leprosy patient produced simultaneously high levels of IFN-gamma and TNF-alpha. |
| 5211 | 10736116 | Post-treatment lepromatous leprosy patients secreted relatively high levels of IL-10 in response to M. leprae, whereas one self-cured tuberculoid leprosy patient produced simultaneously high levels of IFN-gamma and TNF-alpha. |
| 5212 | 10736116 | Vaccination induced amplification of IFN-gamma production with a concomitant decrease in TNF-alpha/IL-10 ratios that resembled the cytokine pattern observed in R contacts. |
| 5213 | 10736116 | Vaccination induced amplification of IFN-gamma production with a concomitant decrease in TNF-alpha/IL-10 ratios that resembled the cytokine pattern observed in R contacts. |
| 5214 | 10736116 | Vaccination induced amplification of IFN-gamma production with a concomitant decrease in TNF-alpha/IL-10 ratios that resembled the cytokine pattern observed in R contacts. |
| 5215 | 10736116 | Vaccination induced amplification of IFN-gamma production with a concomitant decrease in TNF-alpha/IL-10 ratios that resembled the cytokine pattern observed in R contacts. |
| 5216 | 10736116 | Vaccination induced amplification of IFN-gamma production with a concomitant decrease in TNF-alpha/IL-10 ratios that resembled the cytokine pattern observed in R contacts. |
| 5217 | 10727883 | The immune response induced by r-S. typhimurium p30 was accompanied by augmented interferon-gamma (IFN-gamma) and tumor necrosis factor-alpha (TNF-alpha) levels produced by restimulated splenocytes. |
| 5218 | 10725805 | In this presentation we describe that human monocytes undergo spontaneous apoptosis in vitro which involves Fas/FasL interactions, and that proinflammatory cytokines such as tumor necrosis factor-alpha (TNFalpha), interleukin-1beta and granulocyte-monocyte-colony-stimulating factor prevent spontaneous apoptosis. |
| 5219 | 10723942 | We propose that cell mediated immunity comprises two separate elements; protective immunity, driven by IL-12 and IFN; and DTH, mediated by TNF and driven by chemokines. |
| 5220 | 10723942 | These include gamma delta T cells, which we believe control the inflammatory influx of cells; CD4+ NK cells, which may play a role in focussing lymphocytes into lung granulomas; and CD8 T cells, which play a currently undefined role after initial expression of immunity and establishment of chronic disease in the lungs has ensued. |
| 5221 | 10720505 | The mean percentages of CD4+ T cells were 0.11% for VZV and 0.22% for HSV by interferon (IFN)-gamma production; the frequency for HCMV was significantly higher at 1.21%. |
| 5222 | 10720505 | The mean percentages of CD4+ T cells were 0.11% for VZV and 0.22% for HSV by interferon (IFN)-gamma production; the frequency for HCMV was significantly higher at 1.21%. |
| 5223 | 10720505 | Percentages of VZV-, HSV-, and HCMV-specific CD4+ T cells were similar by use of tumor necrosis factor (TNF)-alpha. |
| 5224 | 10720505 | Percentages of VZV-, HSV-, and HCMV-specific CD4+ T cells were similar by use of tumor necrosis factor (TNF)-alpha. |
| 5225 | 10720505 | HCMV-stimulated CD8+ T cells produced IFN-gamma (1.11%) and TNF-alpha (1.71%); VZV- and HSV-specific CD8+ T cells were not detectable. |
| 5226 | 10720505 | HCMV-stimulated CD8+ T cells produced IFN-gamma (1.11%) and TNF-alpha (1.71%); VZV- and HSV-specific CD8+ T cells were not detectable. |
| 5227 | 10713654 | Although culture conditions are extremely diverse, the majority of protocols grow DCs in GM-CSF and either TNF-alpha and/or IL-4. |
| 5228 | 10713654 | The addition of other growth factors such as SCF and Flt-3 ligand can dramatically enhance DC recovery. |
| 5229 | 10708883 | IFN-gamma, TNF-alpha, IL-10 and IL-12 (ELISA). |
| 5230 | 10708883 | IFN-gamma, TNF-alpha, IL-10 and IL-12 (ELISA). |
| 5231 | 10708883 | In similar experiments, a significant increase in the cytolytic activity of HPNK cells was elicited by S. typhi Ty2 but not by mutant strain MEI028; neither of the cytokines assayed (IFN-gamma and TNF-alpha) was detected in the supernatant. |
| 5232 | 10708883 | In similar experiments, a significant increase in the cytolytic activity of HPNK cells was elicited by S. typhi Ty2 but not by mutant strain MEI028; neither of the cytokines assayed (IFN-gamma and TNF-alpha) was detected in the supernatant. |
| 5233 | 10708883 | Incubation with S. typhi Ty2 or MEI028 elicited significant expression of CD69, an early marker of NK cell activation, in PBMC but not in HPNK cell samples (flow cytometry); in similar experiments, the expression of CD16/56 and activation marker CD25 remained essentially unchanged. |
| 5234 | 10708883 | Incubation with S. typhi Ty2 or MEI028 elicited significant expression of CD69, an early marker of NK cell activation, in PBMC but not in HPNK cell samples (flow cytometry); in similar experiments, the expression of CD16/56 and activation marker CD25 remained essentially unchanged. |
| 5235 | 10689137 | The response of NK cells from elderly individuals to IL-2 or other cytokines is also decreased in terms of proliferation, expression of CD69 and killing of NK-resistant cell lines. |
| 5236 | 10689137 | Furthermore early IFN-gamma and chemokine production in response to IL-2 or IL-12 is also decreased. |
| 5237 | 10689137 | However aging does not significantly alter other NK cell functions such as TNF-alpha production or perforin induction in response to IL-2. |
| 5238 | 10689136 | The generation of DC from blood monocytes in response to GM-CSF and IL-4 treatment was similar in cells from young and old persons. |
| 5239 | 10689136 | The DC population thus obtained had a typical dendritic morphology and expressed DC surface markers, such as HLA class II, CD1a, CD11c, CD54, CD80 and CD86, but not CD14 for a period of up to three weeks in culture. |
| 5240 | 10689136 | DC from young and old persons produced IL-12 and TNF-alpha and responded equally well to maturation-inducing stimuli. |
| 5241 | 10678963 | Different phenotypes of Bcg congenic mice were associated with differential expression of the cytokines tumor necrosis factor alpha, interleukin-10, and gamma interferon and production of reactive oxygen intermediates. |
| 5242 | 10687141 | Although a comparable percentage of DCs expressing CD86+ (B7-2), CD40+, and HLA-DR+ were detected in both cultures, higher expression levels were detected in DCs derived from bulk culture (CD86 = MRLFI 3665.1 versus 2662.1 on day 6; CD40 = MRLFI 1786 versus 681.2 on day 6; HLA-DR = MRLFI 6018.2 versus 3444.9 on day 2). |
| 5243 | 10687141 | Cytokines involved in DC maturation were determined by polymerase chain reaction demonstrating interleukin-6 (IL-6), IL-12, interferon-gamma, granulocyte-macrophage colony-stimulating factor, and tumor necrosis factor-alpha mRNA expression by bulk culture cells during the entire 9-day culture period. |
| 5244 | 10687141 | Concurrently, CD3+ CD56-, CD3+ CD25+, and CD3+ TCR+ cell populations increased and cytotoxicity against autologous renal cell carcinoma tumor target was induced. |
| 5245 | 10671197 | Native Gal-lactin stimulated IL-12 p40 / p35 mRNA expression in a dose- and time-dependent manner as measured by reverse transcriptase-PCR. |
| 5246 | 10671197 | IFN-gamma priming augmented Gal-lectin-induced IL-12 mRNA expression independent of TNF-alpha and IL-1beta, and was required for IL-12 p70 protein production from macrophages and human peripheral blood mononuclear cells. |
| 5247 | 10671197 | Gal-lectin plus IFN-gamma stimulated IL-12 p40 and p35 gene transcription with stable mRNA transcripts and a differential requirement for protein synthesis. |
| 5248 | 10654199 | TIL phenotypes studied here indicated CD3 80 +/- 21%, CD4 37 +/- 21%, CD8 44 +/- 18% and HLA DR 69 +/- 24% after IL2 induction, in contrast, to CD3 20 +/- 12%, CD4 10 +/- 7%, CD8 11 +/- 3% and HLA DR 30 +/- 16% before induction. |
| 5249 | 10654199 | The results of a tumor vaccine using TNF-alpha gene transduction demonstrated that the expression of HLA Class I and HLA Class II were dramatically increased 87% and 43%. |
| 5250 | 10651044 | It was found that the biological activity of these LPSs was comparable to those of E. coli LPS in terms of activation of the clotting enzyme of Limulus amoebocyte lysate, mitogenic activity of mouse spleen cells, stimulation of TNF-alpha and nitric oxide production, but IL-6 production could hardly be observed in any LPS. |
| 5251 | 10649619 | After oral or intragastric administration of BCG to mice, comparable numbers of IFN gamma and TNF gamma producing cells were detected in both local (Peyer's patches) and central (spleen) lymphoid organs. |
| 5252 | 10623755 | MVA elicited a Th1 type of immune response, and the main proinflammatory cytokines induced were interleukin-6 and tumor necrosis factor alpha. |
| 5253 | 10607486 | After a 6-h incubation, phenotypic analysis of control-, imiquimod-, or R-848-treated LC indicated that such antigen-presenting cells were in an "intermediate" state of maturation (CD1a(+), HLA-DR, DP, DQ(bright+), CD40(low+), CD86(high+), and CD80(low+)). |
| 5254 | 10607486 | RNase protection assays demonstrated that either imiquimod or R-848 treatments increased steady-state transcripts encoding for IL-12 p40, IL-1beta, TNF-alpha, and IL-1 receptor antagonist by LC. |
| 5255 | 10602382 | The antitumor effect correlated well with a strong and rapid proinflammatory cytokine (TNF-alpha, IL-12 and IFN-gamma) response. |
| 5256 | 10602014 | We investigated the composition of proteasomes of DC derived from human peripheral blood monocytes before and after stimulation by CD40L, LPS, or proinflammatory cytokines (TNF-alpha + IL-6 + IL-1beta). |
| 5257 | 10602014 | Immunoprecipitation of proteasomes and analysis on two-dimensional gels revealed that during maturation the inducible proteasome subunits LMP2, LMP7, and MECL-1 are up-regulated and that the neosynthesis of proteasomes is switched exclusively to the production of immunoproteasomes containing these subunits. |
| 5258 | 10595741 | In an in vitro study, leukemic DCs were generated using granulocyte-macrophage colony-stimulating factor (GM-CSF), tumor necrosis factor-alpha, and interleukin-4 from granulocyte colony-stimulating factor (G-CSF)-mobilized PBSC fraction of this patient, and were found to be Ph1+, and to possess the morphologic and phenotypic characteristics of mature DCs. |
| 5259 | 10587479 | During differentiation of human monocytes (CD14(+)/CD1a(-)) to CD14(-)/CD1a(+)dendritic cells (DC), a drastic decrease in PDE4 activity was observed, while activities of PDE1 and PDE3 substantially increased. |
| 5260 | 10587479 | In addition, rolipram, at PDE4-selective concentrations, blocked TNF release by 37 +/- 5% (P<0.05 vs. control). |
| 5261 | 10579123 | Type 1 T helper (Th1) cells produce interferon-gamma, interleukin (IL)-2, and tumour necrosis factor (TNF)-beta, which activate macrophages and are responsible for cell-mediated immunity and phagocyte-dependent protective responses. |
| 5262 | 10579123 | By contrast, type 2 Th (Th2) cells produce IL-4, IL-5, IL-10, and IL-13, which are responsible for strong antibody production, eosinophil activation, and inhibition of several macrophage functions, thus providing phagocyte-independent protective responses. |
| 5263 | 10555997 | Previously, we demonstrated that a novel low-molecular-weight synthetic immune response modifier, R-848, induces IL-12 and IFN-alpha secretion from monocytes and macrophages. |
| 5264 | 10555997 | Characteristic of dendritic cell maturation, R-848 treatment induces cell surface expression of CD83 and increases cell surface expression of CD80, CD86, CD40, and HLA-DR. |
| 5265 | 10555997 | Additionally, R-848 induces cytokine (IL-6, IL-12, TNF-alpha, IFN-alpha) and chemokine (IL-8, MIP-1alpha, MCP-1) secretion from dendritic cells. |
| 5266 | 10542221 | Vasoactive intestinal peptide and pituitary adenylate cyclase-activating polypeptide inhibit interleukin-12 transcription by regulating nuclear factor kappaB and Ets activation. |
| 5267 | 10542221 | The vasoactive intestinal peptide (VIP) and the structurally related neuropeptide pituitary adenylate cyclase-activating polypeptide (PACAP) act as "macrophage-deactivating factors". |
| 5268 | 10542221 | We showed previously that VIP and PACAP inhibit the production of macrophage-derived tumor necrosis factor-alpha, interleukin (IL)-6, nitric oxide, and IL-12. |
| 5269 | 10542221 | This study examines the molecular mechanisms involved in the VIP/PACAP inhibition of IL-12 production. |
| 5270 | 10542221 | VIP and PACAP inhibit IL-12 (p40) gene expression by affecting both NF-kappaB binding and the composition of the Ets-2 binding complex. |
| 5271 | 10542221 | Both neuropeptides prevent the activation-induced nuclear translocation of the NF-kappaB components p65 and c-Rel by inhibiting the reduction in cytoplasmic IkappaBalpha. |
| 5272 | 10542989 | On admission serum cytokine levels of interleukins 4 and 10 (IL-4, IL-10), interferon gamma (IFN-gamma) and tumour necrosis factor alpha (TNF-alpha) were grossly raised in comparison with a matched control group (P < 0.001). |
| 5273 | 10542989 | On admission serum cytokine levels of interleukins 4 and 10 (IL-4, IL-10), interferon gamma (IFN-gamma) and tumour necrosis factor alpha (TNF-alpha) were grossly raised in comparison with a matched control group (P < 0.001). |
| 5274 | 10542989 | Levels of IL-4, IL-10 and TNF-alpha fell (P < 0.001, P < 0.01 and P < 0.01, respectively) and levels of IFN-gamma rose more (P = 0.005) in immunotherapy recipients than in those receiving chemotherapy alone. |
| 5275 | 10542989 | Levels of IL-4, IL-10 and TNF-alpha fell (P < 0.001, P < 0.01 and P < 0.01, respectively) and levels of IFN-gamma rose more (P = 0.005) in immunotherapy recipients than in those receiving chemotherapy alone. |
| 5276 | 10528174 | We also studied the possible impact of coinjection of plasmid DNA encoding rat cytokines IL-4, IL-10, GM-CSF, and TNF-alpha with the ISS-containing DNA vaccine. |
| 5277 | 10528174 | We also studied the possible impact of coinjection of plasmid DNA encoding rat cytokines IL-4, IL-10, GM-CSF, and TNF-alpha with the ISS-containing DNA vaccine. |
| 5278 | 10528174 | Coinjection of IL-4-, IL-10-, or TNF-alpha-coding cDNA inhibited the suppressive effect of the DNA vaccine on EAE, whereas GM-CSF-coding cDNA had no effect. |
| 5279 | 10528174 | Coinjection of IL-4-, IL-10-, or TNF-alpha-coding cDNA inhibited the suppressive effect of the DNA vaccine on EAE, whereas GM-CSF-coding cDNA had no effect. |
| 5280 | 10525448 | Interleukin (IL)-18 is a newly discovered cytokine, structurally similar to IL-1, with profound effects on T-cell activation. |
| 5281 | 10525448 | Formerly called interferon (IFN) gamma inducing factor (IGIF), IL-18 is the new name of a novel cytokine that plays an important role in the T-cell-helper type 1 (Th1) response, primarily by its ability to induce IFNgamma production in T cells and natural killer (NK) cells. |
| 5282 | 10525448 | Mice deficient in IL-18 have suppressed IFNgamma production despite the presence of IL-12 IL-18 is related to the IL-1 family in terms of structure, receptor family, and function. |
| 5283 | 10525448 | In terms of structure, IL-18 and IL-1beta share primary amino acid sequences of the so-called "signature sequence" motif and are similarly folded as all-beta pleated sheet molecules. |
| 5284 | 10525448 | Also similar to IL-1beta, IL-18 is synthesized as a biologically inactive precursor molecule lacking a signal peptide which requires cleavage into an active, mature molecule by the intracellular cysteine protease called IL-1beta-converting enzyme (ICE, also called caspase-1). |
| 5285 | 10525448 | The activity of mature IL-18 is closely related to that of IL-1. |
| 5286 | 10525448 | IL-18 induces gene expression and synthesis of tumor necrosis factor (TNF), IL-1, Fas ligand, and several chemokines. |
| 5287 | 10525448 | This IL-18R complex is made up of a binding chain termed IL-18Ralpha, a member of the IL-1 receptor family previously identified as the IL-1 receptor-related protein (IL-1Rrp), and a signaling chain, also a member of the IL-1R family. |
| 5288 | 10525448 | The IL-18R complex recruits the IL-1R-activating kinase (IRAK) and TNFR-associated factor-6 (TRAF-6) which phosphorylates nuclear factor kappaB (NFkappaB)-inducing kinase (NIK) with subsequent activation of NFkappaB. |
| 5289 | 10525448 | Thus on the basis of primary structure, three-dimensional structure, receptor family, signal transduction pathways and biological effects, IL-18 appears to be a new member of the IL-1 family. |
| 5290 | 10525448 | Similar to IL-1, IL-18 participates in both innate and acquired immunity. |
| 5291 | 10525446 | The IL-1beta nonapeptide reproduces the immunostimulatory and adjuvant effects of the whole mature IL-1beta, but does not possess any of the IL-1beta inflammatory, vasoactive, tumor-promoting, and systemically toxic effects, nor it can synergize with tumor necrosis factor alpha or other molecules in inducing toxicity and shock. |
| 5292 | 10525053 | Both S. pneumoniae-bound IgA and complement were involved, as demonstrated by a 50% decrease in killing with blocking of Fcalpha receptor (CD89) and CR1/CR3 (CD35/CD11b). |
| 5293 | 10525053 | However, IgA-mediated killing by phagocytes could be reproduced in the absence of opsonic complement by pre-activating phagocytes with the inflammatory products C5a and TNF-alpha. |
| 5294 | 10515123 | Initial rise of all splenic cytokines and serum anti-SEA IgE levels at 6 weeks p.i. was observed, followed by a dramatic drop in the levels of the proinflammatory cytokines IL-2, IFNgamma, IL-4 and TNF-alpha and IgE at 8 weeks of infection. |
| 5295 | 10510391 | IFN-gamma can promote production of TNF and can synergize with this cytokine in its actions on responder cells. |
| 5296 | 10510391 | Furthermore, CD4+ T cells were equally represented in airway populations from the two groups and produced IFN-gamma upon Ag stimulation in vitro. |
| 5297 | 10510336 | The important T-cell stimulatory cytokine IL-12 or the proinflammatory cytokines IL-1beta or TNF-alpha were not detected or were only minimally detected. |
| 5298 | 10510336 | Finally, monocytes pretreated with HRV-14 were greatly inhibited in their production of IL-12 upon stimulation with IFN-gamma/LPS. |
| 5299 | 10505115 | In contrast to the rapid LPS response, CpG DNA-stimulated TNF and IL-6 synthesis in human monocytes was not detectable until 18 h. |
| 5300 | 10505115 | In contrast to the rapid LPS response, CpG DNA-stimulated TNF and IL-6 synthesis in human monocytes was not detectable until 18 h. |
| 5301 | 10505115 | In conclusion, CpG-motifs induce TNF, IL-6 and ICAM-1 expression in human monocytes, but the kinetics of this differ from that induced by LPS, which makes it possible to distinguish immune activation by these agents. |
| 5302 | 10505115 | In conclusion, CpG-motifs induce TNF, IL-6 and ICAM-1 expression in human monocytes, but the kinetics of this differ from that induced by LPS, which makes it possible to distinguish immune activation by these agents. |
| 5303 | 10498601 | Rapid induction of CD40 on a subset of granulocyte colony-stimulating factor-mobilized CD34(+) blood cells identifies myeloid committed progenitors and permits selection of nonimmunogenic CD40(-) progenitor cells. |
| 5304 | 10498601 | Rapid induction of CD40 on a subset of granulocyte colony-stimulating factor-mobilized CD34(+) blood cells identifies myeloid committed progenitors and permits selection of nonimmunogenic CD40(-) progenitor cells. |
| 5305 | 10498601 | Rapid induction of CD40 on a subset of granulocyte colony-stimulating factor-mobilized CD34(+) blood cells identifies myeloid committed progenitors and permits selection of nonimmunogenic CD40(-) progenitor cells. |
| 5306 | 10498601 | Rapid induction of CD40 on a subset of granulocyte colony-stimulating factor-mobilized CD34(+) blood cells identifies myeloid committed progenitors and permits selection of nonimmunogenic CD40(-) progenitor cells. |
| 5307 | 10498601 | Rapid induction of CD40 on a subset of granulocyte colony-stimulating factor-mobilized CD34(+) blood cells identifies myeloid committed progenitors and permits selection of nonimmunogenic CD40(-) progenitor cells. |
| 5308 | 10498601 | CD40 antigen is a costimulatory molecule highly expressed on dendritic cells (DC) and activated B cells, which induces T-cell proliferation through the binding with CD40L receptor. |
| 5309 | 10498601 | CD40 antigen is a costimulatory molecule highly expressed on dendritic cells (DC) and activated B cells, which induces T-cell proliferation through the binding with CD40L receptor. |
| 5310 | 10498601 | CD40 antigen is a costimulatory molecule highly expressed on dendritic cells (DC) and activated B cells, which induces T-cell proliferation through the binding with CD40L receptor. |
| 5311 | 10498601 | CD40 antigen is a costimulatory molecule highly expressed on dendritic cells (DC) and activated B cells, which induces T-cell proliferation through the binding with CD40L receptor. |
| 5312 | 10498601 | CD40 antigen is a costimulatory molecule highly expressed on dendritic cells (DC) and activated B cells, which induces T-cell proliferation through the binding with CD40L receptor. |
| 5313 | 10498601 | CD40, CD80, and CD86 antigens were constitutively expressed on 3.2% +/- 4.5%, 0%, and 1.8% +/- 1.2% CD34(+) blood cells, respectively. |
| 5314 | 10498601 | CD40, CD80, and CD86 antigens were constitutively expressed on 3.2% +/- 4.5%, 0%, and 1.8% +/- 1.2% CD34(+) blood cells, respectively. |
| 5315 | 10498601 | CD40, CD80, and CD86 antigens were constitutively expressed on 3.2% +/- 4.5%, 0%, and 1.8% +/- 1.2% CD34(+) blood cells, respectively. |
| 5316 | 10498601 | CD40, CD80, and CD86 antigens were constitutively expressed on 3.2% +/- 4.5%, 0%, and 1.8% +/- 1.2% CD34(+) blood cells, respectively. |
| 5317 | 10498601 | CD40, CD80, and CD86 antigens were constitutively expressed on 3.2% +/- 4.5%, 0%, and 1.8% +/- 1.2% CD34(+) blood cells, respectively. |
| 5318 | 10498601 | However, after 24 hours in liquid culture with medium alone, or with tumor-necrosis-factor-alpha (TNF-alpha), or with allogeneic mononuclear cells 10.8% +/- 3.8%, 75.3% +/- 15.0% and 53. 7% +/- 17.0% CD34(+) blood cells, respectively, became CD40(+). |
| 5319 | 10498601 | However, after 24 hours in liquid culture with medium alone, or with tumor-necrosis-factor-alpha (TNF-alpha), or with allogeneic mononuclear cells 10.8% +/- 3.8%, 75.3% +/- 15.0% and 53. 7% +/- 17.0% CD34(+) blood cells, respectively, became CD40(+). |
| 5320 | 10498601 | However, after 24 hours in liquid culture with medium alone, or with tumor-necrosis-factor-alpha (TNF-alpha), or with allogeneic mononuclear cells 10.8% +/- 3.8%, 75.3% +/- 15.0% and 53. 7% +/- 17.0% CD34(+) blood cells, respectively, became CD40(+). |
| 5321 | 10498601 | However, after 24 hours in liquid culture with medium alone, or with tumor-necrosis-factor-alpha (TNF-alpha), or with allogeneic mononuclear cells 10.8% +/- 3.8%, 75.3% +/- 15.0% and 53. 7% +/- 17.0% CD34(+) blood cells, respectively, became CD40(+). |
| 5322 | 10498601 | However, after 24 hours in liquid culture with medium alone, or with tumor-necrosis-factor-alpha (TNF-alpha), or with allogeneic mononuclear cells 10.8% +/- 3.8%, 75.3% +/- 15.0% and 53. 7% +/- 17.0% CD34(+) blood cells, respectively, became CD40(+). |
| 5323 | 10498601 | After incubation for 24 hours with TNF-alpha CD34(+)CD40(+) blood cells expressed only myeloid markers and contained less than 5% CD86(+) and CD80(+) cells. |
| 5324 | 10498601 | After incubation for 24 hours with TNF-alpha CD34(+)CD40(+) blood cells expressed only myeloid markers and contained less than 5% CD86(+) and CD80(+) cells. |
| 5325 | 10498601 | After incubation for 24 hours with TNF-alpha CD34(+)CD40(+) blood cells expressed only myeloid markers and contained less than 5% CD86(+) and CD80(+) cells. |
| 5326 | 10498601 | After incubation for 24 hours with TNF-alpha CD34(+)CD40(+) blood cells expressed only myeloid markers and contained less than 5% CD86(+) and CD80(+) cells. |
| 5327 | 10498601 | After incubation for 24 hours with TNF-alpha CD34(+)CD40(+) blood cells expressed only myeloid markers and contained less than 5% CD86(+) and CD80(+) cells. |
| 5328 | 10498601 | Also, a 24-hour priming with TNF-alpha or ligation of CD40 significantly increased the CD34(+) blood cells alloantigen presenting function. |
| 5329 | 10498601 | Also, a 24-hour priming with TNF-alpha or ligation of CD40 significantly increased the CD34(+) blood cells alloantigen presenting function. |
| 5330 | 10498601 | Also, a 24-hour priming with TNF-alpha or ligation of CD40 significantly increased the CD34(+) blood cells alloantigen presenting function. |
| 5331 | 10498601 | Also, a 24-hour priming with TNF-alpha or ligation of CD40 significantly increased the CD34(+) blood cells alloantigen presenting function. |
| 5332 | 10498601 | Also, a 24-hour priming with TNF-alpha or ligation of CD40 significantly increased the CD34(+) blood cells alloantigen presenting function. |
| 5333 | 10498601 | Finally, purified CD34(+)CD40(+) blood cells stimulated an alloreactive T-cell response in MLC, were enriched in granulocytic, monocytic, and dendritic precursors, and generated high numbers of DC in 11-14 d liquid cultures with GM-CSF, SCF, TNF-alpha and FLT-3L. |
| 5334 | 10498601 | Finally, purified CD34(+)CD40(+) blood cells stimulated an alloreactive T-cell response in MLC, were enriched in granulocytic, monocytic, and dendritic precursors, and generated high numbers of DC in 11-14 d liquid cultures with GM-CSF, SCF, TNF-alpha and FLT-3L. |
| 5335 | 10498601 | Finally, purified CD34(+)CD40(+) blood cells stimulated an alloreactive T-cell response in MLC, were enriched in granulocytic, monocytic, and dendritic precursors, and generated high numbers of DC in 11-14 d liquid cultures with GM-CSF, SCF, TNF-alpha and FLT-3L. |
| 5336 | 10498601 | Finally, purified CD34(+)CD40(+) blood cells stimulated an alloreactive T-cell response in MLC, were enriched in granulocytic, monocytic, and dendritic precursors, and generated high numbers of DC in 11-14 d liquid cultures with GM-CSF, SCF, TNF-alpha and FLT-3L. |
| 5337 | 10498601 | Finally, purified CD34(+)CD40(+) blood cells stimulated an alloreactive T-cell response in MLC, were enriched in granulocytic, monocytic, and dendritic precursors, and generated high numbers of DC in 11-14 d liquid cultures with GM-CSF, SCF, TNF-alpha and FLT-3L. |
| 5338 | 10498601 | In conclusion, a short incubation with TNF-alpha allows the selection of CD40(+) blood progenitors, which may be a useful source of DC precursors for antitumor vaccine studies, and also a CD34(+)CD40(-) blood cell fraction that could be exploited in innovative strategies of allogeneic transplantation across HLA barriers. |
| 5339 | 10498601 | In conclusion, a short incubation with TNF-alpha allows the selection of CD40(+) blood progenitors, which may be a useful source of DC precursors for antitumor vaccine studies, and also a CD34(+)CD40(-) blood cell fraction that could be exploited in innovative strategies of allogeneic transplantation across HLA barriers. |
| 5340 | 10498601 | In conclusion, a short incubation with TNF-alpha allows the selection of CD40(+) blood progenitors, which may be a useful source of DC precursors for antitumor vaccine studies, and also a CD34(+)CD40(-) blood cell fraction that could be exploited in innovative strategies of allogeneic transplantation across HLA barriers. |
| 5341 | 10498601 | In conclusion, a short incubation with TNF-alpha allows the selection of CD40(+) blood progenitors, which may be a useful source of DC precursors for antitumor vaccine studies, and also a CD34(+)CD40(-) blood cell fraction that could be exploited in innovative strategies of allogeneic transplantation across HLA barriers. |
| 5342 | 10498601 | In conclusion, a short incubation with TNF-alpha allows the selection of CD40(+) blood progenitors, which may be a useful source of DC precursors for antitumor vaccine studies, and also a CD34(+)CD40(-) blood cell fraction that could be exploited in innovative strategies of allogeneic transplantation across HLA barriers. |
| 5343 | 10497996 | Higher response rates of interferon-gamma but lower response rates of tumor necrosis factor-alpha to four and six peptides, respectively, were observed in Dienga than in Pouma that were independent of the older age of the Gabonese children. |
| 5344 | 10496899 | Gamma interferon (IFN-gamma)-secreting CD4+ T cells have long been established as an essential component of the protective immune response against Mycobacterium tuberculosis. |
| 5345 | 10496899 | It is now becoming evident from studies with the murine model of tuberculosis that an important role also exists for major histocompatibility complex (MHC) class I-restricted CD8+ T cells. |
| 5346 | 10496899 | Using FACScan analysis, we have shown that restimulation with live M. bovis BCG induced more CD8+-T-cell activation than the soluble antigen purified protein derivative and that these cells are actively producing the type 1 cytokines IFN-gamma and tumor necrosis factor alpha (TNF-alpha). |
| 5347 | 10496899 | The use of metabolic inhibitors and blocking antibodies revealed that the CD8+ T cells recognize antigen processed and presented via the classical MHC class I pathway. |
| 5348 | 10496888 | Stimulation of bone marrow macrophages from C3H/HeN mice with the B. burgdorferi lipoprotein OspA resulted in higher-level production of the inflammatory mediators tumor necrosis factor alpha, nitric oxide, and interleukin-6 (IL-6) than that of macrophages from C57BL/6N mice. |
| 5349 | 10482186 | The first is an effort to induce antitumor immunity by enriching the cytokine environment within the primary cancer by intraprostatic injection of Leukocyte Interleukin (Cel-Sci Corp, Vienna, VA), a mixture of natural cytokines that includes interleukin-1 beta (IL-1beta), IL-2, granulocyte-macrophage colony-stimulating factor (GM-CSF), interferon gamma (IFN-gamma), and tumor necrosis factor alpha (TNF-alpha). |
| 5350 | 10482186 | When administered as an emulsion or in association with bacillus Calmette-Guérin (BCG)/cyclophosphamide or GM-CSF with or without IL-2/cyclophosphamide, immunologic tolerance is broken as evidenced by the generation of humoral and cellular immunity. |
| 5351 | 10479117 | As the rash resolved production of IL-2, IL-1beta, tumor necrosis factor-alpha, IL-6, and IL-5 mRNA increased. |
| 5352 | 10477566 | DCs incubated with recombinant S. gordonii were much more efficient than DCs pulsed with soluble C-fragment of tetanus toxin at stimulating specific CD4+ T cells as determined by cell proliferation and IFN-gamma release. |
| 5353 | 10477566 | In particular, S. gordonii dose-dependently up-regulated expression of membrane molecules (MHC I and II, CD80, CD86, CD54, CD40, CD83) and reduced both phagocytic and endocytic activities. |
| 5354 | 10477566 | Furthermore, bacteria promoted in a dose-dependent manner DC release of cytokines (IL-6, TNF-alpha, IL-1beta, IL-12, TGF-beta, and IL-10) and of the chemokines IL-8, RANTES, IFN-gamma-inducible protein-10, and monokine induced by IFN-gamma. |
| 5355 | 10464704 | Enhanced antitumor immune responses of IL-2 gene-modified tumor vaccine by combination with IL-1 and low dose cyclophosphamide. |
| 5356 | 10464704 | To enhance the antitumor immunity induced by IL-2 gene-modified tumor vaccine, we proposed a combined protocol to treat tumor-bearing mice using IL-2 gene-modified tumor vaccine in combination with IL-1 and low-dose Cyclophosphamide(Cy). |
| 5357 | 10464704 | The best therapeutic effect was achieved when the IL-2 gene-modified vaccine was combined with IL-1 and low-dose Cy. |
| 5358 | 10464704 | The cytotoxicity of the splenic CTL, NK, and the levels of IL-2, TNF secreted by splenocytes increased after tumor-bearing mice were treated with the IL-2 gene-modified tumor vaccine. |
| 5359 | 10464704 | The above antitumor immune functions were augmented more significantly when IL-1, low-dose Cy were used in combination with IL-2 genemodified tumor vaccine. |
| 5360 | 10464704 | These results demonstrated that the IL-2 gene modified vaccine could exert more potent anti-metastases effects when it is combined with IL-1 or/and low-dose Cy by activating the specific and non-specific antitumor immune responses more effectively. |
| 5361 | 10457199 | Expression of IFN-gamma or TNF was protective. |
| 5362 | 10457199 | Interleukin-4 exacerbation was T cell independent and was reflected in the failure of macrophage activation, possibly due to suppression of NK cells, which are a source of IFN-gamma early in infection. |
| 5363 | 10418909 | The level of IFN-gamma or TNF-alpha was found to diminish in T. gondii-treated mice as the infection progressed to the late stage. |
| 5364 | 10418909 | The level of IFN-gamma or TNF-alpha was found to diminish in T. gondii-treated mice as the infection progressed to the late stage. |
| 5365 | 10418909 | This declined response of IFN-gamma or TNF-alpha was associated with marked increase in the expression of IL-10, a counterregulatory cytokine. |
| 5366 | 10418909 | This declined response of IFN-gamma or TNF-alpha was associated with marked increase in the expression of IL-10, a counterregulatory cytokine. |
| 5367 | 10418905 | Cryostat sections of cornea were taken at different times after challenge and examined for infiltrating cells containing IL-2, IL-4, IFN-gamma, IL-6, or TNF-alpha. |
| 5368 | 10418905 | By days 3-7, many cells containing IL-4 and IFN-gamma, but few cells containing IL-2, had infiltrated into the corneas of gG or mock vaccinated mice. |
| 5369 | 10418905 | At the same times, many cells containing IL-2, but few cells containing IL-4 or IFN-gamma, were seen in the corneas of gD vaccinated mice. |
| 5370 | 10418905 | In contrast, the corneas of mice vaccinated with gK contained large amounts of IL-2, IFN-gamma, and IL-4. |
| 5371 | 10418905 | Our results suggest that: (1) corneas from gD vaccinated mice had no corneal disease and developed a response highly biased toward IL-2 responses; (2) corneas from gG or mock vaccinated eyes had significant corneal disease and developed a mostly IL-4 and IFN-gamma cytokine response; and (3) corneas from gK vaccinated mice had exacerbated corneal disease and developed strong IL-2, IL-4 and IFN-gamma cytokine responses. |
| 5372 | 10410657 | Including cytokines such as IL-2, IL-12, IFN, TNF or monoclonal antibodies, they have been widely used as biological response modifiers (BRM). |
| 5373 | 10408367 | These iC3b fragments serve to promote the high avidity attachment of the 'iC3b-opsonized' pathogens to the iC3b-receptors (CR3, CD11b/CD18) of phagocytic cells and natural killer (NK) cells, stimulating phagocytosis and/or cytotoxic degranulation. |
| 5374 | 10408367 | Moreover, the cytotoxic activation of beta-glucan-primed NK cell CR3 by iC3b-opsonized tumors is shown to be accompanied by a tumor-localized secretion of the cytokines TNFalpha, IFNalpha, IFNgamma, and IL-6. |
| 5375 | 10390075 | Upregulation of antitumor immunity by IL-12 gene-transfected AK-5 tumor cells in vivo. |
| 5376 | 10390075 | We have earlier demonstrated a significant role for IL-12 in the regression of a rat histiocytic tumor, AK-5. |
| 5377 | 10390075 | Analysis of the serum samples from animals injected with the IL-12 gene-transfected AK-5 cells on different days revealed a significant increase in circulatory IL-12, interferon (IFN)-gamma, tumor necrosis factor (TNF)-alpha and antitumor antibodies, all of which contributed to the reduction in tumor mass. |
| 5378 | 10390075 | Similarly, intraperitoneal transplantation of IL-12 gene-transfected tumor cells in syngeneic Wistar rats induced a significant increase in cellular cytotoxicity, with a concomitant reduction in circulatory IL-12 (p40) protein. |
| 5379 | 10390075 | Administration of antibodies to IL-12 and IFN-gamma reduced the expression of the costimulatory molecules B7.1 and B7.2 and the cytolytic effectors granzyme B and Fas-L, suggesting their involvement in IFN-gamma-dependent antitumor immune response induced by IL-12. |
| 5380 | 10377147 | Stimulation with STF induced rapid de novo synthesis of tumor necrosis factor alpha (TNF-alpha) and interleukin-1beta (IL-1beta), followed by IL-6 and IL-10. |
| 5381 | 10377147 | Stimulation with STF induced rapid de novo synthesis of tumor necrosis factor alpha (TNF-alpha) and interleukin-1beta (IL-1beta), followed by IL-6 and IL-10. |
| 5382 | 10377147 | Intracellular cytokine measurements of STF-stimulated PBMC revealed the existence of monocyte subpopulations that produce only TNF-alpha, IL-1beta or both cytokines. |
| 5383 | 10377147 | Intracellular cytokine measurements of STF-stimulated PBMC revealed the existence of monocyte subpopulations that produce only TNF-alpha, IL-1beta or both cytokines. |
| 5384 | 10361131 | We found that mixtures of irradiated cells expressing granulocyte-macrophage colony-stimulating factor (GM-CSF) plus those expressing interleukin-4 (IL-4) or tumor necrosis factor alpha (TNFalpha) protected mice against WEHI-3B-induced leukemias. |
| 5385 | 10361131 | When bone marrow mononuclear cells (BMMNCs) obtained from mice that had been injected with irradiated, cytokine-expressing tumor cells were injected into tumor-bearing mice, the survival of the latter was significantly prolonged; the longest survival was observed in mice receiving BMMNCs containing an increased number of DCs from animals injected with a mixture of tumor cells expressing GM-CSF with those expressing IL-4. |
| 5386 | 10359214 | This response was augmented following the pretreatment of KS-CD80 cells with interferon-gamma and tumor necrosis factor-alpha. |
| 5387 | 10359214 | Interleukin-4 (IL-4), IL-7, and IL-12 further increased T-cell expansion. |
| 5388 | 10233683 | Further study to find the mechanism underlying this revealed that there was up-regulation of major histocompatibility complex (MHC) class II, CD86 antigens on DC and increased production of interleukin-12 (IL-12) by DC and of IL-2, and tumour necrosis factor-alpha (TNF-alpha) in DC/T-cell cultures when vaccine containing HBsAg was injected in HBV-Tg with potent DC function but not in HBV-Tg with poor DC function. |
| 5389 | 10225908 | We measured proliferation and in vitro production of gamma interferon (IFN-gamma), tumor necrosis factor alpha, and interleukin-10 (IL-10) in response to meningococcal antigens by peripheral blood mononuclear cells (PBMCs) from children convalescing from meningococcal disease and from controls. |
| 5390 | 10225908 | After meningococcal infection, the balance of cytokine production by PBMCs from the youngest children was skewed towards a TH1 response (low IL-10/IFN-gamma ratio), while older children produced more TH2 cytokine (higher IL-10/IFN-gamma ratio). |
| 5391 | 10225849 | To ascertain if immunization with pneumococcal polysaccharide vaccine is associated with rises in the levels of proinflammatory cytokines in the plasma of human immunodeficiency virus type 1 (HIV-1)-infected patients, the levels of tumor necrosis factor alpha (TNF-alpha) and interleukin-6 (IL-6) were measured serially after immunization. |
| 5392 | 10225849 | To ascertain if immunization with pneumococcal polysaccharide vaccine is associated with rises in the levels of proinflammatory cytokines in the plasma of human immunodeficiency virus type 1 (HIV-1)-infected patients, the levels of tumor necrosis factor alpha (TNF-alpha) and interleukin-6 (IL-6) were measured serially after immunization. |
| 5393 | 10225849 | IL-6 levels rose an average of 2.2- and 2.1-fold 6 and 8 h after immunization, respectively, but TNF-alpha levels remained unchanged. |
| 5394 | 10225849 | IL-6 levels rose an average of 2.2- and 2.1-fold 6 and 8 h after immunization, respectively, but TNF-alpha levels remained unchanged. |
| 5395 | 10202049 | A20 is a B cell lymphoma that constitutively expresses the costimulatory molecule B7-2 yet grows readily as a tumor in syngeneic BALB/c mice. |
| 5396 | 10202049 | We have compared the tumorigenicity of A20 variants expressing either B7-1 (A20/B7-1) or B7-2 (A20/B7-2) with an A20 variant expressing B7-1 and B7-2 with 4-1BBL (A20/4-1BBL), a costimulatory member of the TNF family. |
| 5397 | 10202049 | In contrast, mice injected with A20/4-1BBL were tumor free for the 150-day follow-up period, while 25% of mice injected with A20/B7-2 developed tumors. |
| 5398 | 10202049 | Splenocytes from these mice showed high CTL lytic activity against the parental tumor, A20, as well as the syngeneic BALB/c lymphoma K46J, but showed background levels of lytic activity against the congenic SCID thymoma line ST-D2 or the allogeneic EL4 thymoma. |
| 5399 | 10202049 | In vitro blocking experiments with anti-B7-1 plus anti-B7-2 and/or soluble 4-1BB receptor showed B7-1, B7-2, and 4-1BBL all contributed to the CTL activity. |
| 5400 | 10202049 | Thus, the data show that neither B7-1 or B7-2 alone can confer full immunogenicity to the A20 lymphoma but that the addition of 4-1BBL results in a tumor that is highly immunogenic and can confer long-lasting protection against challenge with parental tumor in vivo. |
| 5401 | 10196254 | Three CD4(+) CTL clones were demonstrated to lyse cognate, antigen-presenting target cells by a mechanism that primarily involves perforin, while bystander lysis occurred through Fas/Fas ligand interactions. |
| 5402 | 10196254 | In contrast, one clone used a Fas/Fas ligand mechanism to lyse both cognate and bystander targets. |
| 5403 | 10196254 | In response to stimulation with D2 antigen, CD4(+) T-cell clones produced gamma interferon, tumor necrosis factor alpha (TNF-alpha) and TNF-beta. |
| 5404 | 10190582 | Tumor cells may also become resistant to mediators of apoptosis, such as Fas ligand and tumor necrosis factor-related apoptosis-inducing ligand used by lymphocytes to kill tumor cells. |
| 5405 | 10092812 | Resistance to the mouse pneumonitis (MoPn) strain of Chlamydia trachomatis has been mapped to MHC class II-restricted, IL-12-dependent CD4+ T cells that secrete a type 1 profile of proinflammatory cytokines, which includes IFN-gamma and TNF-alpha. |
| 5406 | 10085019 | Rapid local expression of interleukin-12, tumor necrosis factor alpha, and gamma interferon after cutaneous Francisella tularensis infection in tularemia-immune mice. |
| 5407 | 10085019 | Rapid local expression of interleukin-12, tumor necrosis factor alpha, and gamma interferon after cutaneous Francisella tularensis infection in tularemia-immune mice. |
| 5408 | 10085019 | Rapid local expression of interleukin-12, tumor necrosis factor alpha, and gamma interferon after cutaneous Francisella tularensis infection in tularemia-immune mice. |
| 5409 | 10085019 | Rapid local expression of interleukin-12, tumor necrosis factor alpha, and gamma interferon after cutaneous Francisella tularensis infection in tularemia-immune mice. |
| 5410 | 10085019 | Rapid local expression of interleukin-12, tumor necrosis factor alpha, and gamma interferon after cutaneous Francisella tularensis infection in tularemia-immune mice. |
| 5411 | 10085019 | By immunohistochemistry, skin samples from immune mice showed an intense staining for interleukin-12 (IL-12) and a moderate staining for tumor necrosis factor alpha (TNF-alpha) at 24 h postinoculation, after which staining for both cytokines faded. |
| 5412 | 10085019 | By immunohistochemistry, skin samples from immune mice showed an intense staining for interleukin-12 (IL-12) and a moderate staining for tumor necrosis factor alpha (TNF-alpha) at 24 h postinoculation, after which staining for both cytokines faded. |
| 5413 | 10085019 | By immunohistochemistry, skin samples from immune mice showed an intense staining for interleukin-12 (IL-12) and a moderate staining for tumor necrosis factor alpha (TNF-alpha) at 24 h postinoculation, after which staining for both cytokines faded. |
| 5414 | 10085019 | By immunohistochemistry, skin samples from immune mice showed an intense staining for interleukin-12 (IL-12) and a moderate staining for tumor necrosis factor alpha (TNF-alpha) at 24 h postinoculation, after which staining for both cytokines faded. |
| 5415 | 10085019 | By immunohistochemistry, skin samples from immune mice showed an intense staining for interleukin-12 (IL-12) and a moderate staining for tumor necrosis factor alpha (TNF-alpha) at 24 h postinoculation, after which staining for both cytokines faded. |
| 5416 | 10085019 | In naive mice, the staining for IL-12 was weak at all time points and no staining for TNF-alpha was observed. |
| 5417 | 10085019 | In naive mice, the staining for IL-12 was weak at all time points and no staining for TNF-alpha was observed. |
| 5418 | 10085019 | In naive mice, the staining for IL-12 was weak at all time points and no staining for TNF-alpha was observed. |
| 5419 | 10085019 | In naive mice, the staining for IL-12 was weak at all time points and no staining for TNF-alpha was observed. |
| 5420 | 10085019 | In naive mice, the staining for IL-12 was weak at all time points and no staining for TNF-alpha was observed. |
| 5421 | 10085019 | A quantitative analysis demonstrated higher IFN-gamma and TNF-alpha mRNA levels in immune mice at 24 h postinoculation. |
| 5422 | 10085019 | A quantitative analysis demonstrated higher IFN-gamma and TNF-alpha mRNA levels in immune mice at 24 h postinoculation. |
| 5423 | 10085019 | A quantitative analysis demonstrated higher IFN-gamma and TNF-alpha mRNA levels in immune mice at 24 h postinoculation. |
| 5424 | 10085019 | A quantitative analysis demonstrated higher IFN-gamma and TNF-alpha mRNA levels in immune mice at 24 h postinoculation. |
| 5425 | 10085019 | A quantitative analysis demonstrated higher IFN-gamma and TNF-alpha mRNA levels in immune mice at 24 h postinoculation. |
| 5426 | 10085019 | In conclusion, immunization with F. tularensis LVS conferred a capability to respond to cutaneous reinfection, with rapid local expression of IL-12, TNF-alpha, and IFN-gamma, and this expression was paralleled by containment and mitigation of the infection. |
| 5427 | 10085019 | In conclusion, immunization with F. tularensis LVS conferred a capability to respond to cutaneous reinfection, with rapid local expression of IL-12, TNF-alpha, and IFN-gamma, and this expression was paralleled by containment and mitigation of the infection. |
| 5428 | 10085019 | In conclusion, immunization with F. tularensis LVS conferred a capability to respond to cutaneous reinfection, with rapid local expression of IL-12, TNF-alpha, and IFN-gamma, and this expression was paralleled by containment and mitigation of the infection. |
| 5429 | 10085019 | In conclusion, immunization with F. tularensis LVS conferred a capability to respond to cutaneous reinfection, with rapid local expression of IL-12, TNF-alpha, and IFN-gamma, and this expression was paralleled by containment and mitigation of the infection. |
| 5430 | 10085019 | In conclusion, immunization with F. tularensis LVS conferred a capability to respond to cutaneous reinfection, with rapid local expression of IL-12, TNF-alpha, and IFN-gamma, and this expression was paralleled by containment and mitigation of the infection. |
| 5431 | 10077167 | Long-term survival and complete cures of B16 melanoma-carrying animals after therapy with tumor-targeted IL-2 and SEA. |
| 5432 | 10077167 | In contrast, the immune response after combination therapy was characterized by substantially augmented IFN-gamma and TNF-alpha production and strong CTL activity. |
| 5433 | 10052194 | Modifications of IFN-alpha, TNF-alpha and IFN-gamma serum levels in children vaccinated against measles. |
| 5434 | 10037196 | Here, we demonstrate that functional DCs can be generated from peripheral blood of patients with metastatic renal cell carcinoma (RCC) by culture of monocytes/macrophages (CD14+) in autologous serum containing medium (RPMI) in the presence of granulocyte macrophage colony-stimulating factor and interleukin (IL) 4. |
| 5435 | 10037196 | A synergistic effect of DC-TuLy and IL-2 in stimulating a T cell-dependent immune response was demonstrated by: (a) the increase of growth expansion of TILs (9.4-14.3-fold; day 21); (b) the up-regulation of the CD3+ CD56- TcR+ (both CD4+ and CD8+) cell population; (c) the augmentation of T cell-restricted autologous tumor lysis; and (d) the enhancement of IFN-gamma, tumor necrosis factor-alpha, granulocyte macrophage colony-stimulating factor, and IL-6 mRNA expression by TILs. |
| 5436 | 10024580 | This decreased proliferation was not a result of increased Mphi production of nitric oxide, prostaglandin E2, or oxygen radicals or the release of interleukin-1beta, tumor necrosis factor alpha, interleukin-6, or interleukin-10 following exposure to STF. |
| 5437 | 10023447 | IL-12 also stimulates IFN-gamma production from both T cells and NK cells. |
| 5438 | 10023447 | IL-12 also stimulates IFN-gamma production from both T cells and NK cells. |
| 5439 | 10023447 | In this study, we transfected methylcholanthrene-induced fibrosarcoma (MCA-D) with TNF gene and investigated the therapeutic effect of TNF gene-transduced cancer vaccine and whether the vaccination effect is enhanced by systemic administration of recombinant IL-12 (rIL-12), in a murine model. |
| 5440 | 10023447 | In this study, we transfected methylcholanthrene-induced fibrosarcoma (MCA-D) with TNF gene and investigated the therapeutic effect of TNF gene-transduced cancer vaccine and whether the vaccination effect is enhanced by systemic administration of recombinant IL-12 (rIL-12), in a murine model. |
| 5441 | 10023447 | Our findings show that synergistic enhancement of CTL activity and IFN-gamma production could play an important role in the antitumor effect of combination therapy using TNF gene-transduced cancer vaccine and rIL-12. |
| 5442 | 10023447 | Our findings show that synergistic enhancement of CTL activity and IFN-gamma production could play an important role in the antitumor effect of combination therapy using TNF gene-transduced cancer vaccine and rIL-12. |
| 5443 | 9973521 | Using PBMCs from bladder cancer patients, IFN-alpha was found to substantially enhance the efficacy of BCG to induce IFN-gamma production. |
| 5444 | 9973521 | In addition, IFN-alpha up-regulated BCG-induced IL-12 and TNF-alpha and down-regulated BCG-induced IL-10. |
| 5445 | 9973521 | Neutralizing endogenous IL-10 or adding exogenous IL-12 provided further synergy for IFN-gamma production. |
| 5446 | 9973521 | In clinical practice, intravesical IFN-alpha 2B (50 million units (MU)/dose) was observed to accelerate urinary IFN-gamma production to low-dose BCG (one-tenth or one-third of a full dose) in patients treated with combination therapy compared with BCG alone. |
| 5447 | 9973506 | These include IFN-gamma, IL-12, TNF-alpha, and IL-6, which are important in the control of intracellular bacterial infection. |
| 5448 | 9949802 | The reductase activity of these enzymes is enhanced by TNF-alpha and IL-1 beta. |
| 5449 | 9933432 | Urine of patients showed increased levels of IL-1beta, IL-2, IL-6, tumour necrosis factor-alpha (TNF-alpha), interferon-gamma (IFN-gamma) and macrophage colony-stimulating factor (M-CSF) after BCG instillation. |
| 5450 | 9933432 | Urine of patients showed increased levels of IL-1beta, IL-2, IL-6, tumour necrosis factor-alpha (TNF-alpha), interferon-gamma (IFN-gamma) and macrophage colony-stimulating factor (M-CSF) after BCG instillation. |
| 5451 | 9933432 | Levels of IL-2 and IFN-gamma in the serum also increased after BCG instillation, but IL-1beta, IL-6, TNF-alpha and M-CSF were not detectable. |
| 5452 | 9933432 | Levels of IL-2 and IFN-gamma in the serum also increased after BCG instillation, but IL-1beta, IL-6, TNF-alpha and M-CSF were not detectable. |
| 5453 | 9933432 | Maximal levels of IL-2 and IFN-gamma in the urine or serum were shown after the fourth instillation. |
| 5454 | 9933432 | Maximal levels of IL-2 and IFN-gamma in the urine or serum were shown after the fourth instillation. |
| 5455 | 9927516 | IL-12 p70 production by stimulated human monocytes was inhibited by CT in a dose-dependent manner. |
| 5456 | 9927516 | CT also inhibited the production of IL-12 p70 by monocyte-derived dendritic cells, as well as the production of tumor necrosis factor alpha, but not IL-10, IL-6, or transforming growth factor (TGF)-beta1, by stimulated monocytes. |
| 5457 | 9927516 | The effects of CT were not due to autocrine production of IL-10, TGF-beta1, or prostaglandin E2. |
| 5458 | 9927516 | CT inhibited the production of IFN-gamma by anti-CD3-stimulated human peripheral blood mononuclear cell, due in part to suppression of IL-12 production, but also to the inhibition of expression of the beta1 and beta2 chains of the IL-12 receptor on T cells. |
| 5459 | 9927516 | In vivo, mice given CT before systemic challenge with lipopolysaccharide had markedly reduced serum levels of IL-12 p40 and interferon gamma. |
| 5460 | 9886383 | BmDC cultured under various conditions (granulocyte-macrophage CSF (GM-CSF) or GM-CSF plus IL-4 alone or in combination with Flt3 ligand, TNF-alpha, LPS, or CD40 ligand (CD40L)) were analyzed morphologically, phenotypically, and functionally and were tested for their ability to promote prophylactic and/or therapeutic antitumor immunity. |
| 5461 | 9886383 | Whereas cells cultured in GM-CSF alone were functionally immature, cells incubated with CD40L or LPS were mature BmDC, as evident by morphology, capacity to internalize Ag, migration into regional lymph nodes, IL-12 secretion, and alloantigen or peptide Ag presentation in vitro. |
| 5462 | 9878011 | Immunohistochemical staining was used to enumerate cytokine-producing cells (monokines: interleukin [IL]-1alpha, IL-1beta, IL-6, and tumor necrosis factor [TNF]-alpha; lymphokines: interferon-gamma, IL-2, IL-4, and TNF-beta) in tissues obtained at autopsy from subjects with HPS. |
| 5463 | 9865682 | Most important for its use as an adjuvant in human cancer vaccine are its ability to introduce T-cell costimulatory activity, to prevent anergy induction, and to induce locally chemokines (eg, RANTES, IP-10) and cytokines (eg, interferon alpha, beta [IFN-alpha, beta] and tumor necrosis factor-alpha [TNFalpha]) that affect T-cell recruitment and activation. |
| 5464 | 9829733 | High enrichment of CD34+ HSCs was obtained using an immunomagnetic bead cell separation device. |
| 5465 | 9829733 | After separation, the negative fraction of mobilized PBMCs from normal donors and cancer patients contained undetectable levels of CD34+ HSCs by flow cytometry. |
| 5466 | 9829733 | This fraction of cells was then subjected to plastic adherence, and the adherent cells were cultured for 7 days in GM-CSF (100 ng/ml) and interleukin 4 (50 ng/ml) followed by an additional 7 days in GM-CSF, interleukin 4, and tumor necrosis factor alpha (10 ng/ml) to generate DCs. |
| 5467 | 9829733 | Harvested DCs represented yields of 4.1+/-1.4 and 5.8+/-5.4% of the initial cells plated from the CD34+ cell-depleted mobilized PBMCs of normal donors and cancer patients, respectively, and displayed a high level expression of CD80, CD86, HLA-DR, and CD11c but not CD14. |
| 5468 | 9829733 | Collectively, these results demonstrate the feasibility of obtaining both DCs and CD34+ HSCs from the same leukapheresis collection from G-CSF-primed normal donors and cancer patients in sufficient numbers for the purpose of combined PBSCT and immunization strategies. |
| 5469 | 9815645 | We report here the serial phenotypic characterization of a CTL line directed against an immunodominant epitope (YLSGANLNL, designated CAP-1) of human carcinoembryonic antigen (CEA). |
| 5470 | 9815645 | This CTL line was derived from peripheral blood mononuclear cells of a patient with metastatic carcinoma who had been treated with a recombinant CEA-vaccinia vaccine in a Phase I trial; the CTLs were analyzed through 20 in vitro cycle passages of stimulation with CAP-1 peptide and interleukin 2 in the presence of autologous antigen-presenting cells. |
| 5471 | 9815645 | The CTL line was shown to be phenotypically stable in terms of high levels of cytokine (IFN-gamma, tumor necrosis factor, and granulocyte-macrophage colony-stimulating factor) production, expression of homing-adhesion molecules, ability to lyse peptide-pulsed targets, and ability to lyse human carcinoma cells endogenously expressing CEA in a MHC-restricted manner. |
| 5472 | 9806041 | Regulation of interleukin-12 by interleukin-10, transforming growth factor-beta, tumor necrosis factor-alpha, and interferon-gamma in human monocytes infected with Mycobacterium tuberculosis H37Ra. |
| 5473 | 9806041 | Regulation of interleukin-12 by interleukin-10, transforming growth factor-beta, tumor necrosis factor-alpha, and interferon-gamma in human monocytes infected with Mycobacterium tuberculosis H37Ra. |
| 5474 | 9806041 | Regulation of interleukin-12 by interleukin-10, transforming growth factor-beta, tumor necrosis factor-alpha, and interferon-gamma in human monocytes infected with Mycobacterium tuberculosis H37Ra. |
| 5475 | 9806041 | Regulation of interleukin (IL)-12 production by coexpression of tumor necrosis factor (TNF)-alpha, IL-10, and transforming growth factor (TGF)-beta in human monocytes infected with Mycobacterium tuberculosis H37Ra was analyzed. |
| 5476 | 9806041 | Regulation of interleukin (IL)-12 production by coexpression of tumor necrosis factor (TNF)-alpha, IL-10, and transforming growth factor (TGF)-beta in human monocytes infected with Mycobacterium tuberculosis H37Ra was analyzed. |
| 5477 | 9806041 | Regulation of interleukin (IL)-12 production by coexpression of tumor necrosis factor (TNF)-alpha, IL-10, and transforming growth factor (TGF)-beta in human monocytes infected with Mycobacterium tuberculosis H37Ra was analyzed. |
| 5478 | 9806041 | Also, since IL-12 induces interferon (IFN)-gamma, the effect of IFN-gamma on IL-12 expression was examined. |
| 5479 | 9806041 | Also, since IL-12 induces interferon (IFN)-gamma, the effect of IFN-gamma on IL-12 expression was examined. |
| 5480 | 9806041 | Also, since IL-12 induces interferon (IFN)-gamma, the effect of IFN-gamma on IL-12 expression was examined. |
| 5481 | 9806041 | IL-12 p70 protein paralleled IL-12 p40 protein expression. |
| 5482 | 9806041 | IL-12 p70 protein paralleled IL-12 p40 protein expression. |
| 5483 | 9806041 | IL-12 p70 protein paralleled IL-12 p40 protein expression. |
| 5484 | 9806041 | TNF-alpha protein expression occurred earlier than IL-12 p40 protein but was not required for IL-12 induction. |
| 5485 | 9806041 | TNF-alpha protein expression occurred earlier than IL-12 p40 protein but was not required for IL-12 induction. |
| 5486 | 9806041 | TNF-alpha protein expression occurred earlier than IL-12 p40 protein but was not required for IL-12 induction. |
| 5487 | 9806041 | Addition or neutralization of TGF-beta did not significantly alter IL-12 induction. |
| 5488 | 9806041 | Addition or neutralization of TGF-beta did not significantly alter IL-12 induction. |
| 5489 | 9806041 | Addition or neutralization of TGF-beta did not significantly alter IL-12 induction. |
| 5490 | 9806041 | In contrast, recombinant IL-10 reduced IL-12 and neutralization of IL-10 minimally enhanced IL-12. |
| 5491 | 9806041 | In contrast, recombinant IL-10 reduced IL-12 and neutralization of IL-10 minimally enhanced IL-12. |
| 5492 | 9806041 | In contrast, recombinant IL-10 reduced IL-12 and neutralization of IL-10 minimally enhanced IL-12. |
| 5493 | 9806041 | A pronounced increase in IL-12 followed IFN-gamma pretreatment, which selectively up-regulated IL-12 p35 mRNA. |
| 5494 | 9806041 | A pronounced increase in IL-12 followed IFN-gamma pretreatment, which selectively up-regulated IL-12 p35 mRNA. |
| 5495 | 9806041 | A pronounced increase in IL-12 followed IFN-gamma pretreatment, which selectively up-regulated IL-12 p35 mRNA. |
| 5496 | 9802972 | Immune suppression by recombinant interleukin (rIL)-12 involves interferon gamma induction of nitric oxide synthase 2 (iNOS) activity: inhibitors of NO generation reveal the extent of rIL-12 vaccine adjuvant effect. |
| 5497 | 9802972 | Use of neutralizing antibodies and genetically deficient mice showed that IFN-gamma (but not TNF-alpha) mediated rmIL-12-induced immune suppression. |
| 5498 | 9789739 | Unstimulated DC from young and old individuals had a similar surface expression of MHC class II and CD54 and secreted moderate amounts of IL-12 and TNF-alpha. |
| 5499 | 9784552 | Analysis of the cytokines expressed by the Th cells revealed that all clones expressed gamma interferon and tumor necrosis factor alpha, and most coexpressed interleukin-4. |
| 5500 | 9782116 | Supraoptimal peptide-major histocompatibility complex causes a decrease in bc1-2 levels and allows tumor necrosis factor alpha receptor II-mediated apoptosis of cytotoxic T lymphocytes. |
| 5501 | 9780194 | IFN-gamma, IL-12, and TNF-alpha are required to maintain reduced liver pathology in mice vaccinated with Schistosoma mansoni eggs and IL-12. |
| 5502 | 9780194 | IFN-gamma, IL-12, and TNF-alpha are required to maintain reduced liver pathology in mice vaccinated with Schistosoma mansoni eggs and IL-12. |
| 5503 | 9780194 | IFN-gamma, IL-12, and TNF-alpha are required to maintain reduced liver pathology in mice vaccinated with Schistosoma mansoni eggs and IL-12. |
| 5504 | 9780194 | In this study, we demonstrate that in contrast with egg/IL-12-sensitized animals that showed marked decreases in pathology, mice similarly sensitized but depleted of IFN-gamma, IL-12, or TNF-alpha at the time of egg laying developed granulomas that were similar to the non-IL-12-treated control group. |
| 5505 | 9780194 | In this study, we demonstrate that in contrast with egg/IL-12-sensitized animals that showed marked decreases in pathology, mice similarly sensitized but depleted of IFN-gamma, IL-12, or TNF-alpha at the time of egg laying developed granulomas that were similar to the non-IL-12-treated control group. |
| 5506 | 9780194 | In this study, we demonstrate that in contrast with egg/IL-12-sensitized animals that showed marked decreases in pathology, mice similarly sensitized but depleted of IFN-gamma, IL-12, or TNF-alpha at the time of egg laying developed granulomas that were similar to the non-IL-12-treated control group. |
| 5507 | 9780194 | Moreover, egg/IL-12-sensitized mice depleted of IFN-gamma or IL-12 displayed a partial reduction in IFN-gamma production, suggesting that multiple type 1 cytokines were required to maintain polarized type 1 responses to chronic type 2-inducing stimuli. |
| 5508 | 9780194 | Moreover, egg/IL-12-sensitized mice depleted of IFN-gamma or IL-12 displayed a partial reduction in IFN-gamma production, suggesting that multiple type 1 cytokines were required to maintain polarized type 1 responses to chronic type 2-inducing stimuli. |
| 5509 | 9780194 | Moreover, egg/IL-12-sensitized mice depleted of IFN-gamma or IL-12 displayed a partial reduction in IFN-gamma production, suggesting that multiple type 1 cytokines were required to maintain polarized type 1 responses to chronic type 2-inducing stimuli. |
| 5510 | 9780194 | Together, these data reveal key roles for IFN-gamma, IL-12, and TNF-alpha in the protective effects mediated by this IL-12-based vaccine to prevent pathology. |
| 5511 | 9780194 | Together, these data reveal key roles for IFN-gamma, IL-12, and TNF-alpha in the protective effects mediated by this IL-12-based vaccine to prevent pathology. |
| 5512 | 9780194 | Together, these data reveal key roles for IFN-gamma, IL-12, and TNF-alpha in the protective effects mediated by this IL-12-based vaccine to prevent pathology. |
| 5513 | 9776139 | IFN-gamma, TNF-alpha, IL-4 and IL-10 were evaluated in the PFMC supernatants stimulated by these antigens. |
| 5514 | 9776139 | IFN-gamma, TNF-alpha, IL-4 and IL-10 were evaluated in the PFMC supernatants stimulated by these antigens. |
| 5515 | 9776139 | Both crude and 70-kDa antigens induced higher levels of IFN-gamma, TNF-alpha and IL-10. |
| 5516 | 9776139 | Both crude and 70-kDa antigens induced higher levels of IFN-gamma, TNF-alpha and IL-10. |
| 5517 | 9776139 | There was a significant positive correlation between IFN-gamma and the proliferative response induced by crude M. tuberculosis antigen, and an inverse correlation was identified between IL-10 and cell proliferation. |
| 5518 | 9776139 | There was a significant positive correlation between IFN-gamma and the proliferative response induced by crude M. tuberculosis antigen, and an inverse correlation was identified between IL-10 and cell proliferation. |
| 5519 | 9755879 | Evidence of an antigen-specific CD8+ T cell response (cytotoxicity and/or tumor necrosis factor production) was detected in three of the five CD8+ VIL. |
| 5520 | 9743369 | In contrast to LPS, CpG ODN stimulated FSDDC to produce large amounts of IL-12 but only small amounts of IL-6 and TNF-alpha. |
| 5521 | 9739045 | We coimmunized cDNA expression cassettes encoding the alpha-chemokines IL-8 and SDF-1alpha and the beta-chemokines MIP-1alpha, RANTES, and MCP-1 along with DNA immunogens and analyzed the resulting antigen-specific immune responses. |
| 5522 | 9739045 | In a manner more similar to the traditional immune modulatory role of CD4(+) T cells via the expression of Th1 or Th2 cytokines, CD8(+) T cells appeared to play an important role in immune expansion and effector function by producing chemokines. |
| 5523 | 9739045 | For instance, IL-8 was a strong inducer of CD4(+) T cells, indicated by strong T helper proliferative responses as well as an enhancement of antibody responses. |
| 5524 | 9739045 | Among the chemokines examined, MCP-1 was the most potent activator of CD8(+) CTL activity. |
| 5525 | 9739045 | The enhanced CTL results are supported by the increased expression of Th1 cytokines IFN-gamma and TNF-alpha and the reduction of IgG1/IgG2a ratio. |
| 5526 | 9733870 | Here we apply MVA to human immunodeficiency virus type 1 (HIV-1) vaccine development by incorporating the envelope protein gp160 of HIV-1 primary isolate strain 89.6 (MVA 89.6) and use it to induce mucosal cytotoxic-T-lymphocyte (CTL) immunity. |
| 5527 | 9733870 | Immunization with MVA 89.6 led to (i) the loading of antigen-presenting cells in vivo, as measured by the ex vivo active presentation of the P18-89.6 peptide to an antigen-specific CTL line, and (ii) the significant production of the proinflammatory cytokines (interleukin-6 and tumor necrosis factor alpha) in the mucosal sites. |
| 5528 | 9724878 | In comparative studies of coccidiosis in chickens, in-vivo and in-vitro studies revealed that interferon-gamma, tumor necrosis factor and transforming growth factor-beta are induced following Eimeria infection. |
| 5529 | 9712369 | The TIL cultures were initiated using OKT3 mAb in the presence of moderate concentrations (25-50 U/ml) of IL-2, followed by 100 U/ml of tumor necrosis factor (TNF)-alpha. |
| 5530 | 9712369 | The TIL cultures were initiated using OKT3 mAb in the presence of moderate concentrations (25-50 U/ml) of IL-2, followed by 100 U/ml of tumor necrosis factor (TNF)-alpha. |
| 5531 | 9712369 | TAL were not stimulated with OKT3 mAb, but all were successfully expanded in culture in the presence of IL-2 alone or together with TNF-alpha. |
| 5532 | 9712369 | TAL were not stimulated with OKT3 mAb, but all were successfully expanded in culture in the presence of IL-2 alone or together with TNF-alpha. |
| 5533 | 9711781 | Maturation of human neonatal CD4+ and CD8+ T lymphocytes into Th1/Th2 effectors. |
| 5534 | 9711781 | The activation and maturation of neonatal CD4+ T cells is particularly dependent upon the strength of CD28-mediated cosignal which dictates not only the cytokine profile released upon primary activation but also the response to IL-12. |
| 5535 | 9711781 | Activation of adult as well as neonatal CD4+ T cells in the context of low CD28 costimulation yields to the production of low levels of only one cytokine, i.e. |
| 5536 | 9711781 | In contrast, strong CD28 costimulation supports the production of high levels of type 1 (IL-2, IFN gamma and TNF beta) and low levels of type 2 (IL-4 and IL-13) cytokines by neonatal T cells. |
| 5537 | 9711781 | The low levels of naive T cell-derived IL-4 are sufficient to support their development into high IL-4/IL-5 producers by an autocrine pathway. |
| 5538 | 9711781 | The ability of IL-12 to prime neonatal CD4+ T cells for increased production of IL-4 (in addition to IFN gamma) is observed only when CD28 cosignal is minimal. |
| 5539 | 9711781 | Unlike CD4+ T cells, neonatal CD8+ T cells strictly require exogenous IL-4 to develop into IL-4/IL-5 producers. |
| 5540 | 9711781 | Most importantly, anti-CD3/B7-activated neonatal CD8 T cells coexpress CD4 as well as CCR5 and CXCR4 and are susceptible to HIV-1 infection in vitro. |
| 5541 | 9711774 | We have studied the mechanisms associated with the dysregulation of myeloid lineage cytokines, GM-CSF and M-CSF, and lymphokines, IL-12, and IL-15 in activated CB when compared with APB MNC. |
| 5542 | 9711774 | We have studied the mechanisms associated with the dysregulation of myeloid lineage cytokines, GM-CSF and M-CSF, and lymphokines, IL-12, and IL-15 in activated CB when compared with APB MNC. |
| 5543 | 9711774 | Furthermore, we have studied the effects of IL-12 and IL-15 on induction of IFN-gamma and TNF-alpha production, NK, and LAK activities in CB and APB. |
| 5544 | 9711774 | Furthermore, we have studied the effects of IL-12 and IL-15 on induction of IFN-gamma and TNF-alpha production, NK, and LAK activities in CB and APB. |
| 5545 | 9711774 | GM-CSF, M-CSF, IL-12 and IL-15 protein and mRNA are decreased in activated CB MNC. |
| 5546 | 9711774 | GM-CSF, M-CSF, IL-12 and IL-15 protein and mRNA are decreased in activated CB MNC. |
| 5547 | 9711774 | The impaired ability of CB to produce IL-12 and IL-15 in response to stimulation may contribute to the decrease in IFN-gamma, TNF-alpha production, NK and LAK activities. |
| 5548 | 9711774 | The impaired ability of CB to produce IL-12 and IL-15 in response to stimulation may contribute to the decrease in IFN-gamma, TNF-alpha production, NK and LAK activities. |
| 5549 | 9711774 | Furthermore, combination of low dose IL-12 and IL-15 may augment cytotoxic activities and minimize toxicity. |
| 5550 | 9711774 | Furthermore, combination of low dose IL-12 and IL-15 may augment cytotoxic activities and minimize toxicity. |
| 5551 | 9686610 | Control of IL-12 and IFN-gamma production in response to live or dead bacteria by TNF and other factors. |
| 5552 | 9686610 | Control of IL-12 and IFN-gamma production in response to live or dead bacteria by TNF and other factors. |
| 5553 | 9686610 | Production of IL-12, detected in serum and spleen, was neither increased nor prolonged by injecting Abs to IL-10 or IL-4. |
| 5554 | 9686610 | Production of IL-12, detected in serum and spleen, was neither increased nor prolonged by injecting Abs to IL-10 or IL-4. |
| 5555 | 9686610 | Mice lacking the receptors for TNF (TNFR-/- mice) were severely deficient in IL-12 production, suggesting a controlling role for TNF, which we have previously shown to be triggered by live, rather than dead, bacteria. |
| 5556 | 9686610 | Mice lacking the receptors for TNF (TNFR-/- mice) were severely deficient in IL-12 production, suggesting a controlling role for TNF, which we have previously shown to be triggered by live, rather than dead, bacteria. |
| 5557 | 9686186 | We have shown that IL-12, a powerful inducer of IFN-gamma production by NK cells, is synthesized soon after trypomastigote-macrophage interaction. |
| 5558 | 9686186 | We have shown that IL-12, a powerful inducer of IFN-gamma production by NK cells, is synthesized soon after trypomastigote-macrophage interaction. |
| 5559 | 9686186 | Also, treatment of infected mice with mAb specific for IFN-gamma or TNF-alpha inhibited the protective effect of exogenous IL-12. |
| 5560 | 9686186 | Also, treatment of infected mice with mAb specific for IFN-gamma or TNF-alpha inhibited the protective effect of exogenous IL-12. |
| 5561 | 9686186 | On the other hand, TGF-beta and IL-10 produced by infected macrophages inhibited the induction and effects of IL-12. |
| 5562 | 9686186 | On the other hand, TGF-beta and IL-10 produced by infected macrophages inhibited the induction and effects of IL-12. |
| 5563 | 9686186 | Therefore, while IL-12, TNF-alpha and IFN-gamma correlate with resistance to T. cruzi infection, TGF-beta and IL-10 promote susceptibility. |
| 5564 | 9686186 | Therefore, while IL-12, TNF-alpha and IFN-gamma correlate with resistance to T. cruzi infection, TGF-beta and IL-10 promote susceptibility. |
| 5565 | 9673234 | Protein malnutrition also impaired the abilities of cells from vaccinated LP guinea pigs to produce cytokines, including interferon, tumor necrosis factor alpha (TNF-alpha) and transforming growth factor beta (TGF-beta), in response to PPD, despite the demonstration of higher serum levels of TNF-alpha and TGF-beta after an intravenous injection of PPD into LP guinea pigs. |
| 5566 | 9670850 | However, they produced high levels of IL2, TNFalpha and IL10. |
| 5567 | 9665972 | Inhibition of Mycobacterium bovis BCG-induced tumor necrosis factor alpha secretion in human cells by transforming growth factor beta. |
| 5568 | 9665972 | Inhibition of Mycobacterium bovis BCG-induced tumor necrosis factor alpha secretion in human cells by transforming growth factor beta. |
| 5569 | 9665972 | Inhibition of Mycobacterium bovis BCG-induced tumor necrosis factor alpha secretion in human cells by transforming growth factor beta. |
| 5570 | 9665972 | Inhibition of Mycobacterium bovis BCG-induced tumor necrosis factor alpha secretion in human cells by transforming growth factor beta. |
| 5571 | 9665972 | Inhibition of Mycobacterium bovis BCG-induced tumor necrosis factor alpha secretion in human cells by transforming growth factor beta. |
| 5572 | 9665972 | Inhibition of Mycobacterium bovis BCG-induced tumor necrosis factor alpha secretion in human cells by transforming growth factor beta. |
| 5573 | 9665972 | The effect of exogenous transforming growth factor beta (TGF-beta) on Mycobacterium bovis BCG-induced tumor necrosis factor alpha (TNF-alpha) production by human mononuclear cells was studied. |
| 5574 | 9665972 | The effect of exogenous transforming growth factor beta (TGF-beta) on Mycobacterium bovis BCG-induced tumor necrosis factor alpha (TNF-alpha) production by human mononuclear cells was studied. |
| 5575 | 9665972 | The effect of exogenous transforming growth factor beta (TGF-beta) on Mycobacterium bovis BCG-induced tumor necrosis factor alpha (TNF-alpha) production by human mononuclear cells was studied. |
| 5576 | 9665972 | The effect of exogenous transforming growth factor beta (TGF-beta) on Mycobacterium bovis BCG-induced tumor necrosis factor alpha (TNF-alpha) production by human mononuclear cells was studied. |
| 5577 | 9665972 | The effect of exogenous transforming growth factor beta (TGF-beta) on Mycobacterium bovis BCG-induced tumor necrosis factor alpha (TNF-alpha) production by human mononuclear cells was studied. |
| 5578 | 9665972 | The effect of exogenous transforming growth factor beta (TGF-beta) on Mycobacterium bovis BCG-induced tumor necrosis factor alpha (TNF-alpha) production by human mononuclear cells was studied. |
| 5579 | 9665972 | It was found that TNF-alpha production by human cells stimulated with BCG was significantly inhibited by TGF-beta. |
| 5580 | 9665972 | It was found that TNF-alpha production by human cells stimulated with BCG was significantly inhibited by TGF-beta. |
| 5581 | 9665972 | It was found that TNF-alpha production by human cells stimulated with BCG was significantly inhibited by TGF-beta. |
| 5582 | 9665972 | It was found that TNF-alpha production by human cells stimulated with BCG was significantly inhibited by TGF-beta. |
| 5583 | 9665972 | It was found that TNF-alpha production by human cells stimulated with BCG was significantly inhibited by TGF-beta. |
| 5584 | 9665972 | It was found that TNF-alpha production by human cells stimulated with BCG was significantly inhibited by TGF-beta. |
| 5585 | 9665972 | Furthermore, the suppressive effect of TGF-beta on TNF-alpha secretion in this system was not due to a direct cytotoxic effect, since cell viability was comparable in the presence or absence of TGF-beta. |
| 5586 | 9665972 | Furthermore, the suppressive effect of TGF-beta on TNF-alpha secretion in this system was not due to a direct cytotoxic effect, since cell viability was comparable in the presence or absence of TGF-beta. |
| 5587 | 9665972 | Furthermore, the suppressive effect of TGF-beta on TNF-alpha secretion in this system was not due to a direct cytotoxic effect, since cell viability was comparable in the presence or absence of TGF-beta. |
| 5588 | 9665972 | Furthermore, the suppressive effect of TGF-beta on TNF-alpha secretion in this system was not due to a direct cytotoxic effect, since cell viability was comparable in the presence or absence of TGF-beta. |
| 5589 | 9665972 | Furthermore, the suppressive effect of TGF-beta on TNF-alpha secretion in this system was not due to a direct cytotoxic effect, since cell viability was comparable in the presence or absence of TGF-beta. |
| 5590 | 9665972 | Furthermore, the suppressive effect of TGF-beta on TNF-alpha secretion in this system was not due to a direct cytotoxic effect, since cell viability was comparable in the presence or absence of TGF-beta. |
| 5591 | 9665972 | Interestingly, our results demonstrated comparative suppressive effects of TGF-beta and interleukin-10 on BCG-induced TNF-alpha secretion. |
| 5592 | 9665972 | Interestingly, our results demonstrated comparative suppressive effects of TGF-beta and interleukin-10 on BCG-induced TNF-alpha secretion. |
| 5593 | 9665972 | Interestingly, our results demonstrated comparative suppressive effects of TGF-beta and interleukin-10 on BCG-induced TNF-alpha secretion. |
| 5594 | 9665972 | Interestingly, our results demonstrated comparative suppressive effects of TGF-beta and interleukin-10 on BCG-induced TNF-alpha secretion. |
| 5595 | 9665972 | Interestingly, our results demonstrated comparative suppressive effects of TGF-beta and interleukin-10 on BCG-induced TNF-alpha secretion. |
| 5596 | 9665972 | Interestingly, our results demonstrated comparative suppressive effects of TGF-beta and interleukin-10 on BCG-induced TNF-alpha secretion. |
| 5597 | 9665972 | Together, the data demonstrate, for the first time, that TGF-beta inhibits BCG-induced TNF-alpha secretion by human cells. |
| 5598 | 9665972 | Together, the data demonstrate, for the first time, that TGF-beta inhibits BCG-induced TNF-alpha secretion by human cells. |
| 5599 | 9665972 | Together, the data demonstrate, for the first time, that TGF-beta inhibits BCG-induced TNF-alpha secretion by human cells. |
| 5600 | 9665972 | Together, the data demonstrate, for the first time, that TGF-beta inhibits BCG-induced TNF-alpha secretion by human cells. |
| 5601 | 9665972 | Together, the data demonstrate, for the first time, that TGF-beta inhibits BCG-induced TNF-alpha secretion by human cells. |
| 5602 | 9665972 | Together, the data demonstrate, for the first time, that TGF-beta inhibits BCG-induced TNF-alpha secretion by human cells. |
| 5603 | 9656452 | Neither of the inflammatory cytokines IL-1 beta and TNF alpha were detected in efferent lymph from any animals in this study. |
| 5604 | 9643372 | HIV viral load and type 1 (IL-2 and IFN-gamma) and type 2 (IL-4 and IL-10) cytokine production were evaluated before and 7, 14, and 28 days after vaccination. |
| 5605 | 9643372 | Because polysaccharides of the bacterial cell wall stimulate TNF-alpha production by monocyte-macrophages and TNF-alpha was shown to stimulate HIV replication directly on activation of NF-kappa b after binding the long terminal repeat (LTR) sequences of HIV, we measured TNF-alpha production and observed a significant increase in both groups of vaccines. |
| 5606 | 9573027 | We have recently found in normal human marrow a subset of CD34(+) cells that constitutively expresses HLA-DR and low levels of CD86, a natural ligand for the T cell costimulation receptor CD28. |
| 5607 | 9573027 | We have recently found in normal human marrow a subset of CD34(+) cells that constitutively expresses HLA-DR and low levels of CD86, a natural ligand for the T cell costimulation receptor CD28. |
| 5608 | 9573027 | We have recently found in normal human marrow a subset of CD34(+) cells that constitutively expresses HLA-DR and low levels of CD86, a natural ligand for the T cell costimulation receptor CD28. |
| 5609 | 9573027 | We have recently found in normal human marrow a subset of CD34(+) cells that constitutively expresses HLA-DR and low levels of CD86, a natural ligand for the T cell costimulation receptor CD28. |
| 5610 | 9573027 | In this study, we show that CD34(+)/CD86(+) cells can also present tetanus toxoid antigen to memory CD4(+) T cells. |
| 5611 | 9573027 | In this study, we show that CD34(+)/CD86(+) cells can also present tetanus toxoid antigen to memory CD4(+) T cells. |
| 5612 | 9573027 | In this study, we show that CD34(+)/CD86(+) cells can also present tetanus toxoid antigen to memory CD4(+) T cells. |
| 5613 | 9573027 | In this study, we show that CD34(+)/CD86(+) cells can also present tetanus toxoid antigen to memory CD4(+) T cells. |
| 5614 | 9573027 | CD34(+)/CD86(+) marrow cells cultured in granulocyte-macrophage colony-stimulating factor (GM-CSF)-generated macrophages. |
| 5615 | 9573027 | CD34(+)/CD86(+) marrow cells cultured in granulocyte-macrophage colony-stimulating factor (GM-CSF)-generated macrophages. |
| 5616 | 9573027 | CD34(+)/CD86(+) marrow cells cultured in granulocyte-macrophage colony-stimulating factor (GM-CSF)-generated macrophages. |
| 5617 | 9573027 | CD34(+)/CD86(+) marrow cells cultured in granulocyte-macrophage colony-stimulating factor (GM-CSF)-generated macrophages. |
| 5618 | 9573027 | In contrast, CD34(+)/CD86(-) cells cultured in GM-CSF generated a predominant population of granulocytes. |
| 5619 | 9573027 | In contrast, CD34(+)/CD86(-) cells cultured in GM-CSF generated a predominant population of granulocytes. |
| 5620 | 9573027 | In contrast, CD34(+)/CD86(-) cells cultured in GM-CSF generated a predominant population of granulocytes. |
| 5621 | 9573027 | In contrast, CD34(+)/CD86(-) cells cultured in GM-CSF generated a predominant population of granulocytes. |
| 5622 | 9573027 | CD34(+)/CD86(+) cells cultured in GM-CSF plus tumor necrosis factor-alpha (TNF-alpha) generated almost exclusively CD1a+/CD83(+) dendritic cells. |
| 5623 | 9573027 | CD34(+)/CD86(+) cells cultured in GM-CSF plus tumor necrosis factor-alpha (TNF-alpha) generated almost exclusively CD1a+/CD83(+) dendritic cells. |
| 5624 | 9573027 | CD34(+)/CD86(+) cells cultured in GM-CSF plus tumor necrosis factor-alpha (TNF-alpha) generated almost exclusively CD1a+/CD83(+) dendritic cells. |
| 5625 | 9573027 | CD34(+)/CD86(+) cells cultured in GM-CSF plus tumor necrosis factor-alpha (TNF-alpha) generated almost exclusively CD1a+/CD83(+) dendritic cells. |
| 5626 | 9573027 | In contrast, CD34(+)/CD86(-) cells cultured in GM-CSF plus TNF-alpha generated a variety of cell types, including a small population of dendritic cells. |
| 5627 | 9573027 | In contrast, CD34(+)/CD86(-) cells cultured in GM-CSF plus TNF-alpha generated a variety of cell types, including a small population of dendritic cells. |
| 5628 | 9573027 | In contrast, CD34(+)/CD86(-) cells cultured in GM-CSF plus TNF-alpha generated a variety of cell types, including a small population of dendritic cells. |
| 5629 | 9573027 | In contrast, CD34(+)/CD86(-) cells cultured in GM-CSF plus TNF-alpha generated a variety of cell types, including a small population of dendritic cells. |
| 5630 | 9573027 | In addition, CD34(+)/CD86(+) cells cultured in granulocyte colony-stimulating factor failed to generate CD15(+) granulocytes. |
| 5631 | 9573027 | In addition, CD34(+)/CD86(+) cells cultured in granulocyte colony-stimulating factor failed to generate CD15(+) granulocytes. |
| 5632 | 9573027 | In addition, CD34(+)/CD86(+) cells cultured in granulocyte colony-stimulating factor failed to generate CD15(+) granulocytes. |
| 5633 | 9573027 | In addition, CD34(+)/CD86(+) cells cultured in granulocyte colony-stimulating factor failed to generate CD15(+) granulocytes. |
| 5634 | 9573027 | The ontogeny of dendritic cells was recapitulated by stimulation of CD34(+)/CD86(-) cells with TNF-alpha that induced expression of CD86. |
| 5635 | 9573027 | The ontogeny of dendritic cells was recapitulated by stimulation of CD34(+)/CD86(-) cells with TNF-alpha that induced expression of CD86. |
| 5636 | 9573027 | The ontogeny of dendritic cells was recapitulated by stimulation of CD34(+)/CD86(-) cells with TNF-alpha that induced expression of CD86. |
| 5637 | 9573027 | The ontogeny of dendritic cells was recapitulated by stimulation of CD34(+)/CD86(-) cells with TNF-alpha that induced expression of CD86. |
| 5638 | 9573027 | Subsequent costimulation of CD86(+) cells with GM-CSF plus TNF-alpha lead to expression of CD83 and produced terminal dendritic cell differentiation. |
| 5639 | 9573027 | Subsequent costimulation of CD86(+) cells with GM-CSF plus TNF-alpha lead to expression of CD83 and produced terminal dendritic cell differentiation. |
| 5640 | 9573027 | Subsequent costimulation of CD86(+) cells with GM-CSF plus TNF-alpha lead to expression of CD83 and produced terminal dendritic cell differentiation. |
| 5641 | 9573027 | Subsequent costimulation of CD86(+) cells with GM-CSF plus TNF-alpha lead to expression of CD83 and produced terminal dendritic cell differentiation. |
| 5642 | 9616162 | The role of tumor necrosis factor alpha in modulating the quantity of peripheral blood-derived, cytokine-driven human dendritic cells and its role in enhancing the quality of dendritic cell function in presenting soluble antigens to CD4+ T cells in vitro. |
| 5643 | 9616162 | The role of tumor necrosis factor alpha in modulating the quantity of peripheral blood-derived, cytokine-driven human dendritic cells and its role in enhancing the quality of dendritic cell function in presenting soluble antigens to CD4+ T cells in vitro. |
| 5644 | 9616162 | DC progenitors from peripheral blood mononuclear cells (PBMC) were enriched by adherence to plastic, and the adherent cells were then cultured in serum-free XVIVO-15 medium (SFM) for 7 days with added granulocyte-macrophage colony-stimulating factor (GM-CSF) and interleukin-4 (IL-4). |
| 5645 | 9616162 | DC progenitors from peripheral blood mononuclear cells (PBMC) were enriched by adherence to plastic, and the adherent cells were then cultured in serum-free XVIVO-15 medium (SFM) for 7 days with added granulocyte-macrophage colony-stimulating factor (GM-CSF) and interleukin-4 (IL-4). |
| 5646 | 9616162 | Moreover, 14-day cultured DC generated in the presence of TNFalpha (when added at day 7) demonstrated marked enhancement in their capacity to stimulate a primary allogeneic mixed leukocyte reaction (8-fold increase in stimulation index [SI]) as well as to present soluble tetanus toxoid and candida albicans (10- to 100-fold increases in SI) to purified CD4+ T cells. |
| 5647 | 9616162 | Moreover, 14-day cultured DC generated in the presence of TNFalpha (when added at day 7) demonstrated marked enhancement in their capacity to stimulate a primary allogeneic mixed leukocyte reaction (8-fold increase in stimulation index [SI]) as well as to present soluble tetanus toxoid and candida albicans (10- to 100-fold increases in SI) to purified CD4+ T cells. |
| 5648 | 9616162 | When compared with non-TNFalpha-supplemented cultures, these DC also displayed an increased surface expression of CD83 as well as the costimulatory molecules, CD80 and CD86. |
| 5649 | 9616162 | When compared with non-TNFalpha-supplemented cultures, these DC also displayed an increased surface expression of CD83 as well as the costimulatory molecules, CD80 and CD86. |
| 5650 | 9620291 | In the ex vivo tumor vaccine approach, B16 melanoma cells, transduced in vitro by adenovirus containing either interleukin (IL)-2, granulocyte-macrophage colony stimulating factor (GM-CSF), or tumor necrosis factor-alpha cytokine genes and gamma irradiated, were subcutaneously injected into the flank and a distant subcutaneous challenge injection of unmodified B16 melanoma cells was performed 15 d later. |
| 5651 | 9620291 | In the ex vivo tumor vaccine approach, B16 melanoma cells, transduced in vitro by adenovirus containing either interleukin (IL)-2, granulocyte-macrophage colony stimulating factor (GM-CSF), or tumor necrosis factor-alpha cytokine genes and gamma irradiated, were subcutaneously injected into the flank and a distant subcutaneous challenge injection of unmodified B16 melanoma cells was performed 15 d later. |
| 5652 | 9620291 | Significant reductions in challenge tumor volume were observed in the IL-2 group (75% reduction; p = 0.02) and in the GM-CSF group (88% reduction; p = 0.0006), whereas the effect for tumor necrosis factor-alpha was not statistically significant. |
| 5653 | 9620291 | Significant reductions in challenge tumor volume were observed in the IL-2 group (75% reduction; p = 0.02) and in the GM-CSF group (88% reduction; p = 0.0006), whereas the effect for tumor necrosis factor-alpha was not statistically significant. |
| 5654 | 9620291 | In the in vivo treatment of established melanomas, this cytokine approach was combined with a suicide gene therapy and subcutaneous B16 melanomas were directly injected with (i) IL-2/recombinant, replication-deficient adenovirus (adv) and thymidine kinase (tk)/adv, (ii) GM-CSF/adv, IL-2/adv, and tk/adv, or (iii) control beta-galactosidase (beta-gal)/adv and tk/adv. |
| 5655 | 9620291 | In the in vivo treatment of established melanomas, this cytokine approach was combined with a suicide gene therapy and subcutaneous B16 melanomas were directly injected with (i) IL-2/recombinant, replication-deficient adenovirus (adv) and thymidine kinase (tk)/adv, (ii) GM-CSF/adv, IL-2/adv, and tk/adv, or (iii) control beta-galactosidase (beta-gal)/adv and tk/adv. |
| 5656 | 9620291 | Challenge tumor growth was reduced by 56% for the IL-2/tk/adv/GCV treatment (p = 0.041) and by 77% for the GM-CSF/IL-2/tk/adv/GCV treatment p (p = 0.037), in comparison with the beta-gal/tk/GCV control group. |
| 5657 | 9620291 | Challenge tumor growth was reduced by 56% for the IL-2/tk/adv/GCV treatment (p = 0.041) and by 77% for the GM-CSF/IL-2/tk/adv/GCV treatment p (p = 0.037), in comparison with the beta-gal/tk/GCV control group. |
| 5658 | 9619487 | The use of recombinant ovine IL-1beta and TNF-alpha as natural adjuvants and their physiological effects in vivo. |
| 5659 | 9619487 | The use of recombinant ovine IL-1beta and TNF-alpha as natural adjuvants and their physiological effects in vivo. |
| 5660 | 9619487 | The use of recombinant ovine IL-1beta and TNF-alpha as natural adjuvants and their physiological effects in vivo. |
| 5661 | 9619487 | The use of recombinant ovine IL-1beta and TNF-alpha as natural adjuvants and their physiological effects in vivo. |
| 5662 | 9619487 | The use of recombinant ovine IL-1beta and TNF-alpha as natural adjuvants and their physiological effects in vivo. |
| 5663 | 9619487 | In the present study we have investigated the use of recombinant ovine IL-1beta and TNF-alpha both alone and in combination, as natural adjuvants in vaccination trials in sheep. |
| 5664 | 9619487 | In the present study we have investigated the use of recombinant ovine IL-1beta and TNF-alpha both alone and in combination, as natural adjuvants in vaccination trials in sheep. |
| 5665 | 9619487 | In the present study we have investigated the use of recombinant ovine IL-1beta and TNF-alpha both alone and in combination, as natural adjuvants in vaccination trials in sheep. |
| 5666 | 9619487 | In the present study we have investigated the use of recombinant ovine IL-1beta and TNF-alpha both alone and in combination, as natural adjuvants in vaccination trials in sheep. |
| 5667 | 9619487 | In the present study we have investigated the use of recombinant ovine IL-1beta and TNF-alpha both alone and in combination, as natural adjuvants in vaccination trials in sheep. |
| 5668 | 9619487 | The incorporation of either IL-1beta or TNF-alpha in aqueous or Al(OH)3 vaccine formulations enhanced antibody responses to a recombinant antigen from the cestode parasite Taenia ovis. |
| 5669 | 9619487 | The incorporation of either IL-1beta or TNF-alpha in aqueous or Al(OH)3 vaccine formulations enhanced antibody responses to a recombinant antigen from the cestode parasite Taenia ovis. |
| 5670 | 9619487 | The incorporation of either IL-1beta or TNF-alpha in aqueous or Al(OH)3 vaccine formulations enhanced antibody responses to a recombinant antigen from the cestode parasite Taenia ovis. |
| 5671 | 9619487 | The incorporation of either IL-1beta or TNF-alpha in aqueous or Al(OH)3 vaccine formulations enhanced antibody responses to a recombinant antigen from the cestode parasite Taenia ovis. |
| 5672 | 9619487 | The incorporation of either IL-1beta or TNF-alpha in aqueous or Al(OH)3 vaccine formulations enhanced antibody responses to a recombinant antigen from the cestode parasite Taenia ovis. |
| 5673 | 9619487 | When 10 microg of both IL-1beta and TNF-alpha were incorporated in the aqueous or Al(OH)3 vaccine formulations, increases of 21-fold and 25-fold, respectively, were observed in antibody levels. |
| 5674 | 9619487 | When 10 microg of both IL-1beta and TNF-alpha were incorporated in the aqueous or Al(OH)3 vaccine formulations, increases of 21-fold and 25-fold, respectively, were observed in antibody levels. |
| 5675 | 9619487 | When 10 microg of both IL-1beta and TNF-alpha were incorporated in the aqueous or Al(OH)3 vaccine formulations, increases of 21-fold and 25-fold, respectively, were observed in antibody levels. |
| 5676 | 9619487 | When 10 microg of both IL-1beta and TNF-alpha were incorporated in the aqueous or Al(OH)3 vaccine formulations, increases of 21-fold and 25-fold, respectively, were observed in antibody levels. |
| 5677 | 9619487 | When 10 microg of both IL-1beta and TNF-alpha were incorporated in the aqueous or Al(OH)3 vaccine formulations, increases of 21-fold and 25-fold, respectively, were observed in antibody levels. |
| 5678 | 9619487 | The adjuvant activity of IL-1beta and TNF-alpha in combination in the Al(OH)3-based vaccine resulted in antibody levels commensurate with those obtained using Quil A or IFA. |
| 5679 | 9619487 | The adjuvant activity of IL-1beta and TNF-alpha in combination in the Al(OH)3-based vaccine resulted in antibody levels commensurate with those obtained using Quil A or IFA. |
| 5680 | 9619487 | The adjuvant activity of IL-1beta and TNF-alpha in combination in the Al(OH)3-based vaccine resulted in antibody levels commensurate with those obtained using Quil A or IFA. |
| 5681 | 9619487 | The adjuvant activity of IL-1beta and TNF-alpha in combination in the Al(OH)3-based vaccine resulted in antibody levels commensurate with those obtained using Quil A or IFA. |
| 5682 | 9619487 | The adjuvant activity of IL-1beta and TNF-alpha in combination in the Al(OH)3-based vaccine resulted in antibody levels commensurate with those obtained using Quil A or IFA. |
| 5683 | 9573098 | Optimal activation requires the presence of T-cell-derived gamma interferon (IFN-gamma) and other signals, including tumor necrosis factor (TNF). |
| 5684 | 9573098 | Optimal activation requires the presence of T-cell-derived gamma interferon (IFN-gamma) and other signals, including tumor necrosis factor (TNF). |
| 5685 | 9573098 | Optimal activation requires the presence of T-cell-derived gamma interferon (IFN-gamma) and other signals, including tumor necrosis factor (TNF). |
| 5686 | 9573098 | When RAW264.7 cells were pretreated with human TNF or TNF(70-80) in the presence of IFN-gamma, there was a dose-dependent reduction in the replication of BCG as measured by the uptake of 3H-labeled uracil and a concomitant release of nitric oxide as measured by the nitrite in the culture supernatants. |
| 5687 | 9573098 | When RAW264.7 cells were pretreated with human TNF or TNF(70-80) in the presence of IFN-gamma, there was a dose-dependent reduction in the replication of BCG as measured by the uptake of 3H-labeled uracil and a concomitant release of nitric oxide as measured by the nitrite in the culture supernatants. |
| 5688 | 9573098 | When RAW264.7 cells were pretreated with human TNF or TNF(70-80) in the presence of IFN-gamma, there was a dose-dependent reduction in the replication of BCG as measured by the uptake of 3H-labeled uracil and a concomitant release of nitric oxide as measured by the nitrite in the culture supernatants. |
| 5689 | 9573098 | TNF- or TNF(70-80)-induced macrophage activation was dependent on IFN-gamma and was inhibited by neutralizing monoclonal antibody to human TNF and by anti-IFN-gamma antisera. |
| 5690 | 9573098 | TNF- or TNF(70-80)-induced macrophage activation was dependent on IFN-gamma and was inhibited by neutralizing monoclonal antibody to human TNF and by anti-IFN-gamma antisera. |
| 5691 | 9573098 | TNF- or TNF(70-80)-induced macrophage activation was dependent on IFN-gamma and was inhibited by neutralizing monoclonal antibody to human TNF and by anti-IFN-gamma antisera. |
| 5692 | 9573069 | Nramp1 regulates macrophage activation and has multiple pleiotropic effects, including regulation of tumor necrosis factor alpha, interleukin 1beta (IL-1beta), and major histocompatibility complex class II molecules, all of which influence antigen processing and presentation. |
| 5693 | 9573069 | Results show that congenic mice carrying the wild-type (S. typhimurium resistance) Nramp1 allele mount a predominantly T-helper-1 (IL-2 and gamma interferon) response to vaccination and show enhanced resolution of lesions following challenge infection with Leishmania major. |
| 5694 | 9573069 | In contrast, mice carrying mutant (S. typhimurium susceptibility) Nramp1 mount a T-helper-2 (immunoglobulin E and IL-4) response and show exacerbated lesion growth upon challenge. |
| 5695 | 9573061 | Proliferative responses to both infected autologous endothelial cells and monocytes were characterized by expansion of a mixture of CD4+, CD8+, and gammadelta T cells. |
| 5696 | 9573061 | Reverse transcription-PCR analysis of cytokine expression by C. ruminantium-specific T-cell lines and immune PBMC revealed weak interleukin-2 (IL-2), IL-4, and gamma interferon (IFN-gamma) transcripts at 3 to 24 h after stimulation. |
| 5697 | 9573061 | Strong expression of IFN-gamma, tumor necrosis factor alpha (TNF-alpha), TNF-beta, and IL-2 receptor alpha-chain mRNA was detected in T-cell lines 48 h after antigen stimulation. |
| 5698 | 9570545 | Protective effect on Leishmania major infection of migration inhibitory factor, TNF-alpha, and IFN-gamma administered orally via attenuated Salmonella typhimurium. |
| 5699 | 9570545 | Protective effect on Leishmania major infection of migration inhibitory factor, TNF-alpha, and IFN-gamma administered orally via attenuated Salmonella typhimurium. |
| 5700 | 9570545 | The genes encoding murine macrophage migration inhibitory factor (MIF), IL-2, IFN-gamma or TNF-alpha were cloned individually into an expression plasmid under the control of the inducible promoter nirB and transfected into the aroA- aroD- deletion mutant strain of Salmonella typhimurium (BRD509). |
| 5701 | 9570545 | The genes encoding murine macrophage migration inhibitory factor (MIF), IL-2, IFN-gamma or TNF-alpha were cloned individually into an expression plasmid under the control of the inducible promoter nirB and transfected into the aroA- aroD- deletion mutant strain of Salmonella typhimurium (BRD509). |
| 5702 | 9541605 | Recently we and others reported that specific immune responses generated by DNA vaccine could be modulated by co-delivery of gene expression cassettes encoding for IL-12, granulocyte-macrophage colony-stimulating factor and the co-stimulatory molecule CD86. |
| 5703 | 9541605 | Recently we and others reported that specific immune responses generated by DNA vaccine could be modulated by co-delivery of gene expression cassettes encoding for IL-12, granulocyte-macrophage colony-stimulating factor and the co-stimulatory molecule CD86. |
| 5704 | 9541605 | Recently we and others reported that specific immune responses generated by DNA vaccine could be modulated by co-delivery of gene expression cassettes encoding for IL-12, granulocyte-macrophage colony-stimulating factor and the co-stimulatory molecule CD86. |
| 5705 | 9541605 | To further engineer the immune response in vivo, we investigated the induction and regulation of immune responses following the co-delivery of pro-inflammatory cytokine (IL-1 alpha, TNF-alpha, and TNF-beta), Th1 cytokine (IL-2, IL-12, IL-15, and IL-18), and Th2 cytokine (IL-4, IL-5 and IL-10) genes. |
| 5706 | 9541605 | To further engineer the immune response in vivo, we investigated the induction and regulation of immune responses following the co-delivery of pro-inflammatory cytokine (IL-1 alpha, TNF-alpha, and TNF-beta), Th1 cytokine (IL-2, IL-12, IL-15, and IL-18), and Th2 cytokine (IL-4, IL-5 and IL-10) genes. |
| 5707 | 9541605 | To further engineer the immune response in vivo, we investigated the induction and regulation of immune responses following the co-delivery of pro-inflammatory cytokine (IL-1 alpha, TNF-alpha, and TNF-beta), Th1 cytokine (IL-2, IL-12, IL-15, and IL-18), and Th2 cytokine (IL-4, IL-5 and IL-10) genes. |
| 5708 | 9541605 | We observed enhancement of antigen-specific humoral response with the co-delivery of Th2 cytokine genes IL-4, IL-5, and IL-10 as well as those of IL-2 and IL-18. |
| 5709 | 9541605 | We observed enhancement of antigen-specific humoral response with the co-delivery of Th2 cytokine genes IL-4, IL-5, and IL-10 as well as those of IL-2 and IL-18. |
| 5710 | 9541605 | We observed enhancement of antigen-specific humoral response with the co-delivery of Th2 cytokine genes IL-4, IL-5, and IL-10 as well as those of IL-2 and IL-18. |
| 5711 | 9541605 | A dramatic increase in antigen-specific T helper cell proliferation was seen with IL-2 and TNF-alpha gene co-injections. |
| 5712 | 9541605 | A dramatic increase in antigen-specific T helper cell proliferation was seen with IL-2 and TNF-alpha gene co-injections. |
| 5713 | 9541605 | A dramatic increase in antigen-specific T helper cell proliferation was seen with IL-2 and TNF-alpha gene co-injections. |
| 5714 | 9541605 | In addition, we observed a significant enhancement of the cytotoxic response with the co-administration of TNF-alpha and IL-15 genes with HIV-1 DNA immunogens. |
| 5715 | 9541605 | In addition, we observed a significant enhancement of the cytotoxic response with the co-administration of TNF-alpha and IL-15 genes with HIV-1 DNA immunogens. |
| 5716 | 9541605 | In addition, we observed a significant enhancement of the cytotoxic response with the co-administration of TNF-alpha and IL-15 genes with HIV-1 DNA immunogens. |
| 5717 | 9550413 | Identification of Trypanosoma cruzi trans-sialidase family members as targets of protective CD8+ TC1 responses. |
| 5718 | 9550413 | Peptide-specific CD8+ T cell lines were cytotoxic, secreted IFN-gamma and TNF-alpha, but low to undetectable levels of IL-4 and IL-5, and were able, upon adoptive transfer, to confer a high degree of protection against challenge infection. |
| 5719 | 9545516 | Glycophosphatidyl inositol membrane anchors of parasite proteins possess insulin like activity and induce TNF synthesis. |
| 5720 | 9544573 | The percentage of mononuclear cells (MN) containing IL-1beta, TNF-alpha, MCP-1, and IL-8 mRNAs was highest in 1- to 3-day lesions, apparently because of the nonspecific inflammatory response caused by the tubercle bacilli in the BCG vaccine. |
| 5721 | 9544573 | The percentage of mononuclear cells (MN) containing IL-1beta, TNF-alpha, MCP-1, and IL-8 mRNAs was highest in 1- to 3-day lesions, apparently because of the nonspecific inflammatory response caused by the tubercle bacilli in the BCG vaccine. |
| 5722 | 9544573 | In general, MCP-1 and TNF-alpha proteins and the vascular adhesion molecules, ICAM, VCAM, and perhaps ELAM, peaked at about 3 days. |
| 5723 | 9544573 | In general, MCP-1 and TNF-alpha proteins and the vascular adhesion molecules, ICAM, VCAM, and perhaps ELAM, peaked at about 3 days. |
| 5724 | 9515809 | Interleukin 12 gene therapy of MHC-negative murine melanoma metastases. |
| 5725 | 9515809 | In situ hybridization with cytokine probes detected a strong increase in the proportion of leukocytes positive for IFN-gamma, tumor necrosis factor alpha, IL-1beta, and IFN-inducible protein 10 at the site of rejection of IL-12-engineered tumor cells. |
| 5726 | 9515809 | In conclusion, tumor therapy based on IL-12 gene transduction was effective on a MHC-negative metastatic tumor, suggesting a possible application to MHC-defective human neoplasms. |
| 5727 | 9507233 | AA supplementation caused significant increases in the in vitro secretion of LTB4, and PGE2, but it did not alter the in vitro secretion of tumor necrosis factor alpha; interleukins 1 beta, 2, 6; and the receptor for interleukin 2. |
| 5728 | 9498462 | Interleukin-1 receptor antagonist (IL-1ra) concentration was significantly elevated in all subjects on day 2 after vaccination. |
| 5729 | 9498462 | In a control group receiving non-live vaccinations, TNF and IL-1ra concentrations were unchanged. |
| 5730 | 9485028 | The Her-2/neu oncogene encodes a Mr 185,000 transmembrane protein with homology to the epidermal growth factor receptor. |
| 5731 | 9485028 | CTLs induced with DCs generated in the presence of TNF-alpha elicited a higher cytotoxic activity when they were stimulated with the cognate peptide than did CTLs induced with DCs grown in granulocyte macrophage colony-stimulating factor and interleukin 4 alone. |
| 5732 | 9485028 | Furthermore, these CTLs lysed, in a MHC- and antigen-restricted fashion, not only breast cancer cells but also colon carcinoma and RCC cell lines expressing Her-2/neu. |
| 5733 | 9475357 | Whole-cell pertussis found in diphtheria-tetanus-pertussis (DTP) vaccine can produce symptoms reminiscent of biological responses to circulating proinflammatory monokines such as IL-6, IL-1beta, and TNFalpha. |
| 5734 | 9475357 | Whole-cell pertussis found in diphtheria-tetanus-pertussis (DTP) vaccine can produce symptoms reminiscent of biological responses to circulating proinflammatory monokines such as IL-6, IL-1beta, and TNFalpha. |
| 5735 | 9475357 | Whole-cell pertussis found in diphtheria-tetanus-pertussis (DTP) vaccine can produce symptoms reminiscent of biological responses to circulating proinflammatory monokines such as IL-6, IL-1beta, and TNFalpha. |
| 5736 | 9475357 | The whole-cell pertussis vaccine induced significantly more IL-6, IL-1beta, and TNFalpha production than did the acellular pertussis or diphtheria-tetanus-only vaccine. |
| 5737 | 9475357 | The whole-cell pertussis vaccine induced significantly more IL-6, IL-1beta, and TNFalpha production than did the acellular pertussis or diphtheria-tetanus-only vaccine. |
| 5738 | 9475357 | The whole-cell pertussis vaccine induced significantly more IL-6, IL-1beta, and TNFalpha production than did the acellular pertussis or diphtheria-tetanus-only vaccine. |
| 5739 | 9475357 | These results indicate that in vitro whole-cell vaccine is a potent stimulator of IL-6, IL-1beta, and TNFalpha. |
| 5740 | 9475357 | These results indicate that in vitro whole-cell vaccine is a potent stimulator of IL-6, IL-1beta, and TNFalpha. |
| 5741 | 9475357 | These results indicate that in vitro whole-cell vaccine is a potent stimulator of IL-6, IL-1beta, and TNFalpha. |
| 5742 | 9464831 | While IL-12 is key to their T helper cell (Th)1-promoting adjuvant activity, secretion of toxic levels of TNF-alpha is harmful in that it promotes toxic shock. |
| 5743 | 9464831 | While IL-12 is key to their T helper cell (Th)1-promoting adjuvant activity, secretion of toxic levels of TNF-alpha is harmful in that it promotes toxic shock. |
| 5744 | 9464831 | While IL-12 is key to their T helper cell (Th)1-promoting adjuvant activity, secretion of toxic levels of TNF-alpha is harmful in that it promotes toxic shock. |
| 5745 | 9464831 | CpG oligodeoxynucleotides (ODN) which differentially activate IL-12 versus TNF-alpha cytokine production in APC. |
| 5746 | 9464831 | CpG oligodeoxynucleotides (ODN) which differentially activate IL-12 versus TNF-alpha cytokine production in APC. |
| 5747 | 9464831 | CpG oligodeoxynucleotides (ODN) which differentially activate IL-12 versus TNF-alpha cytokine production in APC. |
| 5748 | 9464831 | While its potential to induce IL-12 is preserved, its ability to trigger TNF-alpha release is strongly curtailed both in vitro and in vivo. |
| 5749 | 9464831 | While its potential to induce IL-12 is preserved, its ability to trigger TNF-alpha release is strongly curtailed both in vitro and in vivo. |
| 5750 | 9464831 | While its potential to induce IL-12 is preserved, its ability to trigger TNF-alpha release is strongly curtailed both in vitro and in vivo. |
| 5751 | 9389728 | Partial interferon-gamma receptor 1 deficiency in a child with tuberculoid bacillus Calmette-Guérin infection and a sibling with clinical tuberculosis. |
| 5752 | 9389728 | Complete interferon-gamma receptor 1 (IFNgammaR1) deficiency has been identified previously as a cause of fatal bacillus Calmette-Guérin (BCG) infection with lepromatoid granulomas, and of disseminated nontuberculous mycobacterial (NTM) infection in children who had not been inoculated with BCG. |
| 5753 | 9389728 | Impaired response to IFN-gamma was documented in B cells by signal transducer and activator of transcription 1 nuclear translocation, in fibroblasts by cell surface HLA class II induction, and in monocytes by cell surface CD64 induction and TNF-alpha secretion. |
| 5754 | 9414288 | Gene immunotherapy in murine acute myeloid leukemia: granulocyte-macrophage colony-stimulating factor tumor cell vaccines elicit more potent antitumor immunity compared with B7 family and other cytokine vaccines. |
| 5755 | 9414288 | Gene immunotherapy in murine acute myeloid leukemia: granulocyte-macrophage colony-stimulating factor tumor cell vaccines elicit more potent antitumor immunity compared with B7 family and other cytokine vaccines. |
| 5756 | 9414288 | In this report, we question whether CD86 (B7.2) or the cytokines granulocyte-macrophage colony-stimulating factor (GM-CSF), interleukin-4 (IL-4), or tumor necrosis factor-alpha (TNF-alpha) can improve the vaccination potential of AML cells. |
| 5757 | 9414288 | In this report, we question whether CD86 (B7.2) or the cytokines granulocyte-macrophage colony-stimulating factor (GM-CSF), interleukin-4 (IL-4), or tumor necrosis factor-alpha (TNF-alpha) can improve the vaccination potential of AML cells. |
| 5758 | 9414288 | Our studies show that (1) mice vaccinated with a leukemogenic number of AML cells engineered to express B7.2 (B7.2-AML) or to secrete GM-CSF, IL-4, or TNF-alpha (GM-, IL-4-, TNF-alpha-AML) do not develop leukemia; (2) GM-AML cells are tumorigenic in sublethally irradiated SJL/J mice but not in Swiss nu/nu mice, indicating that killing of tumor cells is not T-cell-dependent; (3) vaccines with irradiated GM-AML, but not B7.2-, IL-4-, or TNF-alpha-AML cells, can elicit leukemia-specific protective and therapeutic immunity; and (4) in head-to-head comparison experiments, vaccination with irradiated GM-AML is more potent than B7.1-AML, curing 80% and providing 20% prolonged survival of the leukemic mice at week 2, as opposed to cures only up to 1 week with B7.1-AML vaccines. |
| 5759 | 9414288 | Our studies show that (1) mice vaccinated with a leukemogenic number of AML cells engineered to express B7.2 (B7.2-AML) or to secrete GM-CSF, IL-4, or TNF-alpha (GM-, IL-4-, TNF-alpha-AML) do not develop leukemia; (2) GM-AML cells are tumorigenic in sublethally irradiated SJL/J mice but not in Swiss nu/nu mice, indicating that killing of tumor cells is not T-cell-dependent; (3) vaccines with irradiated GM-AML, but not B7.2-, IL-4-, or TNF-alpha-AML cells, can elicit leukemia-specific protective and therapeutic immunity; and (4) in head-to-head comparison experiments, vaccination with irradiated GM-AML is more potent than B7.1-AML, curing 80% and providing 20% prolonged survival of the leukemic mice at week 2, as opposed to cures only up to 1 week with B7.1-AML vaccines. |
| 5760 | 9450626 | Modulation of MHC class II+ Langerhans cell numbers in corticosteroid treated epidermis by GM-CSF in combination with TNF-alpha. |
| 5761 | 9450626 | Modulation of MHC class II+ Langerhans cell numbers in corticosteroid treated epidermis by GM-CSF in combination with TNF-alpha. |
| 5762 | 9450626 | Modulation of MHC class II+ Langerhans cell numbers in corticosteroid treated epidermis by GM-CSF in combination with TNF-alpha. |
| 5763 | 9450626 | Modulation of MHC class II+ Langerhans cell numbers in corticosteroid treated epidermis by GM-CSF in combination with TNF-alpha. |
| 5764 | 9450626 | Modulation of MHC class II+ Langerhans cell numbers in corticosteroid treated epidermis by GM-CSF in combination with TNF-alpha. |
| 5765 | 9450626 | Modulation of MHC class II+ Langerhans cell numbers in corticosteroid treated epidermis by GM-CSF in combination with TNF-alpha. |
| 5766 | 9450626 | Modulation of MHC class II+ Langerhans cell numbers in corticosteroid treated epidermis by GM-CSF in combination with TNF-alpha. |
| 5767 | 9450626 | To identify cytokines which could increase DC in tissues we tested the ability of GM-CSF, TNF-alpha and IL-6 to partially prevent steroid depletion of Langerhans cells (LC) from the epidermis. |
| 5768 | 9450626 | To identify cytokines which could increase DC in tissues we tested the ability of GM-CSF, TNF-alpha and IL-6 to partially prevent steroid depletion of Langerhans cells (LC) from the epidermis. |
| 5769 | 9450626 | To identify cytokines which could increase DC in tissues we tested the ability of GM-CSF, TNF-alpha and IL-6 to partially prevent steroid depletion of Langerhans cells (LC) from the epidermis. |
| 5770 | 9450626 | To identify cytokines which could increase DC in tissues we tested the ability of GM-CSF, TNF-alpha and IL-6 to partially prevent steroid depletion of Langerhans cells (LC) from the epidermis. |
| 5771 | 9450626 | To identify cytokines which could increase DC in tissues we tested the ability of GM-CSF, TNF-alpha and IL-6 to partially prevent steroid depletion of Langerhans cells (LC) from the epidermis. |
| 5772 | 9450626 | To identify cytokines which could increase DC in tissues we tested the ability of GM-CSF, TNF-alpha and IL-6 to partially prevent steroid depletion of Langerhans cells (LC) from the epidermis. |
| 5773 | 9450626 | To identify cytokines which could increase DC in tissues we tested the ability of GM-CSF, TNF-alpha and IL-6 to partially prevent steroid depletion of Langerhans cells (LC) from the epidermis. |
| 5774 | 9450626 | In the presence of serum, GM-CSF or TNF-alpha could increase LC frequency compared to the control; but in the absence of serum neither of these cytokines were effective unless they were combined with each other. |
| 5775 | 9450626 | In the presence of serum, GM-CSF or TNF-alpha could increase LC frequency compared to the control; but in the absence of serum neither of these cytokines were effective unless they were combined with each other. |
| 5776 | 9450626 | In the presence of serum, GM-CSF or TNF-alpha could increase LC frequency compared to the control; but in the absence of serum neither of these cytokines were effective unless they were combined with each other. |
| 5777 | 9450626 | In the presence of serum, GM-CSF or TNF-alpha could increase LC frequency compared to the control; but in the absence of serum neither of these cytokines were effective unless they were combined with each other. |
| 5778 | 9450626 | In the presence of serum, GM-CSF or TNF-alpha could increase LC frequency compared to the control; but in the absence of serum neither of these cytokines were effective unless they were combined with each other. |
| 5779 | 9450626 | In the presence of serum, GM-CSF or TNF-alpha could increase LC frequency compared to the control; but in the absence of serum neither of these cytokines were effective unless they were combined with each other. |
| 5780 | 9450626 | In the presence of serum, GM-CSF or TNF-alpha could increase LC frequency compared to the control; but in the absence of serum neither of these cytokines were effective unless they were combined with each other. |
| 5781 | 9450626 | In the presence of serum the combination of GM-CSF with TNF-alpha was ineffective. |
| 5782 | 9450626 | In the presence of serum the combination of GM-CSF with TNF-alpha was ineffective. |
| 5783 | 9450626 | In the presence of serum the combination of GM-CSF with TNF-alpha was ineffective. |
| 5784 | 9450626 | In the presence of serum the combination of GM-CSF with TNF-alpha was ineffective. |
| 5785 | 9450626 | In the presence of serum the combination of GM-CSF with TNF-alpha was ineffective. |
| 5786 | 9450626 | In the presence of serum the combination of GM-CSF with TNF-alpha was ineffective. |
| 5787 | 9450626 | In the presence of serum the combination of GM-CSF with TNF-alpha was ineffective. |
| 5788 | 9450626 | The data support the hypotheses that GM-CSF and TNF-alpha are both important in regulating LC numbers in the epidermis in vivo. |
| 5789 | 9450626 | The data support the hypotheses that GM-CSF and TNF-alpha are both important in regulating LC numbers in the epidermis in vivo. |
| 5790 | 9450626 | The data support the hypotheses that GM-CSF and TNF-alpha are both important in regulating LC numbers in the epidermis in vivo. |
| 5791 | 9450626 | The data support the hypotheses that GM-CSF and TNF-alpha are both important in regulating LC numbers in the epidermis in vivo. |
| 5792 | 9450626 | The data support the hypotheses that GM-CSF and TNF-alpha are both important in regulating LC numbers in the epidermis in vivo. |
| 5793 | 9450626 | The data support the hypotheses that GM-CSF and TNF-alpha are both important in regulating LC numbers in the epidermis in vivo. |
| 5794 | 9450626 | The data support the hypotheses that GM-CSF and TNF-alpha are both important in regulating LC numbers in the epidermis in vivo. |
| 5795 | 9450626 | Serum may modulate how each of these cytokines, separately or in combination, affect LC frequency in the epidermis - GM-CSF and TNF-alpha separately probably interact with other factors present in serum to increase LC frequency, whereas in combination it is possible that these separate effects are cancelled in the presence of serum. |
| 5796 | 9450626 | Serum may modulate how each of these cytokines, separately or in combination, affect LC frequency in the epidermis - GM-CSF and TNF-alpha separately probably interact with other factors present in serum to increase LC frequency, whereas in combination it is possible that these separate effects are cancelled in the presence of serum. |
| 5797 | 9450626 | Serum may modulate how each of these cytokines, separately or in combination, affect LC frequency in the epidermis - GM-CSF and TNF-alpha separately probably interact with other factors present in serum to increase LC frequency, whereas in combination it is possible that these separate effects are cancelled in the presence of serum. |
| 5798 | 9450626 | Serum may modulate how each of these cytokines, separately or in combination, affect LC frequency in the epidermis - GM-CSF and TNF-alpha separately probably interact with other factors present in serum to increase LC frequency, whereas in combination it is possible that these separate effects are cancelled in the presence of serum. |
| 5799 | 9450626 | Serum may modulate how each of these cytokines, separately or in combination, affect LC frequency in the epidermis - GM-CSF and TNF-alpha separately probably interact with other factors present in serum to increase LC frequency, whereas in combination it is possible that these separate effects are cancelled in the presence of serum. |
| 5800 | 9450626 | Serum may modulate how each of these cytokines, separately or in combination, affect LC frequency in the epidermis - GM-CSF and TNF-alpha separately probably interact with other factors present in serum to increase LC frequency, whereas in combination it is possible that these separate effects are cancelled in the presence of serum. |
| 5801 | 9450626 | Serum may modulate how each of these cytokines, separately or in combination, affect LC frequency in the epidermis - GM-CSF and TNF-alpha separately probably interact with other factors present in serum to increase LC frequency, whereas in combination it is possible that these separate effects are cancelled in the presence of serum. |
| 5802 | 9450626 | TNF-alpha and GM-CSF together, in the absence of serum, form one combination of a minimum number of cytokines which can regulate LC frequency in the epidermis; and IL-6 alone, or in combination with GM-CSF, does not increase LC frequency. |
| 5803 | 9450626 | TNF-alpha and GM-CSF together, in the absence of serum, form one combination of a minimum number of cytokines which can regulate LC frequency in the epidermis; and IL-6 alone, or in combination with GM-CSF, does not increase LC frequency. |
| 5804 | 9450626 | TNF-alpha and GM-CSF together, in the absence of serum, form one combination of a minimum number of cytokines which can regulate LC frequency in the epidermis; and IL-6 alone, or in combination with GM-CSF, does not increase LC frequency. |
| 5805 | 9450626 | TNF-alpha and GM-CSF together, in the absence of serum, form one combination of a minimum number of cytokines which can regulate LC frequency in the epidermis; and IL-6 alone, or in combination with GM-CSF, does not increase LC frequency. |
| 5806 | 9450626 | TNF-alpha and GM-CSF together, in the absence of serum, form one combination of a minimum number of cytokines which can regulate LC frequency in the epidermis; and IL-6 alone, or in combination with GM-CSF, does not increase LC frequency. |
| 5807 | 9450626 | TNF-alpha and GM-CSF together, in the absence of serum, form one combination of a minimum number of cytokines which can regulate LC frequency in the epidermis; and IL-6 alone, or in combination with GM-CSF, does not increase LC frequency. |
| 5808 | 9450626 | TNF-alpha and GM-CSF together, in the absence of serum, form one combination of a minimum number of cytokines which can regulate LC frequency in the epidermis; and IL-6 alone, or in combination with GM-CSF, does not increase LC frequency. |
| 5809 | 9436032 | Cytokine genes (tumor necrosis factor-alpha, interleukin 2, interferon gamma) and costimulatory molecule, B7-1, were incorporated into canarypox virus, ALVAC, which does not replicate in infected mammalian cells, and highly attenuated vaccinia virus, NYVAC. |
| 5810 | 9424847 | NS1 protein expressed by adenovirus increased the level of the key interleukins (IL) interferon, tumor necrosis factor, IL-1 beta, IL-2, and, probably, IL-4. |
| 5811 | 9421852 | However, postoperative increase of soluble TNF-receptors p55 and p75 was also significant in patients transfused with allogenic blood (p = .022; p = .0014). |
| 5812 | 9394829 | IC formed of tetanus toxoid and polyclonal anti-tetanus toxoid antiserum as well as heat-aggregated human serum IgG almost completely inhibited IL-12 (p70 and p40) secretion induced by interferon-gamma and lipopolysaccharide in human blood-derived monocytes. |
| 5813 | 9394829 | IC formed of tetanus toxoid and polyclonal anti-tetanus toxoid antiserum as well as heat-aggregated human serum IgG almost completely inhibited IL-12 (p70 and p40) secretion induced by interferon-gamma and lipopolysaccharide in human blood-derived monocytes. |
| 5814 | 9394829 | IC formed of tetanus toxoid and polyclonal anti-tetanus toxoid antiserum as well as heat-aggregated human serum IgG almost completely inhibited IL-12 (p70 and p40) secretion induced by interferon-gamma and lipopolysaccharide in human blood-derived monocytes. |
| 5815 | 9394829 | Neutralizing anti-IL-10 antibodies plus indomethacin restored IL-12 secretion in the presence of IC to a high extent, indicating that IL-10 and prostaglandin (PG) partially mediate the IC-induced inhibition of IL-12 secretion. |
| 5816 | 9394829 | Neutralizing anti-IL-10 antibodies plus indomethacin restored IL-12 secretion in the presence of IC to a high extent, indicating that IL-10 and prostaglandin (PG) partially mediate the IC-induced inhibition of IL-12 secretion. |
| 5817 | 9394829 | Neutralizing anti-IL-10 antibodies plus indomethacin restored IL-12 secretion in the presence of IC to a high extent, indicating that IL-10 and prostaglandin (PG) partially mediate the IC-induced inhibition of IL-12 secretion. |
| 5818 | 9394829 | However, neutralization of tumor necrosis factor (TNF)-alpha by specific antibodies also incompletely restored IL-12 secretion. |
| 5819 | 9394829 | However, neutralization of tumor necrosis factor (TNF)-alpha by specific antibodies also incompletely restored IL-12 secretion. |
| 5820 | 9394829 | However, neutralization of tumor necrosis factor (TNF)-alpha by specific antibodies also incompletely restored IL-12 secretion. |
| 5821 | 9394829 | We found that exogenously added TNF-alpha caused a profound inhibition of monocytic IL-12 secretion in the absence of IC, again mediated via the induction of IL-10 and PG. |
| 5822 | 9394829 | We found that exogenously added TNF-alpha caused a profound inhibition of monocytic IL-12 secretion in the absence of IC, again mediated via the induction of IL-10 and PG. |
| 5823 | 9394829 | We found that exogenously added TNF-alpha caused a profound inhibition of monocytic IL-12 secretion in the absence of IC, again mediated via the induction of IL-10 and PG. |
| 5824 | 9394829 | In summary, IC inhibit IL-12 secretion via TNF-alpha-induced IL-10 and PG synthesis. |
| 5825 | 9394829 | In summary, IC inhibit IL-12 secretion via TNF-alpha-induced IL-10 and PG synthesis. |
| 5826 | 9394829 | In summary, IC inhibit IL-12 secretion via TNF-alpha-induced IL-10 and PG synthesis. |
| 5827 | 9364689 | However, the lipid As of H. pylori and P. gingivalis showed lower activities in inducing tumour necrosis factor alpha (TNF-alpha) production by human PBMC and IL-8 production by human gingival fibroblasts than that of compound 506. |
| 5828 | 9341792 | BCG infection was also accompanied by an impairment of the capacity of monocytes to secrete IL-10 and by an induction of the capacity to secrete tumor necrosis factor-alpha, two cytokines known to induce and prevent human monocyte apoptosis, respectively. |
| 5829 | 9341778 | We and others have demonstrated that single-stranded (ss) DNA containing the motif CpG flanked by two 5' purines and two 3' pyrimidines are mitogenic for B cells and activate macrophages to release tumor necrosis factor-alpha, interferon-gamma, interleukin (IL)-6 or IL-12. |
| 5830 | 9307066 | Functionally mature Vgamma9Vdelta2 T cells display a potent natural killer (NK)-like cytotoxic activity, share with NK cells the expression of inhibitory receptors for HLA class I molecules, and release a plethora of cytokines, most notably interferon-gamma and tumor necrosis factor alpha. |
| 5831 | 9322065 | Three forms of OspA vaccine candidates were investigated by the induction of the cytokines interleukin (IL)-1 beta, IL-6, tumor necrosis factor (TNF)-alpha, IL-10 and interferon (IFN)-gamma as markers of monocyte activation and immune stimulation: lipidated OspA (L-OspA), non-lipidated OspA (NL-OspA), and a fusion protein of 81 amino acids of the nonstructural protein 1 of influenza virus with OspA (NS1-OspA). |
| 5832 | 9322065 | Three forms of OspA vaccine candidates were investigated by the induction of the cytokines interleukin (IL)-1 beta, IL-6, tumor necrosis factor (TNF)-alpha, IL-10 and interferon (IFN)-gamma as markers of monocyte activation and immune stimulation: lipidated OspA (L-OspA), non-lipidated OspA (NL-OspA), and a fusion protein of 81 amino acids of the nonstructural protein 1 of influenza virus with OspA (NS1-OspA). |
| 5833 | 9322065 | Three forms of OspA vaccine candidates were investigated by the induction of the cytokines interleukin (IL)-1 beta, IL-6, tumor necrosis factor (TNF)-alpha, IL-10 and interferon (IFN)-gamma as markers of monocyte activation and immune stimulation: lipidated OspA (L-OspA), non-lipidated OspA (NL-OspA), and a fusion protein of 81 amino acids of the nonstructural protein 1 of influenza virus with OspA (NS1-OspA). |
| 5834 | 9322065 | All OspA preparations induced IL-1 beta, IL-6 and TNF-alpha in a concentration-dependent manner with peak levels at 12-24 h. |
| 5835 | 9322065 | All OspA preparations induced IL-1 beta, IL-6 and TNF-alpha in a concentration-dependent manner with peak levels at 12-24 h. |
| 5836 | 9322065 | All OspA preparations induced IL-1 beta, IL-6 and TNF-alpha in a concentration-dependent manner with peak levels at 12-24 h. |
| 5837 | 9322065 | In peripheral blood mononuclear cells from 10 healthy donors, L-OspA at 10 micrograms ml-1 induced up to 4-fold more IL-1 beta, IL-6, and TNF-alpha than the other OspA preparations (P < or = 0.0068), followed by NS1-OspA, which was still superior to NL-OspA. |
| 5838 | 9322065 | In peripheral blood mononuclear cells from 10 healthy donors, L-OspA at 10 micrograms ml-1 induced up to 4-fold more IL-1 beta, IL-6, and TNF-alpha than the other OspA preparations (P < or = 0.0068), followed by NS1-OspA, which was still superior to NL-OspA. |
| 5839 | 9322065 | In peripheral blood mononuclear cells from 10 healthy donors, L-OspA at 10 micrograms ml-1 induced up to 4-fold more IL-1 beta, IL-6, and TNF-alpha than the other OspA preparations (P < or = 0.0068), followed by NS1-OspA, which was still superior to NL-OspA. |
| 5840 | 9322065 | L-OspA also induced high levels of IL-10 within 24 h but no significant amounts of IFN-gamma. |
| 5841 | 9322065 | L-OspA also induced high levels of IL-10 within 24 h but no significant amounts of IFN-gamma. |
| 5842 | 9322065 | L-OspA also induced high levels of IL-10 within 24 h but no significant amounts of IFN-gamma. |
| 5843 | 9300722 | Induction of TNF-alpha in human peripheral blood mononuclear cells by the mannoprotein of Cryptococcus neoformans involves human mannose binding protein. |
| 5844 | 9300722 | Induction of TNF-alpha in human peripheral blood mononuclear cells by the mannoprotein of Cryptococcus neoformans involves human mannose binding protein. |
| 5845 | 9300722 | Induction of TNF-alpha in human peripheral blood mononuclear cells by the mannoprotein of Cryptococcus neoformans involves human mannose binding protein. |
| 5846 | 9300722 | Induction of TNF-alpha in human peripheral blood mononuclear cells by the mannoprotein of Cryptococcus neoformans involves human mannose binding protein. |
| 5847 | 9300722 | Induction of TNF-alpha in human peripheral blood mononuclear cells by the mannoprotein of Cryptococcus neoformans involves human mannose binding protein. |
| 5848 | 9300722 | Induction of TNF-alpha in human peripheral blood mononuclear cells by the mannoprotein of Cryptococcus neoformans involves human mannose binding protein. |
| 5849 | 9300722 | We have shown previously that specific receptors on PBMCs and a serum factor other than Ab and complement are involved in the TNF-alpha response to cryptococcal mannoprotein (MP2). |
| 5850 | 9300722 | We have shown previously that specific receptors on PBMCs and a serum factor other than Ab and complement are involved in the TNF-alpha response to cryptococcal mannoprotein (MP2). |
| 5851 | 9300722 | We have shown previously that specific receptors on PBMCs and a serum factor other than Ab and complement are involved in the TNF-alpha response to cryptococcal mannoprotein (MP2). |
| 5852 | 9300722 | We have shown previously that specific receptors on PBMCs and a serum factor other than Ab and complement are involved in the TNF-alpha response to cryptococcal mannoprotein (MP2). |
| 5853 | 9300722 | We have shown previously that specific receptors on PBMCs and a serum factor other than Ab and complement are involved in the TNF-alpha response to cryptococcal mannoprotein (MP2). |
| 5854 | 9300722 | We have shown previously that specific receptors on PBMCs and a serum factor other than Ab and complement are involved in the TNF-alpha response to cryptococcal mannoprotein (MP2). |
| 5855 | 9300722 | Beta-Glucan laminarin produced background inhibition. mAbs against CD14, CD11b, and CD18 did not prevent FITC-MP2 binding to PBMCs, implying that these receptors are not involved in MP2 recognition by PBMCs. mAb against CD14 blocked (>90%) MP2-induced TNF-alpha release by PBMCs, while mAbs against CD11b/CD18 caused no inhibition. |
| 5856 | 9300722 | Beta-Glucan laminarin produced background inhibition. mAbs against CD14, CD11b, and CD18 did not prevent FITC-MP2 binding to PBMCs, implying that these receptors are not involved in MP2 recognition by PBMCs. mAb against CD14 blocked (>90%) MP2-induced TNF-alpha release by PBMCs, while mAbs against CD11b/CD18 caused no inhibition. |
| 5857 | 9300722 | Beta-Glucan laminarin produced background inhibition. mAbs against CD14, CD11b, and CD18 did not prevent FITC-MP2 binding to PBMCs, implying that these receptors are not involved in MP2 recognition by PBMCs. mAb against CD14 blocked (>90%) MP2-induced TNF-alpha release by PBMCs, while mAbs against CD11b/CD18 caused no inhibition. |
| 5858 | 9300722 | Beta-Glucan laminarin produced background inhibition. mAbs against CD14, CD11b, and CD18 did not prevent FITC-MP2 binding to PBMCs, implying that these receptors are not involved in MP2 recognition by PBMCs. mAb against CD14 blocked (>90%) MP2-induced TNF-alpha release by PBMCs, while mAbs against CD11b/CD18 caused no inhibition. |
| 5859 | 9300722 | Beta-Glucan laminarin produced background inhibition. mAbs against CD14, CD11b, and CD18 did not prevent FITC-MP2 binding to PBMCs, implying that these receptors are not involved in MP2 recognition by PBMCs. mAb against CD14 blocked (>90%) MP2-induced TNF-alpha release by PBMCs, while mAbs against CD11b/CD18 caused no inhibition. |
| 5860 | 9300722 | Beta-Glucan laminarin produced background inhibition. mAbs against CD14, CD11b, and CD18 did not prevent FITC-MP2 binding to PBMCs, implying that these receptors are not involved in MP2 recognition by PBMCs. mAb against CD14 blocked (>90%) MP2-induced TNF-alpha release by PBMCs, while mAbs against CD11b/CD18 caused no inhibition. |
| 5861 | 9300722 | Removal of human mannose binding protein (hMBP) by preincubation of serum with a specific mAb abrogated TNF-alpha induction by MP2 and strongly inhibited its binding to PBMCs. |
| 5862 | 9300722 | Removal of human mannose binding protein (hMBP) by preincubation of serum with a specific mAb abrogated TNF-alpha induction by MP2 and strongly inhibited its binding to PBMCs. |
| 5863 | 9300722 | Removal of human mannose binding protein (hMBP) by preincubation of serum with a specific mAb abrogated TNF-alpha induction by MP2 and strongly inhibited its binding to PBMCs. |
| 5864 | 9300722 | Removal of human mannose binding protein (hMBP) by preincubation of serum with a specific mAb abrogated TNF-alpha induction by MP2 and strongly inhibited its binding to PBMCs. |
| 5865 | 9300722 | Removal of human mannose binding protein (hMBP) by preincubation of serum with a specific mAb abrogated TNF-alpha induction by MP2 and strongly inhibited its binding to PBMCs. |
| 5866 | 9300722 | Removal of human mannose binding protein (hMBP) by preincubation of serum with a specific mAb abrogated TNF-alpha induction by MP2 and strongly inhibited its binding to PBMCs. |
| 5867 | 9300722 | Recombinant hMBP enhanced TNF-alpha induction by MP2 as well as binding of FITC-MP2 to PBMCs. |
| 5868 | 9300722 | Recombinant hMBP enhanced TNF-alpha induction by MP2 as well as binding of FITC-MP2 to PBMCs. |
| 5869 | 9300722 | Recombinant hMBP enhanced TNF-alpha induction by MP2 as well as binding of FITC-MP2 to PBMCs. |
| 5870 | 9300722 | Recombinant hMBP enhanced TNF-alpha induction by MP2 as well as binding of FITC-MP2 to PBMCs. |
| 5871 | 9300722 | Recombinant hMBP enhanced TNF-alpha induction by MP2 as well as binding of FITC-MP2 to PBMCs. |
| 5872 | 9300722 | Recombinant hMBP enhanced TNF-alpha induction by MP2 as well as binding of FITC-MP2 to PBMCs. |
| 5873 | 9300722 | In addition, incubation of serum with MP2-coated beads and analysis by SDS-PAGE resulted in the detection of a protein of approximately 33/34 kDa that could be partially removed by preincubating the serum with hMBP mAb. |
| 5874 | 9300722 | In addition, incubation of serum with MP2-coated beads and analysis by SDS-PAGE resulted in the detection of a protein of approximately 33/34 kDa that could be partially removed by preincubating the serum with hMBP mAb. |
| 5875 | 9300722 | In addition, incubation of serum with MP2-coated beads and analysis by SDS-PAGE resulted in the detection of a protein of approximately 33/34 kDa that could be partially removed by preincubating the serum with hMBP mAb. |
| 5876 | 9300722 | In addition, incubation of serum with MP2-coated beads and analysis by SDS-PAGE resulted in the detection of a protein of approximately 33/34 kDa that could be partially removed by preincubating the serum with hMBP mAb. |
| 5877 | 9300722 | In addition, incubation of serum with MP2-coated beads and analysis by SDS-PAGE resulted in the detection of a protein of approximately 33/34 kDa that could be partially removed by preincubating the serum with hMBP mAb. |
| 5878 | 9300722 | In addition, incubation of serum with MP2-coated beads and analysis by SDS-PAGE resulted in the detection of a protein of approximately 33/34 kDa that could be partially removed by preincubating the serum with hMBP mAb. |
| 5879 | 9300722 | We conclude that hMBP is involved in the binding of MP2 to PBMCs and the release of TNF-alpha. |
| 5880 | 9300722 | We conclude that hMBP is involved in the binding of MP2 to PBMCs and the release of TNF-alpha. |
| 5881 | 9300722 | We conclude that hMBP is involved in the binding of MP2 to PBMCs and the release of TNF-alpha. |
| 5882 | 9300722 | We conclude that hMBP is involved in the binding of MP2 to PBMCs and the release of TNF-alpha. |
| 5883 | 9300722 | We conclude that hMBP is involved in the binding of MP2 to PBMCs and the release of TNF-alpha. |
| 5884 | 9300722 | We conclude that hMBP is involved in the binding of MP2 to PBMCs and the release of TNF-alpha. |
| 5885 | 9278339 | Previous studies showed that mouse spleen cells produced IL-12, TNF-alpha, and IFN-gamma when stimulated with phagocytosable-size chitin particles (N-acetyl-D-glucosamine polymers). |
| 5886 | 9278339 | Previous studies showed that mouse spleen cells produced IL-12, TNF-alpha, and IFN-gamma when stimulated with phagocytosable-size chitin particles (N-acetyl-D-glucosamine polymers). |
| 5887 | 9278339 | Previous studies showed that mouse spleen cells produced IL-12, TNF-alpha, and IFN-gamma when stimulated with phagocytosable-size chitin particles (N-acetyl-D-glucosamine polymers). |
| 5888 | 9278339 | Previous studies showed that mouse spleen cells produced IL-12, TNF-alpha, and IFN-gamma when stimulated with phagocytosable-size chitin particles (N-acetyl-D-glucosamine polymers). |
| 5889 | 9278339 | We found that these particles induced IL-12, TNF-alpha, and IFN-gamma. |
| 5890 | 9278339 | We found that these particles induced IL-12, TNF-alpha, and IFN-gamma. |
| 5891 | 9278339 | We found that these particles induced IL-12, TNF-alpha, and IFN-gamma. |
| 5892 | 9278339 | We found that these particles induced IL-12, TNF-alpha, and IFN-gamma. |
| 5893 | 9278339 | The treatments with soluble mannan or with cytochalasin D, in sharp contrast, did not inhibit LPS-induced IL-12/IFN-gamma production or exogenous IL-12-induced IFN-gamma production. |
| 5894 | 9278339 | The treatments with soluble mannan or with cytochalasin D, in sharp contrast, did not inhibit LPS-induced IL-12/IFN-gamma production or exogenous IL-12-induced IFN-gamma production. |
| 5895 | 9278339 | The treatments with soluble mannan or with cytochalasin D, in sharp contrast, did not inhibit LPS-induced IL-12/IFN-gamma production or exogenous IL-12-induced IFN-gamma production. |
| 5896 | 9278339 | The treatments with soluble mannan or with cytochalasin D, in sharp contrast, did not inhibit LPS-induced IL-12/IFN-gamma production or exogenous IL-12-induced IFN-gamma production. |
| 5897 | 9278339 | Finally, spleen cells from C3H/HeJ mice also showed comparable levels of IL-12/TNF-alpha/IFN-gamma production when induced by 1 to 10 microm chitin particles. |
| 5898 | 9278339 | Finally, spleen cells from C3H/HeJ mice also showed comparable levels of IL-12/TNF-alpha/IFN-gamma production when induced by 1 to 10 microm chitin particles. |
| 5899 | 9278339 | Finally, spleen cells from C3H/HeJ mice also showed comparable levels of IL-12/TNF-alpha/IFN-gamma production when induced by 1 to 10 microm chitin particles. |
| 5900 | 9278339 | Finally, spleen cells from C3H/HeJ mice also showed comparable levels of IL-12/TNF-alpha/IFN-gamma production when induced by 1 to 10 microm chitin particles. |
| 5901 | 9278339 | Taken together, our results indicate that mannose receptor-mediated phagocytosis, but not the receptor-mediated pinocytosis, is highly associated with the production of IFN-gamma-inducing extracellular signaling factors such as IL-12 and TNF-alpha. |
| 5902 | 9278339 | Taken together, our results indicate that mannose receptor-mediated phagocytosis, but not the receptor-mediated pinocytosis, is highly associated with the production of IFN-gamma-inducing extracellular signaling factors such as IL-12 and TNF-alpha. |
| 5903 | 9278339 | Taken together, our results indicate that mannose receptor-mediated phagocytosis, but not the receptor-mediated pinocytosis, is highly associated with the production of IFN-gamma-inducing extracellular signaling factors such as IL-12 and TNF-alpha. |
| 5904 | 9278339 | Taken together, our results indicate that mannose receptor-mediated phagocytosis, but not the receptor-mediated pinocytosis, is highly associated with the production of IFN-gamma-inducing extracellular signaling factors such as IL-12 and TNF-alpha. |
| 5905 | 9583995 | Severe graft-versus-host disease in SCID mice is associated with a decrease of selective donor cell TCR Vbeta specificities and increased expression of IFN-gamma and IL-4. |
| 5906 | 9583995 | At that time, cells in BM of B6 and CBA/J injected recipients were augmented in intracellular IL-4, IL-10, and TNF-alpha, whereas only cells in B6 treated BM were increased in IFN-gamma, and both treated groups of mice had up-regulated endogenous MHC class I and class II expression in the three organs. |
| 5907 | 9314076 | Extensive studies of the molecular basis of the latter phenomenon led to the conclusion that the most decisive step from non-specific microabscess formation to granulomatous inflammation is the activation of non-specifically invading CD4+ T cells, which results in high local concentrations of TNF-alpha and IFN-gamma in the presence of IL-2. |
| 5908 | 9314076 | Extensive studies of the molecular basis of the latter phenomenon led to the conclusion that the most decisive step from non-specific microabscess formation to granulomatous inflammation is the activation of non-specifically invading CD4+ T cells, which results in high local concentrations of TNF-alpha and IFN-gamma in the presence of IL-2. |
| 5909 | 9314076 | Because any attempt to neutralize the effects of TNF-alpha and IFN-gamma to modulate T-cell-mediated inflammation will also dramatically decrease host resistance, other anti-inflammatory strategies based on the modulation of TNF-alpha and IFN-gamma-induced mechanisms of monocyte accumulation must be developed. |
| 5910 | 9314076 | Because any attempt to neutralize the effects of TNF-alpha and IFN-gamma to modulate T-cell-mediated inflammation will also dramatically decrease host resistance, other anti-inflammatory strategies based on the modulation of TNF-alpha and IFN-gamma-induced mechanisms of monocyte accumulation must be developed. |
| 5911 | 9234802 | Inhibition of anti-B. burgdorferi antibody production was observed after 3 days, but not after 2 days, of exposure of the antigen-presenting cells to tumor necrosis factor alpha +/- granulocyte-macrophage colony-stimulating factor. |
| 5912 | 9217054 | VEE-induced cytokine gene expression was 100-fold elevated over that of untreated controls for IFN-gamma and IL-6 and 10-fold increased for IL-12, IL-10, and TNF-alpha. |
| 5913 | 9276872 | Pancreatic cancer is extremely resistant to various cancer therapies, however, variety of new therapies for pancreatic cancer have been investigated: (1) immunotherapy including cytokines like TNF, adoptive immunotherapy with lymphokine-activated killer cells or cytotoxic T-lymphocytes, and tumor vaccines using mutated Ki-ras oncoprotein or irradiated tumor cells which were transfected by cytokine genes; (2) gene therapy including transfer of cytokine genes or antisense Ki-ras oncogene, and a combination of gene transfer of herpes simplex virus thymidine kinase and subsequent administration of ganciclovir; (3) differentiation therapy including a quinolinone derivative, vesnarinone; (4) endocrine therapy including cholecystokinin-receptor antagonist, CR1505 or L364,718; (5) heavy water, and etc. |
| 5914 | 9252123 | Degenerate cytotoxic T cell epitopes from P. falciparum restricted by multiple HLA-A and HLA-B supertype alleles. |
| 5915 | 9252123 | Positive cytotoxic T lymphocyte recall and cytokine (interferon-gamma and tumor necrosis factor alpha) responses were detected for all peptides; all were recognized in the context of more than one HLA class I molecule; and at least 12 of the 17 were recognized in the context of all HLA alleles studied. |
| 5916 | 9199462 | A murine model of pneumonia due to the mouse pneumonitis agent (MoPn [murine Chlamydia trachomatis]) in mice deficient in CD4+ T-cell function (major histocompatibility complex [MHC] class II function [class II-/-], CD8+ T-cell function (beta2-microglobulin deficient, MHC class I deficient [Beta2m-/-]), B-cell function (C57BL/10J-Igh(tm1Cgn) [Igh-/-]), and gamma interferon (IFN-gamma) (C57BL/6-Ifg(tm1) [Ifg-/-]) or interleukin-4 (C57BL/6J(tm1Cgn29) [IL4-/-]) production was employed to determine if each of these mechanisms was critical to resistance against reinfection by C. trachomatis or if alternate compensatory mechanisms existed in their absence which could potentially be exploited in vaccine development. |
| 5917 | 9199462 | A murine model of pneumonia due to the mouse pneumonitis agent (MoPn [murine Chlamydia trachomatis]) in mice deficient in CD4+ T-cell function (major histocompatibility complex [MHC] class II function [class II-/-], CD8+ T-cell function (beta2-microglobulin deficient, MHC class I deficient [Beta2m-/-]), B-cell function (C57BL/10J-Igh(tm1Cgn) [Igh-/-]), and gamma interferon (IFN-gamma) (C57BL/6-Ifg(tm1) [Ifg-/-]) or interleukin-4 (C57BL/6J(tm1Cgn29) [IL4-/-]) production was employed to determine if each of these mechanisms was critical to resistance against reinfection by C. trachomatis or if alternate compensatory mechanisms existed in their absence which could potentially be exploited in vaccine development. |
| 5918 | 9199462 | A murine model of pneumonia due to the mouse pneumonitis agent (MoPn [murine Chlamydia trachomatis]) in mice deficient in CD4+ T-cell function (major histocompatibility complex [MHC] class II function [class II-/-], CD8+ T-cell function (beta2-microglobulin deficient, MHC class I deficient [Beta2m-/-]), B-cell function (C57BL/10J-Igh(tm1Cgn) [Igh-/-]), and gamma interferon (IFN-gamma) (C57BL/6-Ifg(tm1) [Ifg-/-]) or interleukin-4 (C57BL/6J(tm1Cgn29) [IL4-/-]) production was employed to determine if each of these mechanisms was critical to resistance against reinfection by C. trachomatis or if alternate compensatory mechanisms existed in their absence which could potentially be exploited in vaccine development. |
| 5919 | 9199462 | A murine model of pneumonia due to the mouse pneumonitis agent (MoPn [murine Chlamydia trachomatis]) in mice deficient in CD4+ T-cell function (major histocompatibility complex [MHC] class II function [class II-/-], CD8+ T-cell function (beta2-microglobulin deficient, MHC class I deficient [Beta2m-/-]), B-cell function (C57BL/10J-Igh(tm1Cgn) [Igh-/-]), and gamma interferon (IFN-gamma) (C57BL/6-Ifg(tm1) [Ifg-/-]) or interleukin-4 (C57BL/6J(tm1Cgn29) [IL4-/-]) production was employed to determine if each of these mechanisms was critical to resistance against reinfection by C. trachomatis or if alternate compensatory mechanisms existed in their absence which could potentially be exploited in vaccine development. |
| 5920 | 9199462 | CD4 T-cell-deficient MHC class II-/- mice were very susceptible to reinfection with MoPn, showing the critical importance of this cell to resistance. |
| 5921 | 9199462 | CD4 T-cell-deficient MHC class II-/- mice were very susceptible to reinfection with MoPn, showing the critical importance of this cell to resistance. |
| 5922 | 9199462 | CD4 T-cell-deficient MHC class II-/- mice were very susceptible to reinfection with MoPn, showing the critical importance of this cell to resistance. |
| 5923 | 9199462 | CD4 T-cell-deficient MHC class II-/- mice were very susceptible to reinfection with MoPn, showing the critical importance of this cell to resistance. |
| 5924 | 9199462 | These mice lacked antibody production but did produce IFN-gamma, apparently by mechanisms involving NK and CD8+ T cells. |
| 5925 | 9199462 | These mice lacked antibody production but did produce IFN-gamma, apparently by mechanisms involving NK and CD8+ T cells. |
| 5926 | 9199462 | These mice lacked antibody production but did produce IFN-gamma, apparently by mechanisms involving NK and CD8+ T cells. |
| 5927 | 9199462 | These mice lacked antibody production but did produce IFN-gamma, apparently by mechanisms involving NK and CD8+ T cells. |
| 5928 | 9199462 | Levels of lung IFN-gamma and TNF-alpha were elevated in Igh-/- mice compared to those in controls. |
| 5929 | 9199462 | Levels of lung IFN-gamma and TNF-alpha were elevated in Igh-/- mice compared to those in controls. |
| 5930 | 9199462 | Levels of lung IFN-gamma and TNF-alpha were elevated in Igh-/- mice compared to those in controls. |
| 5931 | 9199462 | Levels of lung IFN-gamma and TNF-alpha were elevated in Igh-/- mice compared to those in controls. |
| 5932 | 9199462 | Of most importance, however, congenitally IFN-gamma-deficient Ifg-/- mice (which have elevated levels of other cytokines, including TNF-alpha and granulocyte-macrophage colony-stimulating factor) are paradoxically more resistant to MoPn rechallenge than controls, showing that IFN-gamma is not an absolute requirement for acquired resistance and implying the presence of very effective compensatory host defense mechanism(s). |
| 5933 | 9199462 | Of most importance, however, congenitally IFN-gamma-deficient Ifg-/- mice (which have elevated levels of other cytokines, including TNF-alpha and granulocyte-macrophage colony-stimulating factor) are paradoxically more resistant to MoPn rechallenge than controls, showing that IFN-gamma is not an absolute requirement for acquired resistance and implying the presence of very effective compensatory host defense mechanism(s). |
| 5934 | 9199462 | Of most importance, however, congenitally IFN-gamma-deficient Ifg-/- mice (which have elevated levels of other cytokines, including TNF-alpha and granulocyte-macrophage colony-stimulating factor) are paradoxically more resistant to MoPn rechallenge than controls, showing that IFN-gamma is not an absolute requirement for acquired resistance and implying the presence of very effective compensatory host defense mechanism(s). |
| 5935 | 9199462 | Of most importance, however, congenitally IFN-gamma-deficient Ifg-/- mice (which have elevated levels of other cytokines, including TNF-alpha and granulocyte-macrophage colony-stimulating factor) are paradoxically more resistant to MoPn rechallenge than controls, showing that IFN-gamma is not an absolute requirement for acquired resistance and implying the presence of very effective compensatory host defense mechanism(s). |
| 5936 | 9199462 | Thus, resistance to reinfection in this model is flexible and multifactorial and is heavily dependent on CD4+ T cells, with a probable role for IFN-gamma and TNF-alpha and a possible modest role for Th1-dependent antibody. |
| 5937 | 9199462 | Thus, resistance to reinfection in this model is flexible and multifactorial and is heavily dependent on CD4+ T cells, with a probable role for IFN-gamma and TNF-alpha and a possible modest role for Th1-dependent antibody. |
| 5938 | 9199462 | Thus, resistance to reinfection in this model is flexible and multifactorial and is heavily dependent on CD4+ T cells, with a probable role for IFN-gamma and TNF-alpha and a possible modest role for Th1-dependent antibody. |
| 5939 | 9199462 | Thus, resistance to reinfection in this model is flexible and multifactorial and is heavily dependent on CD4+ T cells, with a probable role for IFN-gamma and TNF-alpha and a possible modest role for Th1-dependent antibody. |
| 5940 | 9199462 | Since IFN-gamma was dispensable in host defense, the highly effective mechanism or mechanisms which can compensate for its absence (which include TNF-alpha) deserve further study. |
| 5941 | 9199462 | Since IFN-gamma was dispensable in host defense, the highly effective mechanism or mechanisms which can compensate for its absence (which include TNF-alpha) deserve further study. |
| 5942 | 9199462 | Since IFN-gamma was dispensable in host defense, the highly effective mechanism or mechanisms which can compensate for its absence (which include TNF-alpha) deserve further study. |
| 5943 | 9199462 | Since IFN-gamma was dispensable in host defense, the highly effective mechanism or mechanisms which can compensate for its absence (which include TNF-alpha) deserve further study. |
| 5944 | 10851462 | Cytokine detection in patients' sera by ELISA showed significant increases (p < 0.05) for IFN-gamma and TNF-alpha but not for IFN-alpha four h post vaccination. |
| 5945 | 9234526 | Ag85A and Ag85B encoding plasmids induced a robust Th1-like response towards native Ag85, characterized by elevated levels of interleukin (IL)-2, interferon-gamma, and TNF-alpha. |
| 5946 | 9234526 | Levels of IL-4, IL-6, and IL-10 were low or undetectable. |
| 5947 | 9139889 | The capacity of rVV-M to generate HLA-A2.1-restricted MART-1/Melan A-specific CTL was demonstrated from tumor-infiltrating-lymphocyte (TIL) cultures and from healthy donors' peripheral-blood mononuclear cells (PBMC). |
| 5948 | 9139889 | MART-1/Melan-A27-35-specific CTL were generated from TIL after 2 weekly stimulation courses. |
| 5949 | 9139889 | In addition, TNF-alpha production could be induced in rVV-M-stimulated CTL upon co-culture with COS-7 cells transiently transfected with MART-1/Melan-A and HLA-A2.1 genes. |
| 5950 | 9297347 | The parameters of nonspecific immunity (interferon, interleukin-1, tumor necrosis factor, and natural killers) changed in immune BALB/c mice after challenge with Machupo virus in doses of 1000 and 5000 PFU. |
| 5951 | 9297347 | The parameters of nonspecific immunity (interferon, interleukin-1, tumor necrosis factor, and natural killers) changed in immune BALB/c mice after challenge with Machupo virus in doses of 1000 and 5000 PFU. |
| 5952 | 9297347 | After challenge with 5000 PFU the maximal values of interferon, interleukin-1, tumor necrosis factor, and natural killers were observed on days 5-7, the animals dying at the height of these values. |
| 5953 | 9297347 | After challenge with 5000 PFU the maximal values of interferon, interleukin-1, tumor necrosis factor, and natural killers were observed on days 5-7, the animals dying at the height of these values. |
| 5954 | 9226467 | In order to improve suppressed immunogenicity of QRpP cells with the high levels of PGE2, the author transfected QRpP cells with an effective expression vector containing cDNA for IL-2, IFN-gamma and TNF-alpha. |
| 5955 | 9226467 | In order to improve suppressed immunogenicity of QRpP cells with the high levels of PGE2, the author transfected QRpP cells with an effective expression vector containing cDNA for IL-2, IFN-gamma and TNF-alpha. |
| 5956 | 9226467 | In order to improve suppressed immunogenicity of QRpP cells with the high levels of PGE2, the author transfected QRpP cells with an effective expression vector containing cDNA for IL-2, IFN-gamma and TNF-alpha. |
| 5957 | 9226467 | These transfected clones expressed mRNA for IL-2, IFN-gamma and TNF-alpha, respectively, and produced high levels of cytokines in their culture supernatants. |
| 5958 | 9226467 | These transfected clones expressed mRNA for IL-2, IFN-gamma and TNF-alpha, respectively, and produced high levels of cytokines in their culture supernatants. |
| 5959 | 9226467 | These transfected clones expressed mRNA for IL-2, IFN-gamma and TNF-alpha, respectively, and produced high levels of cytokines in their culture supernatants. |
| 5960 | 9226467 | Consequentry, QRpP cells transfected with IL-2 (QRpP-IL-2), IFN-gamma (QRpP-IFN-gamma), IL-2 and IFN-gamma (QRpP-IL-2/IFN-gamma), TNF-alpha (QRpP-TNF-alpha) lowered in tumorigenicity. |
| 5961 | 9226467 | Consequentry, QRpP cells transfected with IL-2 (QRpP-IL-2), IFN-gamma (QRpP-IFN-gamma), IL-2 and IFN-gamma (QRpP-IL-2/IFN-gamma), TNF-alpha (QRpP-TNF-alpha) lowered in tumorigenicity. |
| 5962 | 9226467 | Consequentry, QRpP cells transfected with IL-2 (QRpP-IL-2), IFN-gamma (QRpP-IFN-gamma), IL-2 and IFN-gamma (QRpP-IL-2/IFN-gamma), TNF-alpha (QRpP-TNF-alpha) lowered in tumorigenicity. |
| 5963 | 9127013 | HIV-1 env DNA vaccine administered to rhesus monkeys elicits MHC class II-restricted CD4+ T helper cells that secrete IFN-gamma and TNF-alpha. |
| 5964 | 9127013 | HIV-1 env DNA vaccine administered to rhesus monkeys elicits MHC class II-restricted CD4+ T helper cells that secrete IFN-gamma and TNF-alpha. |
| 5965 | 9127013 | All of the CD4+ T cell lines responded to Env peptide by secreting IFN-gamma and TNF-alpha without appreciable IL-4 production. |
| 5966 | 9127013 | All of the CD4+ T cell lines responded to Env peptide by secreting IFN-gamma and TNF-alpha without appreciable IL-4 production. |
| 5967 | 9127013 | Demonstration of a nucleotide vaccine eliciting a Th1-like immune response is consistent with the well documented ability of naked DNA vaccines to induce durable CD8+ CTL responses. |
| 5968 | 9127013 | Demonstration of a nucleotide vaccine eliciting a Th1-like immune response is consistent with the well documented ability of naked DNA vaccines to induce durable CD8+ CTL responses. |
| 5969 | 9125592 | Intraperitoneal administration of these preparations induced production of tumor necrosis factor alpha (TNF-alpha) and interleukin 6 (IL-6) in serum 2 h after injections. |
| 5970 | 9125592 | Intraperitoneal administration of these preparations induced production of tumor necrosis factor alpha (TNF-alpha) and interleukin 6 (IL-6) in serum 2 h after injections. |
| 5971 | 9125592 | Intraperitoneal administration of these preparations induced production of tumor necrosis factor alpha (TNF-alpha) and interleukin 6 (IL-6) in serum 2 h after injections. |
| 5972 | 9125592 | However, repeated doses of low- and high-toxicity preparations induced lower amounts of TNF-alpha and IL-6, i.e., LOS tolerance. |
| 5973 | 9125592 | However, repeated doses of low- and high-toxicity preparations induced lower amounts of TNF-alpha and IL-6, i.e., LOS tolerance. |
| 5974 | 9125592 | However, repeated doses of low- and high-toxicity preparations induced lower amounts of TNF-alpha and IL-6, i.e., LOS tolerance. |
| 5975 | 9125592 | Peritoneal macrophages from tolerant mice pretreated with either high- or low-toxicity LOS preparations produced only a fraction of the amounts of TNF-alpha and IL-6 produced by control groups in response to LOS ex vivo. |
| 5976 | 9125592 | Peritoneal macrophages from tolerant mice pretreated with either high- or low-toxicity LOS preparations produced only a fraction of the amounts of TNF-alpha and IL-6 produced by control groups in response to LOS ex vivo. |
| 5977 | 9125592 | Peritoneal macrophages from tolerant mice pretreated with either high- or low-toxicity LOS preparations produced only a fraction of the amounts of TNF-alpha and IL-6 produced by control groups in response to LOS ex vivo. |
| 5978 | 9125582 | Production of tumor necrosis factor and nitric oxide by macrophages infected with live and dead mycobacteria and their suppression by an interleukin-10-secreting recombinant. |
| 5979 | 9125582 | Production of tumor necrosis factor and nitric oxide by macrophages infected with live and dead mycobacteria and their suppression by an interleukin-10-secreting recombinant. |
| 5980 | 9125582 | Expression of interleukin-10 by a recombinant strain of Mycobacterium smegmatis caused reduced production of TNF-alpha and nitric oxide during the early stages of infection. |
| 5981 | 9125582 | Expression of interleukin-10 by a recombinant strain of Mycobacterium smegmatis caused reduced production of TNF-alpha and nitric oxide during the early stages of infection. |
| 5982 | 9125535 | In contrast, no increases in interleukin-4 production were observed in the first 24 h and tumor necrosis factor alpha levels increased equally in both nonlethal and lethal infections. |
| 5983 | 9125535 | In contrast, no increases in interleukin-4 production were observed in the first 24 h and tumor necrosis factor alpha levels increased equally in both nonlethal and lethal infections. |
| 5984 | 9125535 | Infecting mice with increasing numbers of lethal P. yoelii and Plasmodium berghei parasites did not increase the amount of gamma interferon, interleukin-4, and tumor necrosis factor alpha produced in a dose-dependent fashion. |
| 5985 | 9125535 | Infecting mice with increasing numbers of lethal P. yoelii and Plasmodium berghei parasites did not increase the amount of gamma interferon, interleukin-4, and tumor necrosis factor alpha produced in a dose-dependent fashion. |
| 5986 | 9103465 | Cytokine-in-adjuvant steering of the immune response phenotype to HIV-1 vaccine constructs: granulocyte-macrophage colony-stimulating factor and TNF-alpha synergize with IL-12 to enhance induction of cytotoxic T lymphocytes. |
| 5987 | 9103465 | Cytokine-in-adjuvant steering of the immune response phenotype to HIV-1 vaccine constructs: granulocyte-macrophage colony-stimulating factor and TNF-alpha synergize with IL-12 to enhance induction of cytotoxic T lymphocytes. |
| 5988 | 9103465 | Cytokine-in-adjuvant steering of the immune response phenotype to HIV-1 vaccine constructs: granulocyte-macrophage colony-stimulating factor and TNF-alpha synergize with IL-12 to enhance induction of cytotoxic T lymphocytes. |
| 5989 | 9103465 | Here we study the effects of IL-2, IL-4, IL-7, IL-1beta, IL-12, IFN-gamma, TNF-alpha, and granulocyte-macrophage CSF (GM-CSF) incorporated with peptide in adjuvant on a variety of responses elicited: CTL, T cell proliferation, cytokine production and message, and Ab isotype. |
| 5990 | 9103465 | Here we study the effects of IL-2, IL-4, IL-7, IL-1beta, IL-12, IFN-gamma, TNF-alpha, and granulocyte-macrophage CSF (GM-CSF) incorporated with peptide in adjuvant on a variety of responses elicited: CTL, T cell proliferation, cytokine production and message, and Ab isotype. |
| 5991 | 9103465 | Here we study the effects of IL-2, IL-4, IL-7, IL-1beta, IL-12, IFN-gamma, TNF-alpha, and granulocyte-macrophage CSF (GM-CSF) incorporated with peptide in adjuvant on a variety of responses elicited: CTL, T cell proliferation, cytokine production and message, and Ab isotype. |
| 5992 | 9103465 | GM-CSF synergized with IL-12 for CTL induction in BALB/c mice concomitant with suppression of Th2 cytokines IL-4 and IL-10. |
| 5993 | 9103465 | GM-CSF synergized with IL-12 for CTL induction in BALB/c mice concomitant with suppression of Th2 cytokines IL-4 and IL-10. |
| 5994 | 9103465 | GM-CSF synergized with IL-12 for CTL induction in BALB/c mice concomitant with suppression of Th2 cytokines IL-4 and IL-10. |
| 5995 | 9103465 | TNF-alpha also synergized with IL-12, but by a different mechanism, inducing IFN-gamma production in BALB/c mice and thus shifting the response to a Th1 phenotype. |
| 5996 | 9103465 | TNF-alpha also synergized with IL-12, but by a different mechanism, inducing IFN-gamma production in BALB/c mice and thus shifting the response to a Th1 phenotype. |
| 5997 | 9103465 | TNF-alpha also synergized with IL-12, but by a different mechanism, inducing IFN-gamma production in BALB/c mice and thus shifting the response to a Th1 phenotype. |
| 5998 | 9103465 | The results presented here suggest that in addition to IL-2, optimum induction of CD8+ CTL in vivo requires a combination of cytokines, including GM-CSF (probably acting to enhance Ag presentation and CD4+ cell help) and IL-12 (steering the Th response toward Th1 cytokines). |
| 5999 | 9103465 | The results presented here suggest that in addition to IL-2, optimum induction of CD8+ CTL in vivo requires a combination of cytokines, including GM-CSF (probably acting to enhance Ag presentation and CD4+ cell help) and IL-12 (steering the Th response toward Th1 cytokines). |
| 6000 | 9103465 | The results presented here suggest that in addition to IL-2, optimum induction of CD8+ CTL in vivo requires a combination of cytokines, including GM-CSF (probably acting to enhance Ag presentation and CD4+ cell help) and IL-12 (steering the Th response toward Th1 cytokines). |
| 6001 | 9100988 | We have previously demonstrated that immunization of HIV-1-infected individuals with the common recall antigen, tetanus, induced transient increases in plasma viremia as well as an increased ability to isolate virus from CD8+ T cell-depleted peripheral blood mononuclear cells (PBMCs) under minimally stimulated culture conditions (IL-2 plus IL-4) postimmunization. |
| 6002 | 9100988 | In four of these patients, virus could also be isolated from CD8+ T cell-depleted PBMCs in the presence of tetanus without the addition of any exogenous IL-2. |
| 6003 | 9100988 | HIV-1 was isolated predominantly from CD4+ T cells with a CD45RO+, CD25+ phenotype and was associated with a trend to elevated levels in culture supernatants of IFN-gamma, IL-6, TNF-alpha, and IL-4. |
| 6004 | 9101513 | The synovitis took a neutrophilic form, with marked synovial membrane content of interleukin 8 (IL-8) and tumor necrosis factor alpha (TNF-alpha). |
| 6005 | 9101513 | The synovitis took a neutrophilic form, with marked synovial membrane content of interleukin 8 (IL-8) and tumor necrosis factor alpha (TNF-alpha). |
| 6006 | 9101513 | It subsequently developed into chronic lymphoplasmacytoid synovitis, similar to rheumatoid arthritis (RA), with decreased IL-8 but continuing IL-1 and TNF-alpha production in the synovial membrane. |
| 6007 | 9101513 | It subsequently developed into chronic lymphoplasmacytoid synovitis, similar to rheumatoid arthritis (RA), with decreased IL-8 but continuing IL-1 and TNF-alpha production in the synovial membrane. |
| 6008 | 9207755 | Dh-Ag was more potent than M. leprae in the induction of immunostimulatory/proinflammatory cytokines, interleukin-1 (IL-1), IL-6 and tumor necrosis factor (TNF). |
| 6009 | 9207755 | Dh-Ag was more potent than M. leprae in the induction of immunostimulatory/proinflammatory cytokines, interleukin-1 (IL-1), IL-6 and tumor necrosis factor (TNF). |
| 6010 | 9207755 | Nevertheless, when monocytes were pretreated with the lipids followed by stimulation with Dh-Ag, productions of IL-1, IL-6 and TNF were all inhibited in a dose-dependent manner. |
| 6011 | 9207755 | Nevertheless, when monocytes were pretreated with the lipids followed by stimulation with Dh-Ag, productions of IL-1, IL-6 and TNF were all inhibited in a dose-dependent manner. |
| 6012 | 9382749 | Subsequent studies have shown that the protective immune mechanisms were dependent on antigen specific CD4+ T cells, the activation of alveolar macrophages, the recruitment and activation of polymorphs, predominantly neutrophils, the controlled secretion of TNF-alpha, IL-1 and IFN gamma and the presence of antibody. |
| 6013 | 9181927 | Even if the mechanism by which BCG mediate antitumor activity are not clearly established, an association between the immunological response and antitumoral activity is known IL-1 and TNF alfa are the monokines that have multiple biological effects, including linfocyte proliferation, production of fever, augmentation of cytotoxicity and production of cytokines. |
| 6014 | 9181927 | Even if the mechanism by which BCG mediate antitumor activity are not clearly established, an association between the immunological response and antitumoral activity is known IL-1 and TNF alfa are the monokines that have multiple biological effects, including linfocyte proliferation, production of fever, augmentation of cytotoxicity and production of cytokines. |
| 6015 | 9181927 | The goal of this study is show the response from LPS induced and not peripheral monocytes of superficial bladder cancer patients BCG treated and not, i.e. the levels of TNF alfa, IL-1 and not IL-6. |
| 6016 | 9181927 | The goal of this study is show the response from LPS induced and not peripheral monocytes of superficial bladder cancer patients BCG treated and not, i.e. the levels of TNF alfa, IL-1 and not IL-6. |
| 6017 | 8995646 | For both SIVmac239 and its nef-deleted derivative, strong expression was observed as early as 7 days postinfection for interleukin 1beta (IL-1beta), IL-6, tumor necrosis factor alpha, gamma interferon, and IL-13. |
| 6018 | 8995646 | Primary infection with SIVmac239 was characterized by a higher level of IL-4, IL-10, MIP-1alpha, MIP-1beta, MCP-1, and RANTES gene expression and a lower level of IL-12 and granzyme B gene expression compared with infection with SIVmac239 delta nef. |
| 6019 | 24493438 | Several observations are remarkable: the high efficacy of local cytokines to induce an antitumor response in the absence of systemic toxicity; a surprisingly large number of cytokines possess antitumor activity in this assay (IL-1, IL-2, IL-4, IL-6, IL-7, TNF, LT, IFN-γ, MCAF, G-CSF, GM-CSF, IP-10); and in several models, cytokine-producing tumors were heavily infiltrated by T-lymphocytes that contributed to tumor destruction (for review see ref. 1). |
| 6020 | 24493438 | Several observations are remarkable: the high efficacy of local cytokines to induce an antitumor response in the absence of systemic toxicity; a surprisingly large number of cytokines possess antitumor activity in this assay (IL-1, IL-2, IL-4, IL-6, IL-7, TNF, LT, IFN-γ, MCAF, G-CSF, GM-CSF, IP-10); and in several models, cytokine-producing tumors were heavily infiltrated by T-lymphocytes that contributed to tumor destruction (for review see ref. 1). |
| 6021 | 24493438 | Currently, three cytokine gene therapy variations with IL-2, IL-4, TNF, IFN-γ, or GM-CSF genes are tested: transfected autologous tumor cells; transfected allogeneic tumor cells; and transfected autologous fibroblasts mixed with tumor cells as vaccine. |
| 6022 | 24493438 | Currently, three cytokine gene therapy variations with IL-2, IL-4, TNF, IFN-γ, or GM-CSF genes are tested: transfected autologous tumor cells; transfected allogeneic tumor cells; and transfected autologous fibroblasts mixed with tumor cells as vaccine. |
| 6023 | 9597079 | In a primary cascade of cytokine production at the site of antigen + adjuvant injection, TNF-alpha promotes the migration of dendritic cells (DC) to lymphoid tissues while GM-CSF accelerates the differentiation of DC into efficient presenters of antigens to T cells. |
| 6024 | 9408967 | Recent evidence suggests that cytokine combinations, such as IL-2, IL-6, and TNF alpha, can activate both naive and memory T cells in vitro. |
| 6025 | 9266414 | The examination of an experimental animal model for MS, experimental allergic encephalomyelitis (EAE), demonstrated that myelin basic protein-(MBP) or proteolipidprotein-(PLP) specific T cells mediate the destruction of CNS myelin. |
| 6026 | 9266414 | In recent years, elegant studies in EAE showed that encephalitogenic T cells recognize short peptides of MBP or PLP in the context of MHC/HLA-class II molecules, express a restricted number of T cell receptor (TCR) molecules and secrete interferon-gamma and tumor necrosis factor-alpha/beta. |
| 6027 | 9266414 | MBP- and PLP-specific T cells with similar properties could also be isolated from MS patients and control individuals. |
| 6028 | 9079741 | The analysis showed high expression of interleukin (IL)-1 alpha, tumor necrosis factor (TNF)-alpha, IL-2, and interferon (IFN)-tau in BCG (7/7, 7/7, 7/7, 5/7) and N-CWS (9/9, 9/9, 8/9, 8/9) treated tumors in comparison to low expression in controls (3/9, 0/9, 3/9, 3/9). |
| 6029 | 9000497 | The first section delineates the genesis of the inflammatory responses, which initiate with the production of tumor necrosis factor (TNF)-alpha, interferon (IFN)-gamma, interleukin (IL)-1, IL-6, and IL-8 and continue with the recruitment of neutrophilic polymorphonuclear cells, lymphocytes, plasma cells, macrophages and eosinophils, and later with the development and recruitment of specifically committed cells (lymphocytes sensitized to H pylori antigens and B cells producing immunoglobulin (Ig)A, IgG, and possibly IgE antibodies against a variety of H pylori surface and flagellar proteins as well as bacterial toxins). |
| 6030 | 8975923 | The ability to induce TNF-alpha in PBMC by four clinical strains of C. neoformans, a laboratory strain (NIH 37), and the purified cryptococcal components glucuronoxylomannan (GXM), galactoxylomannan (GalXM), and mannoproteins (MP1 and MP2) were investigated under different opsonic conditions. |
| 6031 | 8975923 | The ability to induce TNF-alpha in PBMC by four clinical strains of C. neoformans, a laboratory strain (NIH 37), and the purified cryptococcal components glucuronoxylomannan (GXM), galactoxylomannan (GalXM), and mannoproteins (MP1 and MP2) were investigated under different opsonic conditions. |
| 6032 | 8975923 | The ability to induce TNF-alpha in PBMC by four clinical strains of C. neoformans, a laboratory strain (NIH 37), and the purified cryptococcal components glucuronoxylomannan (GXM), galactoxylomannan (GalXM), and mannoproteins (MP1 and MP2) were investigated under different opsonic conditions. |
| 6033 | 8975923 | The ability to induce TNF-alpha in PBMC by four clinical strains of C. neoformans, a laboratory strain (NIH 37), and the purified cryptococcal components glucuronoxylomannan (GXM), galactoxylomannan (GalXM), and mannoproteins (MP1 and MP2) were investigated under different opsonic conditions. |
| 6034 | 8975923 | The ability to induce TNF-alpha in PBMC by four clinical strains of C. neoformans, a laboratory strain (NIH 37), and the purified cryptococcal components glucuronoxylomannan (GXM), galactoxylomannan (GalXM), and mannoproteins (MP1 and MP2) were investigated under different opsonic conditions. |
| 6035 | 8975923 | Normal human serum (NHS) enhanced TNF-alpha induction by whole cryptococci and the different cryptococcal components, with MP2 being the most potent TNF-alpha inducer. |
| 6036 | 8975923 | Normal human serum (NHS) enhanced TNF-alpha induction by whole cryptococci and the different cryptococcal components, with MP2 being the most potent TNF-alpha inducer. |
| 6037 | 8975923 | Normal human serum (NHS) enhanced TNF-alpha induction by whole cryptococci and the different cryptococcal components, with MP2 being the most potent TNF-alpha inducer. |
| 6038 | 8975923 | Normal human serum (NHS) enhanced TNF-alpha induction by whole cryptococci and the different cryptococcal components, with MP2 being the most potent TNF-alpha inducer. |
| 6039 | 8975923 | Normal human serum (NHS) enhanced TNF-alpha induction by whole cryptococci and the different cryptococcal components, with MP2 being the most potent TNF-alpha inducer. |
| 6040 | 8975923 | In contrast, when MP1, MP2, and GalXM were incubated with HI NHS, 48, 71, and 44%, respectively, of the original TNF-alpha levels remained. |
| 6041 | 8975923 | In contrast, when MP1, MP2, and GalXM were incubated with HI NHS, 48, 71, and 44%, respectively, of the original TNF-alpha levels remained. |
| 6042 | 8975923 | In contrast, when MP1, MP2, and GalXM were incubated with HI NHS, 48, 71, and 44%, respectively, of the original TNF-alpha levels remained. |
| 6043 | 8975923 | In contrast, when MP1, MP2, and GalXM were incubated with HI NHS, 48, 71, and 44%, respectively, of the original TNF-alpha levels remained. |
| 6044 | 8975923 | In contrast, when MP1, MP2, and GalXM were incubated with HI NHS, 48, 71, and 44%, respectively, of the original TNF-alpha levels remained. |
| 6045 | 8975923 | Two anti-CD14 monoclonal antibodies (60BCA and 3C10) inhibited the production of TNF-alpha induced by MP2. |
| 6046 | 8975923 | Two anti-CD14 monoclonal antibodies (60BCA and 3C10) inhibited the production of TNF-alpha induced by MP2. |
| 6047 | 8975923 | Two anti-CD14 monoclonal antibodies (60BCA and 3C10) inhibited the production of TNF-alpha induced by MP2. |
| 6048 | 8975923 | Two anti-CD14 monoclonal antibodies (60BCA and 3C10) inhibited the production of TNF-alpha induced by MP2. |
| 6049 | 8975923 | Two anti-CD14 monoclonal antibodies (60BCA and 3C10) inhibited the production of TNF-alpha induced by MP2. |
| 6050 | 8975923 | The results indicate that (i) induction of TNF-alpha by C. neoformans and GXMs strongly depends on complement, (ii) MP1 and MP2 induction of TNF-alpha is facilitated by a heat-stable serum factor other than Ig, and (iii) CD14 may be involved in the induction of TNF-alpha by MP2. |
| 6051 | 8975923 | The results indicate that (i) induction of TNF-alpha by C. neoformans and GXMs strongly depends on complement, (ii) MP1 and MP2 induction of TNF-alpha is facilitated by a heat-stable serum factor other than Ig, and (iii) CD14 may be involved in the induction of TNF-alpha by MP2. |
| 6052 | 8975923 | The results indicate that (i) induction of TNF-alpha by C. neoformans and GXMs strongly depends on complement, (ii) MP1 and MP2 induction of TNF-alpha is facilitated by a heat-stable serum factor other than Ig, and (iii) CD14 may be involved in the induction of TNF-alpha by MP2. |
| 6053 | 8975923 | The results indicate that (i) induction of TNF-alpha by C. neoformans and GXMs strongly depends on complement, (ii) MP1 and MP2 induction of TNF-alpha is facilitated by a heat-stable serum factor other than Ig, and (iii) CD14 may be involved in the induction of TNF-alpha by MP2. |
| 6054 | 8975923 | The results indicate that (i) induction of TNF-alpha by C. neoformans and GXMs strongly depends on complement, (ii) MP1 and MP2 induction of TNF-alpha is facilitated by a heat-stable serum factor other than Ig, and (iii) CD14 may be involved in the induction of TNF-alpha by MP2. |
| 6055 | 8943063 | This study demonstrates that the beta-chemokines macrophage inflammatory proteins 1 alpha and 1 beta (MIP-1 alpha and MIP-1 beta) and, RANTES (regulated on activation, normally T-cell expressed and secreted) inhibit human immunodeficiency virus (HIV) replication in anti-CD3 or recall antigen-stimulated peripheral blood mononuclear cells (PBMCs) of asymptomatic HIV-infected subjects. |
| 6056 | 8943063 | Significant levels of beta-chemokines were produced by both CD4+ and CD8+ PBMC subsets from HIV-infected individuals. |
| 6057 | 8943063 | Neutralization of endogenous MIP-1 alpha, MIP-1 beta, and RANTES did not rescue HIV replication in cultures to which greater than 10% CD8+ T cells had been added, indicating that the HIV suppressor activity of CD8+ T cells cannot be explained entirely by the beta-chemokines. |
| 6058 | 8943063 | However, significant enhancement of viral replication was observed upon neutralization of endogenous beta-chemokines in CD8-depleted or CD4+ PBMCs from most donors, particularly in cultures with low inducible levels of HIV production. |
| 6059 | 8943063 | These data suggest that the levels of HIV replication in CD4+ PBMC reflect the balance of the opposing effects of endogenous suppressive factors, such as the beta-chemokines, and HIV-inducing cytokines, such as tumor necrosis factor alpha and interleukin 1 beta. |
| 6060 | 9103075 | Virus vaccines prepared on the basis of cells of mammals (rabies, poliomyelitis, measles and hepatitis A vaccines) contain cytokines (IL-1 beta, IL-6, TNF-alpha), whose concentration depends on the kind of the vaccine. |
| 6061 | 9103075 | Virus vaccines prepared on the basis of cells of mammals (rabies, poliomyelitis, measles and hepatitis A vaccines) contain cytokines (IL-1 beta, IL-6, TNF-alpha), whose concentration depends on the kind of the vaccine. |
| 6062 | 9103075 | In Russian and foreign preparations of interferon the presence of IL-1 beta and TNF-alpha has been detected; the content of these cytokines is determined by the specific features of the methods used manufacturing these preparations. |
| 6063 | 9103075 | In Russian and foreign preparations of interferon the presence of IL-1 beta and TNF-alpha has been detected; the content of these cytokines is determined by the specific features of the methods used manufacturing these preparations. |
| 6064 | 9014289 | Increases in expression of both IL-4 and IFN-gamma occur following immunization with either Salmonella construct. |
| 6065 | 9014289 | In addition, other cytokines (IL-6, IL-7, IL-12) increase at similar levels in either BRD509 or KR1 dosed animals. |
| 6066 | 9014289 | Proinflammatory cytokines IL-1 and TNF-alpha are also present but unchanged at early time points (6, 24, and 72 hours), increasing only after 7 days postimmunization. |
| 6067 | 9001822 | An evolving approach is the use of immunotherapy, such as interleukin-2, -6, and -12; interferon-gamma; and alpha-tumor necrosis factor. |
| 6068 | 8892615 | We show here that highly purified CD14(bright) peripheral blood monocytes supplemented with granulocyte-monocyte (GM)-CSF plus IL-4 develop with high efficacy (>95% of input cells) into DC. |
| 6069 | 8892615 | They neo-expressed CD1a, CD1b, CD1c, CD80, and CD5; they massively up-regulated CD40 (109-fold) and HLA-DQ and DP (125- and 87-fold); and significantly (>5-fold) up-regulated HLA-DR, CD4, CD11b, CD11c, CD43, CD45, CD45R0, CD54, CD58, and CD59. |
| 6070 | 8892615 | CD14, CD15s, CD64, and CDw65 molecules were down-regulated to background levels, and no major changes were observed for HLA class I, CD11a, CD32, CD33, CD48, CD50, CD86, CDw92, CD93, or CD97. |
| 6071 | 8892615 | Monocytes cultured in parallel with GM-CSF plus TNF-alpha were more heterogeneous in expression densities but otherwise similar in their surface molecule repertoire. |
| 6072 | 8892615 | Only GM-CSF plus IL-4-cultured cells were found to be potent stimulators in allogeneic and autologous MLR and they presented tetanus toxoid 100- to 1000-fold more efficiently than other cell populations tested. |
| 6073 | 8898937 | The outer surface lipoprotein OspA of Borrelia burgdorferi provides co-stimulatory signals to normal human peripheral CD4+ and CD8+ T lymphocytes. |
| 6074 | 8898937 | The outer surface lipoprotein OspA of Borrelia burgdorferi provides co-stimulatory signals to normal human peripheral CD4+ and CD8+ T lymphocytes. |
| 6075 | 8898937 | Furthermore, incubation of CD2+ T cells or selected CD4+ as well as CD8+ subpopulations with rlip-OspA, but not with rNS1-OspA led to the production of interferon (IFN)-gamma, interleukin (IL)-6 and tumor necrosis factor (TNF)-alpha, but not IL-4. |
| 6076 | 8898937 | Furthermore, incubation of CD2+ T cells or selected CD4+ as well as CD8+ subpopulations with rlip-OspA, but not with rNS1-OspA led to the production of interferon (IFN)-gamma, interleukin (IL)-6 and tumor necrosis factor (TNF)-alpha, but not IL-4. |
| 6077 | 8898937 | In contrast, co-stimulation of the respective T cell populations with anti-CD28 antibodies resulted in the generation of IFN-gamma, IL-4 and TNF-alpha, but not IL-6. |
| 6078 | 8898937 | In contrast, co-stimulation of the respective T cell populations with anti-CD28 antibodies resulted in the generation of IFN-gamma, IL-4 and TNF-alpha, but not IL-6. |
| 6079 | 8898937 | In light of the fact that inflamed tissues of B. burgdorferi-infected hosts contain blood leukocytes together with spirochetes, their degradation products, or both, these results suggest that infiltrating CD4+ and CD8+ T cells of any specificities, including spirochetes, autoantigens, or both, participate in the pathogenesis of Lyme disease. |
| 6080 | 8898937 | In light of the fact that inflamed tissues of B. burgdorferi-infected hosts contain blood leukocytes together with spirochetes, their degradation products, or both, these results suggest that infiltrating CD4+ and CD8+ T cells of any specificities, including spirochetes, autoantigens, or both, participate in the pathogenesis of Lyme disease. |
| 6081 | 8894681 | Indeed, enhanced expression of HLA class I and/or ICAM-1 molecules on the surface of the TNF gene-transduced tumor cells were observed by fluorescence-activated cell sorting (FACS) analysis. |
| 6082 | 10830026 | Experimental studies have demonstrated that most of the pathology in meningitis is mediated by inflammatory cytokines such as tumor necrosis factor (TNF) and interleukin-1 (IL-1), which are produced by host cells in response to bacterial invasion of the meninges. |
| 6083 | 8757623 | T cells from protected and nonprotected strains differed in their production of IFN-gamma and TNF-alpha following immunization with MSP1(19), but it was unclear how the differential patterns of cytokine expression related to the level of protection. |
| 6084 | 8683732 | Localization of IL-1, IL-2, IL-4, IL-8 and TNF in superficial bladder tumors treated with intravesical bacillus Calmette-Guerin. |
| 6085 | 8999669 | Immunization of BALB/c, C57BL/6, CBA/calac mice with strain XJ44 of Argentine hemorrhagic fever resulted in changes of nonspecific immunity parameters, such as interferon, interleukin-1, tumor necrosis factor, and natural killers. |
| 6086 | 8706049 | Bacillus Calmette-Guérin plus interleukin-2 and/or granulocyte/macrophage-colony-stimulating factor enhances immunocompetent cell production of interferon-gamma, which inhibits B16F10 melanoma cell growth in vitro. |
| 6087 | 8706049 | Tumor necrosis factor alpha was substantially weaker (IC50 > 10 ng/ml) but provided synergy with IFN gamma. |
| 6088 | 8706049 | None of the other cytokines such as interleukin-2 (IL-2), IL-4, IL-6, IL-10, IL-12, or granulocyte/macrophage-colony-stimulating factor had direct antitumor activity against B16F10 melanoma cells. |
| 6089 | 8706049 | However, when IL-2 and/or GM-CSF were combined with BCG either by exogenous addition or through endogenous production by novel cytokine-secreting recombinant BCG (rBCG), a substantial increase in INF gamma production by splenocytes was observed. |
| 6090 | 8706049 | These results suggest that BCG may exert part of its antitumor action on melanoma through the induction of IFN gamma, which can be greatly enhanced through the concomitant addition of IL-2 and/or GM-CSF. |
| 6091 | 8704976 | The present study was conducted to determine the extent to which the cytokines tumour necrosis factor-alpha (TNF-alpha) and interferon-gamma (IFN-gamma) are required to protect against primary or secondary murine tularaemia caused by the live vaccine strain of the facultative intracellular bacterium Francisella tularensis. |
| 6092 | 8704976 | The present study was conducted to determine the extent to which the cytokines tumour necrosis factor-alpha (TNF-alpha) and interferon-gamma (IFN-gamma) are required to protect against primary or secondary murine tularaemia caused by the live vaccine strain of the facultative intracellular bacterium Francisella tularensis. |
| 6093 | 8704976 | The present study was conducted to determine the extent to which the cytokines tumour necrosis factor-alpha (TNF-alpha) and interferon-gamma (IFN-gamma) are required to protect against primary or secondary murine tularaemia caused by the live vaccine strain of the facultative intracellular bacterium Francisella tularensis. |
| 6094 | 8704976 | The present study was conducted to determine the extent to which the cytokines tumour necrosis factor-alpha (TNF-alpha) and interferon-gamma (IFN-gamma) are required to protect against primary or secondary murine tularaemia caused by the live vaccine strain of the facultative intracellular bacterium Francisella tularensis. |
| 6095 | 8704976 | It is shown that non-immune mice treated with neutralizing monoclonal antibodies (mAbs) against TNF-alpha and IFN-gamma are rendered defenceless against otherwise sublethal intravenous inocula of the bacterium. |
| 6096 | 8704976 | It is shown that non-immune mice treated with neutralizing monoclonal antibodies (mAbs) against TNF-alpha and IFN-gamma are rendered defenceless against otherwise sublethal intravenous inocula of the bacterium. |
| 6097 | 8704976 | It is shown that non-immune mice treated with neutralizing monoclonal antibodies (mAbs) against TNF-alpha and IFN-gamma are rendered defenceless against otherwise sublethal intravenous inocula of the bacterium. |
| 6098 | 8704976 | It is shown that non-immune mice treated with neutralizing monoclonal antibodies (mAbs) against TNF-alpha and IFN-gamma are rendered defenceless against otherwise sublethal intravenous inocula of the bacterium. |
| 6099 | 8704976 | However, the need for TNF-alpha and IFN-gamma for controlling secondary tularaemia became critical when challenge inocula exceeded 10(6) c.f.u. |
| 6100 | 8704976 | However, the need for TNF-alpha and IFN-gamma for controlling secondary tularaemia became critical when challenge inocula exceeded 10(6) c.f.u. |
| 6101 | 8704976 | However, the need for TNF-alpha and IFN-gamma for controlling secondary tularaemia became critical when challenge inocula exceeded 10(6) c.f.u. |
| 6102 | 8704976 | However, the need for TNF-alpha and IFN-gamma for controlling secondary tularaemia became critical when challenge inocula exceeded 10(6) c.f.u. |
| 6103 | 8704976 | Additionally, they show that the need for TNF-alpha and IFN-gamma to combat secondary infection depends on the size of the challenge inoculum. |
| 6104 | 8704976 | Additionally, they show that the need for TNF-alpha and IFN-gamma to combat secondary infection depends on the size of the challenge inoculum. |
| 6105 | 8704976 | Additionally, they show that the need for TNF-alpha and IFN-gamma to combat secondary infection depends on the size of the challenge inoculum. |
| 6106 | 8704976 | Additionally, they show that the need for TNF-alpha and IFN-gamma to combat secondary infection depends on the size of the challenge inoculum. |
| 6107 | 8647214 | IL-12 also synergizes with B7.1 (CD80) co-stimulation to induce proliferation and cytokine production by both human and murine T cells in vitro. |
| 6108 | 8647214 | The synergistic anti-tumor effects associated with combined application of B7.1- and IL-12-transfected tumors were partially negated by systemic administration of the CD28-B7.1/B7.2 antagonist CTLA4-Ig or by inoculation with neutralizing antibodies directed against murine interferon-gamma or tumor necrosis factor-alpha, two cytokines elicited in response to IL-12 stimulation. |
| 6109 | 9156803 | Enhanced efficacy of combination of IL-2 gene and IL-6 gene-transfected tumor cells in the treatment of established metastatic tumors. |
| 6110 | 9156803 | IL-2 and IL-6 are important cytokines which have potent antitumor effects and can cooperate to induce immune responses more effectively. |
| 6111 | 9156803 | IL-2 gene or IL-6 gene-transfected tumor cells exhibited reduced tumorigenicity and decreased metastatic potential. |
| 6112 | 9156803 | In order to increase the therapeutic efficacy of IL-2 gene-, IL-6 gene-modified tumor vaccines, the experimental pulmonary metastatic melanoma-bearing mice were treated with inactivated IL-2 gene-transfected tumor cells and inactivated IL-6 gene-transfected tumor cells. |
| 6113 | 9156803 | The CTL activity, NK activity and IL-2-induced LAK activity, IL-2 and TNF secretion from the splenocytes of the above tumor-bearing mice increased more significantly than that of tumor-bearing mice vaccinated with IL-2 gene-transfected vaccine or IL-6 gene transfected vaccine alone. |
| 6114 | 9156803 | These results demonstrated that the combined use of IL-2 gene-transfected tumor vaccine and IL-6 gene-transfected tumor vaccine could achieve more potent antitumor effect via more effective activation of specific and non-specific antitumor immune responses. |
| 6115 | 9816208 | Lack of T-cell-mediated recognition of the fusion region of the pml/RAR-alpha hybrid protein by lymphocytes of acute promyelocytic leukemia patients. |
| 6116 | 9816208 | In previous studies, it was shown that the fusion region of the pml/RAR-alpha protein, expressed by acute promyelocytic leukemia (APL) cells, can be specifically recognized in vitro by donor (D. |
| 6117 | 9816208 | G.) with BCR1/25, a 25-mer pml/RAR-alpha, did not elicit either a polyclonal or a clonal immune response specific to the peptide. |
| 6118 | 9816208 | We then generated new donor anti-pml/RAR-alpha CD4(+) T-cell clones. |
| 6119 | 9816208 | One clone (C3/5, CD3(+), CD4(+), CD8(-)) was selected for further analysis. |
| 6120 | 9816208 | Clone C3/5 showed specific proliferation, cytotoxicity, and cytokine (tumor necrosis factor alpha, granulocyte-macrophage colony-stimulating factor) production when challenged with autologous lymphoblastic cell lines pulsed with peptide BCR1/25. |
| 6121 | 9816208 | G. whether the use of 9-mer peptides (BCR1/9) would generate a CD8/HLA class I-restricted response. |
| 6122 | 8861036 | Expression of mRNA for TNF-alpha, IL-12, IFN-gamma, and IL-10 was demonstrated within 48 h of inoculation, the kinetics being similar irrespective of bacterial strain used. |
| 6123 | 8861035 | Production and specificity of antibodies, cytotoxic responses of macrophages and NK-cells, spontaneous production ex vivo of cytokines IL-1 alpha, IL-2, IL-4, IL-6, IL-10, IFN-gamma, and TNF-alpha in spleen cell cultures in C3H/HeJ (Lps(d)) mice in comparison with C3H/HeN (Lps(n)) mice were tested. |
| 6124 | 8861033 | Protective immunity is associated with a CD4 and CD8 T-cell response towards a mosaic of proteins of F. tularensis and due to HLA restriction, each individual selects her own mosaic. |
| 6125 | 8861033 | In mice, intradermal injection of live F. tularensis but not of killed bacteria results in an early cytokine expression in the infected liver, including interleukin-12, tumor necrosis factor-alpha, and interferon-gamma. |
| 6126 | 8598323 | Tumor cells from 7 freshly isolated human ovarian tumors and 2 continuous human ovarian cancer cell lines were analyzed for their surface expression of MHC class-1, class 11 and ICAM-1 surface antigens before and after exposure to gamma-irradiation and/or the cytokines TNF-alpha plus IFN-gamma. |
| 6127 | 8598323 | Tumor cells from 7 freshly isolated human ovarian tumors and 2 continuous human ovarian cancer cell lines were analyzed for their surface expression of MHC class-1, class 11 and ICAM-1 surface antigens before and after exposure to gamma-irradiation and/or the cytokines TNF-alpha plus IFN-gamma. |
| 6128 | 8598323 | Tumor cells from 7 freshly isolated human ovarian tumors and 2 continuous human ovarian cancer cell lines were analyzed for their surface expression of MHC class-1, class 11 and ICAM-1 surface antigens before and after exposure to gamma-irradiation and/or the cytokines TNF-alpha plus IFN-gamma. |
| 6129 | 8598323 | All 7 fresh tumors expressed high levels of MHC class 1 and 1CAM-1 antigens, and levels were markedly up-regulated after exposure to TNF-alpha plus IFN-gamma Similarly, class-11 antigens were either induced (3 out of 7 tumors) or significantly up-regulated by TNF-alpha plus IFN-gamma. |
| 6130 | 8598323 | All 7 fresh tumors expressed high levels of MHC class 1 and 1CAM-1 antigens, and levels were markedly up-regulated after exposure to TNF-alpha plus IFN-gamma Similarly, class-11 antigens were either induced (3 out of 7 tumors) or significantly up-regulated by TNF-alpha plus IFN-gamma. |
| 6131 | 8598323 | All 7 fresh tumors expressed high levels of MHC class 1 and 1CAM-1 antigens, and levels were markedly up-regulated after exposure to TNF-alpha plus IFN-gamma Similarly, class-11 antigens were either induced (3 out of 7 tumors) or significantly up-regulated by TNF-alpha plus IFN-gamma. |
| 6132 | 8598323 | Exposure to high doses of gamma-irradiation also increased the expression of MHC class-1 and ICAM-1 antigens, albeit to a modest degree. |
| 6133 | 8598323 | Exposure to high doses of gamma-irradiation also increased the expression of MHC class-1 and ICAM-1 antigens, albeit to a modest degree. |
| 6134 | 8598323 | Exposure to high doses of gamma-irradiation also increased the expression of MHC class-1 and ICAM-1 antigens, albeit to a modest degree. |
| 6135 | 8598323 | MHC class 1 and ICAM-1 antigens expression was much lower on continuous human ovarian cell lines than on the fresh tumors. |
| 6136 | 8598323 | MHC class 1 and ICAM-1 antigens expression was much lower on continuous human ovarian cell lines than on the fresh tumors. |
| 6137 | 8598323 | MHC class 1 and ICAM-1 antigens expression was much lower on continuous human ovarian cell lines than on the fresh tumors. |
| 6138 | 8598323 | Exposure of these cells to TNF-alpha plus IFN-gamma markedly up-regulated antigen expression to levels comparable to those expressed on the freshly isolated tumors. |
| 6139 | 8598323 | Exposure of these cells to TNF-alpha plus IFN-gamma markedly up-regulated antigen expression to levels comparable to those expressed on the freshly isolated tumors. |
| 6140 | 8598323 | Exposure of these cells to TNF-alpha plus IFN-gamma markedly up-regulated antigen expression to levels comparable to those expressed on the freshly isolated tumors. |
| 6141 | 8934653 | Induction of TNF-alpha, IL-1 beta and IL-6 cytokine mRNA transcription in macrophages was determined by reverse transcriptase-polymerase chain reaction. |
| 6142 | 8832908 | LPS 25 mu g/mouse was injected via the tail vein, and Interferon (IFN)/Tumor necrosis factor-alpha (TNF-alpha) in serum were determined. |
| 6143 | 8832908 | LPS 25 mu g/mouse was injected via the tail vein, and Interferon (IFN)/Tumor necrosis factor-alpha (TNF-alpha) in serum were determined. |
| 6144 | 8832908 | LPS 25 mu g/mouse was injected via the tail vein, and Interferon (IFN)/Tumor necrosis factor-alpha (TNF-alpha) in serum were determined. |
| 6145 | 8832908 | The productions of IFN and TNF-alpha were suppressed significantly. |
| 6146 | 8832908 | The productions of IFN and TNF-alpha were suppressed significantly. |
| 6147 | 8832908 | The productions of IFN and TNF-alpha were suppressed significantly. |
| 6148 | 8832908 | IFN and TNF-alpha in the supernatant were determined. |
| 6149 | 8832908 | IFN and TNF-alpha in the supernatant were determined. |
| 6150 | 8832908 | IFN and TNF-alpha in the supernatant were determined. |
| 6151 | 8619443 | The upregulation of CD36 and intercellular adhesion molecule-1 by soluble recombinant (sr)-tumor necrosis factor-alpha or sr-interferon-gamma did not modify the IRBC interactions with SBECs at the ultrastructural level. |
| 6152 | 8717394 | In the present work the kinetics of some indices of immunity (tumor necrosis factor (TNF), interferon (IFN), natural killer cells (NK), lymphocyte proliferation activity, virus-specific antibodies, CD4/CD8 ratio) in response to Marburg virus infection in Macaca mulatta were studied. |
| 6153 | 8717394 | In the present work the kinetics of some indices of immunity (tumor necrosis factor (TNF), interferon (IFN), natural killer cells (NK), lymphocyte proliferation activity, virus-specific antibodies, CD4/CD8 ratio) in response to Marburg virus infection in Macaca mulatta were studied. |
| 6154 | 8717394 | In the present work the kinetics of some indices of immunity (tumor necrosis factor (TNF), interferon (IFN), natural killer cells (NK), lymphocyte proliferation activity, virus-specific antibodies, CD4/CD8 ratio) in response to Marburg virus infection in Macaca mulatta were studied. |
| 6155 | 8717394 | A comparison of the indices of IFN, TNF and spontaneous lymphocyte proliferation activity in Macaca mulatta infected with Marburg virus at different stages of life shows the relationship between the increase of these indices and the decrease in the animals' lifespan. |
| 6156 | 8717394 | A comparison of the indices of IFN, TNF and spontaneous lymphocyte proliferation activity in Macaca mulatta infected with Marburg virus at different stages of life shows the relationship between the increase of these indices and the decrease in the animals' lifespan. |
| 6157 | 8717394 | A comparison of the indices of IFN, TNF and spontaneous lymphocyte proliferation activity in Macaca mulatta infected with Marburg virus at different stages of life shows the relationship between the increase of these indices and the decrease in the animals' lifespan. |
| 6158 | 8717394 | Marburg virus immunosuppressive properties were corroborated by studying lymphocyte proliferation activity in response to antigenic stimulation in vitro and the CD4/CD8 index during experimental Marburg virus infection in Macaca mulatta. |
| 6159 | 8717394 | Marburg virus immunosuppressive properties were corroborated by studying lymphocyte proliferation activity in response to antigenic stimulation in vitro and the CD4/CD8 index during experimental Marburg virus infection in Macaca mulatta. |
| 6160 | 8717394 | Marburg virus immunosuppressive properties were corroborated by studying lymphocyte proliferation activity in response to antigenic stimulation in vitro and the CD4/CD8 index during experimental Marburg virus infection in Macaca mulatta. |
| 6161 | 8717394 | We conclude that the disease outcome depends on the dynamics of certain immunologic indices such as TNF and IFN. |
| 6162 | 8717394 | We conclude that the disease outcome depends on the dynamics of certain immunologic indices such as TNF and IFN. |
| 6163 | 8717394 | We conclude that the disease outcome depends on the dynamics of certain immunologic indices such as TNF and IFN. |
| 6164 | 8543823 | Development and characterization of recombinant adenoviruses encoding MART1 or gp100 for cancer therapy. |
| 6165 | 8543823 | The human melanoma tumor Ags, MART1 and gp100, are specifically recognized by HLA-A2-restricted CD8+ CTLs derived from melanoma patients and appear to be involved in tumor regression. |
| 6166 | 8543823 | Infection of non-Ag expressing HLA-A2+ cell lines A375 and MDA-231 with the vectors resulted in recognition by Ag-specific CTLs as demonstrated by specific target cell lysis and release of cytokines, including IFN-gamma, TNF-alpha, and granulocyte-macrophage-CSF. |
| 6167 | 8543823 | Because of the suspected homology between the human MART1 and gp100 genes and their murine counterparts, we immunized C57BL/6 mice with these recombinant adenoviruses and demonstrated that immunization with Ad2CMV-gp100 could protect mice from murine melanoma B16 challenge administered intradermally. |
| 6168 | 8543823 | Depletion of CD8+ but not CD4+ T cells in vivo from Ad2CMV-gp100-vaccinated mice eliminated the protective effect. |
| 6169 | 9224970 | Th1 favor rejection (tumoral, fetal or of transplants) through the elaboration of IL-2, IFN and TNF while Th2 led to tolerance or acceptation through the production of IL-4, IL-5 and IL-10: both functions neutralize each other establishing a "normal" equilibrium Th1 vs Th2. |
| 6170 | 9065029 | Two experimental models of immune complexes were used to study the secretion of interleukin (IL)-10, IL-6, IL-1 beta and TNF-alpha by human monocytes in vitro. |
| 6171 | 9065029 | Two experimental models of immune complexes were used to study the secretion of interleukin (IL)-10, IL-6, IL-1 beta and TNF-alpha by human monocytes in vitro. |
| 6172 | 9065029 | Immune complexes formed of tetanus toxoid and polyclonal anti-tetanus toxoid antiserum as well as heat-aggregated human serum immunoglobulins induced the release of IL-6 and IL-10 in a dose- and antigen: antibody ratio-dependent manner. |
| 6173 | 9065029 | Immune complexes formed of tetanus toxoid and polyclonal anti-tetanus toxoid antiserum as well as heat-aggregated human serum immunoglobulins induced the release of IL-6 and IL-10 in a dose- and antigen: antibody ratio-dependent manner. |
| 6174 | 9065029 | Additionally, we demonstrated that endogenously synthesized IL-10 limited the immune complex-induced secretion of proinflammatory cytokines tumor necrosis factor-alpha, IL-6 and IL-1 beta. |
| 6175 | 9065029 | Additionally, we demonstrated that endogenously synthesized IL-10 limited the immune complex-induced secretion of proinflammatory cytokines tumor necrosis factor-alpha, IL-6 and IL-1 beta. |
| 6176 | 8963198 | The purpose of the study was to identify sites of gp 120, which are responsible for CD4 binding and induce tumor necrosis factor-alpha (TNF-alpha) synthesis. |
| 6177 | 8963198 | The purpose of the study was to identify sites of gp 120, which are responsible for CD4 binding and induce tumor necrosis factor-alpha (TNF-alpha) synthesis. |
| 6178 | 8963198 | The purpose of the study was to identify sites of gp 120, which are responsible for CD4 binding and induce tumor necrosis factor-alpha (TNF-alpha) synthesis. |
| 6179 | 8963198 | The peptides 420-440, 426-452, 369-384, 255-272 bind to T-lymphocytic CD4 and induced TNF-alpha. |
| 6180 | 8963198 | The peptides 420-440, 426-452, 369-384, 255-272 bind to T-lymphocytic CD4 and induced TNF-alpha. |
| 6181 | 8963198 | The peptides 420-440, 426-452, 369-384, 255-272 bind to T-lymphocytic CD4 and induced TNF-alpha. |
| 6182 | 8963198 | The peptide 436-451 binds to CD4, but failed to induced TNF-alpha, which suggests that the latter may be used as a basis for HIV-infection vaccine. |
| 6183 | 8963198 | The peptide 436-451 binds to CD4, but failed to induced TNF-alpha, which suggests that the latter may be used as a basis for HIV-infection vaccine. |
| 6184 | 8963198 | The peptide 436-451 binds to CD4, but failed to induced TNF-alpha, which suggests that the latter may be used as a basis for HIV-infection vaccine. |
| 6185 | 8910923 | When B-16 melanoma cells, used here as a model, were first treated for 72 h with interferon-gamma or tumor necrosis factor-alpha at concentrations of 10 and 100 units/ml, respectively, followed by application of pressure and cross-linking (PCL), the surface presentation of H2b molecules increased by 40% compared to treatment with cytokines alone, and by up to 1,700% when compared to treatment with PCL alone. |
| 6186 | 8804738 | It is important in the construction of adenovirus vectors not to delete a major portion of the early region 3 (E3) because: the E3 19 kD glycoprotein markedly reduces the capacity of the Class I major histocompatibility complex (Class I MHC) from transporting viral antigens to the surfaces of infected cells; and the E3 14.7 kD protein significantly inhibits the production of TNF-alpha and, therefore, reduces the polymorphonuclear response. |
| 6187 | 8742064 | To investigate the spectrum of cytokines expressed by peripheral blood mononuclear cells (PBMC) from cynomolgus macaques (Macaca fascicularis), we used a semi-quantitative RT-PCR to determine levels of mRNA coding for IL-1 beta, IL-2, IL-4, IL-6, IL-10, IFN-gamma, and TNF-alpha. |
| 6188 | 8742064 | To investigate the spectrum of cytokines expressed by peripheral blood mononuclear cells (PBMC) from cynomolgus macaques (Macaca fascicularis), we used a semi-quantitative RT-PCR to determine levels of mRNA coding for IL-1 beta, IL-2, IL-4, IL-6, IL-10, IFN-gamma, and TNF-alpha. |
| 6189 | 8742064 | While transcripts or IL-2, IL-4 and IFN-gamma were either low or not detected in unmanipulated PBMCs, varying levels of IL-1 beta, IL-5, IL-10, and TNF-alpha were readily detected in the same samples. |
| 6190 | 8742064 | While transcripts or IL-2, IL-4 and IFN-gamma were either low or not detected in unmanipulated PBMCs, varying levels of IL-1 beta, IL-5, IL-10, and TNF-alpha were readily detected in the same samples. |
| 6191 | 8551248 | Furthermore, depletion of either CD4+ or CD8+ T cells from tumor-bearing mice before therapy totally suppressed the therapeutic efficacy of DC pulsed with tumor-derived peptides. |
| 6192 | 8551248 | The analysis of the cytokine pattern in the draining lymph nodes and spleens of tumor-bearing mice immunized with DC pulsed with tumor-eluted peptides revealed a marked upregulation of interleukin (IL) 4 and interferon (IFN) gamma production, as compared with mice immunized with DC alone or DC pulsed with irrelevant peptides. |
| 6193 | 8551248 | DC-induced antitumor effects were completely blocked by coadministration of neutralizing monoclonal antibody directed against T helper cell 1-associated cytokines (such as IL-12, tumor necrosis factor alpha, IFN-gamma), and eventually, but not initially, blocked by anti-mIL-4 mAb. |
| 6194 | 8546443 | Tick countermeasures to host defenses reduce T-lymphocyte proliferation, elaboration of the TH1 cytokines interleukin-2 and interferon-gamma, production of macrophage cytokines interleukin-1 and tumor necrosis factor, and antibody responses. |
| 6195 | 8618848 | In 6 of 10 subjects (1 control subject, 3 HIV-seropositive patients with CD4+ cell number > 400 cells per microliters, and 2 HIV-positive patients with CD4+ cell number < 400 cells per microliters), these fluctuations in TNF-alpha were coupled to the known rhythm of electroencephalogram delta amplitude (square root of power) during sleep. |
| 6196 | 8618848 | In 6 of 10 subjects (1 control subject, 3 HIV-seropositive patients with CD4+ cell number > 400 cells per microliters, and 2 HIV-positive patients with CD4+ cell number < 400 cells per microliters), these fluctuations in TNF-alpha were coupled to the known rhythm of electroencephalogram delta amplitude (square root of power) during sleep. |
| 6197 | 8618848 | In 5 HIV subjects with abnormally low CD4+ cell counts ( < 400 cells per microliters), the number of days since seroconversion correlated significantly with low correlation between TNF-alpha and delta amplitude. |
| 6198 | 8618848 | In 5 HIV subjects with abnormally low CD4+ cell counts ( < 400 cells per microliters), the number of days since seroconversion correlated significantly with low correlation between TNF-alpha and delta amplitude. |
| 6199 | 7499860 | Neutralization of IFN-gamma and TNF-alpha caused a complete inhibition of nitrite production. |
| 6200 | 7499860 | Neutralization of IFN-gamma and TNF-alpha caused a complete inhibition of nitrite production. |
| 6201 | 7499860 | The present study showed that the ability of viable BCG to induce NO production is superior to that of killed BCG, and both IFN-gamma and TNF-alpha are essential for BCG-induced NO production by spleen cells. |
| 6202 | 7499860 | The present study showed that the ability of viable BCG to induce NO production is superior to that of killed BCG, and both IFN-gamma and TNF-alpha are essential for BCG-induced NO production by spleen cells. |
| 6203 | 8525336 | Though the relationships among the components of the immune response are complex, it seems likely that in response to mycobacterial infection associated with active disease, cytokines such as TNF-alpha and IL-1 beta are produced; these cytokines serve to recruit more lymphocytes, generally of the T(H) (T helper) phenotype, which then produces substances such as the macrophage activating factor interferon-gamma. |
| 6204 | 8525336 | The role of other cytokines, such as IL-6 and IL-8, both of which are induced by M. tuberculosis or its cell was components, is less clear. |
| 6205 | 8635884 | Experiments involving adoptive transfer of T-cell sub-populations and in vivo depletion of specific T-cells have shown that CD4+ T-cells and to a lesser extent CD8+ T-cells are important in immune responses which limit primary infection. |
| 6206 | 8635884 | Experiments involving adoptive transfer of T-cell sub-populations and in vivo depletion of specific T-cells have shown that CD4+ T-cells and to a lesser extent CD8+ T-cells are important in immune responses which limit primary infection. |
| 6207 | 8635884 | In contrast, CD8+ T-cells are more important in subsequent infections with CD4+ T-cells having a lesser role. |
| 6208 | 8635884 | In contrast, CD8+ T-cells are more important in subsequent infections with CD4+ T-cells having a lesser role. |
| 6209 | 8635884 | Most attention has concentrated on interferon-gamma (IFN-gamma) and tumour necrosis factor-alpha (TNF-alpha) because these cytokines have been shown to limit other protozoan infections. |
| 6210 | 8635884 | Most attention has concentrated on interferon-gamma (IFN-gamma) and tumour necrosis factor-alpha (TNF-alpha) because these cytokines have been shown to limit other protozoan infections. |
| 6211 | 8635884 | Mechanisms by which IFN-gamma and TNF-alpha modulate parasite reproduction have not been identified. |
| 6212 | 8635884 | Mechanisms by which IFN-gamma and TNF-alpha modulate parasite reproduction have not been identified. |
| 6213 | 8573663 | All patients responded with a short pulse of increased synthesis of the cytokines tumor necrosis factor, interleukin-1, and interleukin-6 and elevated body temperature for several hours. |
| 6214 | 8562166 | Our data demonstrate the IFN gamma, TNF alpha and IL-1 alpha can decrease the expression of EGFR on some bladder tumour cell lines. |
| 6215 | 8562166 | Our data demonstrate the IFN gamma, TNF alpha and IL-1 alpha can decrease the expression of EGFR on some bladder tumour cell lines. |
| 6216 | 8562166 | IFN gamma reduced EGFR expression on two of eight cell lines (RT4, SD). |
| 6217 | 8562166 | IFN gamma reduced EGFR expression on two of eight cell lines (RT4, SD). |
| 6218 | 8562166 | However, IL-1 and TNF did not share this activity. |
| 6219 | 8562166 | However, IL-1 and TNF did not share this activity. |
| 6220 | 7593618 | In this report we identify HCV-specific CTL responses restricted by the HLA class I molecules A2, A3, A11, A23, B7, B8, and B53. |
| 6221 | 7593618 | These HCV-specific CTL were shown to produce cytokines including IFN-gamma, TNF-alpha, GM-CSF, IL-8, and IL-10 in an antigen- and HLA class I-specific manner. |
| 6222 | 8697075 | [Antitumor effect of interleukin-2 gene-transfected tumor vaccine in combination with interleukin-6 gene-transfected tumor vaccine]. |
| 6223 | 8697075 | It has been shown that IL-2 and IL-6 can cooperate to induce immune responses more effectively. |
| 6224 | 8697075 | In order to increase the therapeutic efficacy of cytokine gene-transfected tumor vaccines, we treated the experimental pulmonary metastatic melanoma-bearing mice with IL-2 gene-transfected tumor vaccine and IL-6 gene-transfected tumor vaccine. |
| 6225 | 8697075 | The CTL activity, NK activity and IL-2-induced LAK activity, IL-2 and TNF secretion from the splenocytes of the above tumor-bearing mice increased more significantly than that of tumor-bearing mice treated with IL-2 gene-transfected vaccine or IL-6 gene-transfected vaccine alone. |
| 6226 | 8697075 | These results demonstrated that the combined use of IL-2 gene-transfected tumor vaccine and IL-6 gene-transfected tumor vaccine could achieve more potent antitumor effect via more efficient activation of immune functions. |
| 6227 | 7490119 | In addition, Kupffer cells colonized by L-forms constitutively synthesized mRNA for interleukin-6 (IL-6) and tumour necrosis factor-alpha (TNF-alpha). |
| 6228 | 8933818 | Northern blot analysis revealed that 2 h after CA-5d, PECs expressed a high level of IL-2, IFN-gamma, IL-1 beta and a low level of IL-10 and TNF-alpha mRNAs, while IL-4 and IL-5 mRNAs were absent, suggesting the development of TH1 subset. |
| 6229 | 8933818 | Northern blot analysis revealed that 2 h after CA-5d, PECs expressed a high level of IL-2, IFN-gamma, IL-1 beta and a low level of IL-10 and TNF-alpha mRNAs, while IL-4 and IL-5 mRNAs were absent, suggesting the development of TH1 subset. |
| 6230 | 8933818 | At 24 h, while IL-2 mRNA remained high, IL-1 beta and IFN-gamma expression had decreased and IL-10 and TNF-alpha mRNAs were no longer detectable. |
| 6231 | 8933818 | At 24 h, while IL-2 mRNA remained high, IL-1 beta and IFN-gamma expression had decreased and IL-10 and TNF-alpha mRNAs were no longer detectable. |
| 6232 | 8933818 | Instead, in spleens of CA-treated mice, examined up to 5 days after CA-5d, only IL-2 and IL-1 beta mRNAs were detectable, but the expression level was similar to that of untreated control mice. |
| 6233 | 8933818 | Instead, in spleens of CA-treated mice, examined up to 5 days after CA-5d, only IL-2 and IL-1 beta mRNAs were detectable, but the expression level was similar to that of untreated control mice. |
| 6234 | 7553683 | We tested biopsy specimens of eight subcutaneous metastases that had developed inflammation following vaccine treatment for expression of mRNA for interferon gamma (IFN gamma), interleukin-4 (IL-4), tumor necrosis factor alpha (TNF alpha), and IL-10. |
| 6235 | 7553683 | We tested biopsy specimens of eight subcutaneous metastases that had developed inflammation following vaccine treatment for expression of mRNA for interferon gamma (IFN gamma), interleukin-4 (IL-4), tumor necrosis factor alpha (TNF alpha), and IL-10. |
| 6236 | 7553683 | We tested biopsy specimens of eight subcutaneous metastases that had developed inflammation following vaccine treatment for expression of mRNA for interferon gamma (IFN gamma), interleukin-4 (IL-4), tumor necrosis factor alpha (TNF alpha), and IL-10. |
| 6237 | 7553683 | Post-vaccine, inflamed biopsies contained mRNA for IFN gamma (5/8), IL-4 (4/8) or both (3/8), and for TNF alpha (4/7). |
| 6238 | 7553683 | Post-vaccine, inflamed biopsies contained mRNA for IFN gamma (5/8), IL-4 (4/8) or both (3/8), and for TNF alpha (4/7). |
| 6239 | 7553683 | Post-vaccine, inflamed biopsies contained mRNA for IFN gamma (5/8), IL-4 (4/8) or both (3/8), and for TNF alpha (4/7). |
| 6240 | 7553683 | In contrast, IFN gamma mRNA was detected in only 1/17 and TNF alpha mRNA in 2/16 control specimens (pre-treatment lymph node metastases or non-inflamed subcutaneous metastases). mRNA for IL-10, a cytokine with anti-inflammatory properties, was detected in 24/25 melanoma metastases and was independent of lymphoid content; in situ the reverse transcriptase/polymerase chain reaction confirmed that melanoma cells were the major source. |
| 6241 | 7553683 | In contrast, IFN gamma mRNA was detected in only 1/17 and TNF alpha mRNA in 2/16 control specimens (pre-treatment lymph node metastases or non-inflamed subcutaneous metastases). mRNA for IL-10, a cytokine with anti-inflammatory properties, was detected in 24/25 melanoma metastases and was independent of lymphoid content; in situ the reverse transcriptase/polymerase chain reaction confirmed that melanoma cells were the major source. |
| 6242 | 7553683 | In contrast, IFN gamma mRNA was detected in only 1/17 and TNF alpha mRNA in 2/16 control specimens (pre-treatment lymph node metastases or non-inflamed subcutaneous metastases). mRNA for IL-10, a cytokine with anti-inflammatory properties, was detected in 24/25 melanoma metastases and was independent of lymphoid content; in situ the reverse transcriptase/polymerase chain reaction confirmed that melanoma cells were the major source. |
| 6243 | 7664800 | Systemic immunization induces protective CD4+ and CD8+ T cell-mediated immune responses in murine Listeria monocytogenes meningoencephalitis. |
| 6244 | 7664800 | The immune mechanisms underlying immunization-induced protection of mice from lethal central nervous system (CNS) listeriosis were evaluated by immunohistochemistry, flow cytometry of leukocytes isolated from the brain, reverse transcription-polymerase chain reaction analysis of intracerebral (i.c.) tumor-necrosis factor-alpha, interferon-gamma, interleukin (IL)-2, IL-1 beta, IL-10, granulocyte/macrophage colony-stimulating factor, and inducible nitric oxide synthase mRNA expression, and T cell depletion experiments. |
| 6245 | 7664800 | The data demonstrate that active immunization of mice prior to an i.c. infection with Listeria monocytogenes prevents the development of a fatal necrotizing encephalitis and accelerates the recruitment of an increased number of alpha beta T cell receptor (TcR)+ CD4+ and CD8+ T cells, gamma delta TcR+ T cells, B cells, granulocytes and macrophages to the brain compared to non-immunized animals. |
| 6246 | 7664800 | The protective effects of immunization were completely abolished by depletion of CD4+, CD8+, or both T cell subsets. |
| 6247 | 7664800 | The severity of disease was only slightly different between CD4+, CD8+ and CD4+/CD8+ T cell depleted mice, indicating that both subsets of T cells are required for an effective i.c. immune response to L. monocytogenes. |
| 6248 | 7495519 | Such genes include the murine MHC class I gene, Ld (toxoplasmosis), HLA-BW53, HLA DRB1* 1302-DQ B10s01 and TNF2 (malaria), murine Nramp (toxoplasmosis, leishmaniasis and tuberculosis), gene(s) modulating the T-helper type 1 and type 2 dichotomy (leishmaniasis, leprosy and HIV infection) and the natural killer cell complex (cytomegalovirus infection). |
| 6249 | 7493774 | Tuberculin-induced expression of IFN-gamma, IL2, IL4, IL10 and TNF-alpha mRNA occurred in the skin biopsies of all of the lesioned, M. bovis inoculated animals except for an absence of tuberculin-induced TNF-alpha mRNA expression in two animals. |
| 6250 | 7493774 | Tuberculin-induced expression of IFN-gamma, IL2, IL4, IL10 and TNF-alpha mRNA occurred in the skin biopsies of all of the lesioned, M. bovis inoculated animals except for an absence of tuberculin-induced TNF-alpha mRNA expression in two animals. |
| 6251 | 7493774 | By 28 weeks after vaccination, the three BCG-vaccinated, sham-inoculated cattle displayed minimal skin swelling response to tuberculin, but tuberculin-induced expression of IFN-gamma, IL2, IL4, IL10 and TNF-alpha mRNA was observed in skin biopsies of all of these animals. |
| 6252 | 7493774 | By 28 weeks after vaccination, the three BCG-vaccinated, sham-inoculated cattle displayed minimal skin swelling response to tuberculin, but tuberculin-induced expression of IFN-gamma, IL2, IL4, IL10 and TNF-alpha mRNA was observed in skin biopsies of all of these animals. |
| 6253 | 7583930 | Levels of interleukin 6 and tumor necrosis factor in serum from humans vaccinated with live, attenuated Francisella tularensis. |
| 6254 | 7583930 | Levels of interleukin 6 and tumor necrosis factor in serum from humans vaccinated with live, attenuated Francisella tularensis. |
| 6255 | 7583930 | The levels of interleukin 6 (IL-6) and tumor necrosis factor alpha in serum did not change significantly during the course of immunization with the live vaccine strain of Francisella tularensis. |
| 6256 | 7583930 | The levels of interleukin 6 (IL-6) and tumor necrosis factor alpha in serum did not change significantly during the course of immunization with the live vaccine strain of Francisella tularensis. |
| 6257 | 7571278 | Infection evokes complex changes which are thought to be caused by production and release of pro-inflammatory cytokines such as tumour necrosis factor (TNF-alpha), interferons (INFs), and interleukins (ILs). |
| 6258 | 7571278 | Infection evokes complex changes which are thought to be caused by production and release of pro-inflammatory cytokines such as tumour necrosis factor (TNF-alpha), interferons (INFs), and interleukins (ILs). |
| 6259 | 7571278 | Infection evokes complex changes which are thought to be caused by production and release of pro-inflammatory cytokines such as tumour necrosis factor (TNF-alpha), interferons (INFs), and interleukins (ILs). |
| 6260 | 7571278 | To improve our understanding of the pathophysiology of pro-inflammatory cytokines in ruminants, studies have been performed with TNF-alpha, IL1-alpha/beta, and IFN-alpha/ gamma as well as with cytokine-inducers in dwarf goats. |
| 6261 | 7571278 | To improve our understanding of the pathophysiology of pro-inflammatory cytokines in ruminants, studies have been performed with TNF-alpha, IL1-alpha/beta, and IFN-alpha/ gamma as well as with cytokine-inducers in dwarf goats. |
| 6262 | 7571278 | To improve our understanding of the pathophysiology of pro-inflammatory cytokines in ruminants, studies have been performed with TNF-alpha, IL1-alpha/beta, and IFN-alpha/ gamma as well as with cytokine-inducers in dwarf goats. |
| 6263 | 7571278 | Although studies of the actions of corticosteroids, nonsteroidal anti-inflammatory and antipyretic agents, antibodies to endotoxin, TNF-alpha, or IL-1, synthetic E. coli lipid A precursors, hydrazine, isoniazid, chloroquine, polymyxin B, bicyclic imidazoles, hydroxamates, and tyrosine kinase inhibitors in endotoxaemic animals have shed further light on inflammatory processes, clinical studies in this field are urgently required to evaluate their beneficial effect. |
| 6264 | 7571278 | Although studies of the actions of corticosteroids, nonsteroidal anti-inflammatory and antipyretic agents, antibodies to endotoxin, TNF-alpha, or IL-1, synthetic E. coli lipid A precursors, hydrazine, isoniazid, chloroquine, polymyxin B, bicyclic imidazoles, hydroxamates, and tyrosine kinase inhibitors in endotoxaemic animals have shed further light on inflammatory processes, clinical studies in this field are urgently required to evaluate their beneficial effect. |
| 6265 | 7571278 | Although studies of the actions of corticosteroids, nonsteroidal anti-inflammatory and antipyretic agents, antibodies to endotoxin, TNF-alpha, or IL-1, synthetic E. coli lipid A precursors, hydrazine, isoniazid, chloroquine, polymyxin B, bicyclic imidazoles, hydroxamates, and tyrosine kinase inhibitors in endotoxaemic animals have shed further light on inflammatory processes, clinical studies in this field are urgently required to evaluate their beneficial effect. |
| 6266 | 7502485 | Additionally, supernatants derived from human PBML were screened for interferons (IFN) alpha and gamma as well as for tumor necrosis factor by enzyme-linked immunosorbent assay. |
| 6267 | 7502485 | IFN alpha/beta was found to be responsible for the antiviral effect. |
| 6268 | 7502485 | Supernatants derived from human, porcine and ovine PBML stimulated with replicable PPV, native VV MVA and MVA lacZ recombinant or native APV and APV lacZ recombinant virus regularly contained IFN alpha. |
| 6269 | 7730632 | Interestingly, other cytokines (mGM-CSF, mTNF-alpha, and mIFN-gamma) inserted into the rVV genome did not modify the efficacy of the rVV constructs. |
| 6270 | 7722323 | IL-12-treated animals displayed a marked increase in pulmonary IFN-gamma and IL-12 p40 mRNA expression, while levels of IL-4, IL-5, and IL-13 were suppressed significantly during the period of vaccination. |
| 6271 | 7722323 | Surprisingly, IL-12-treated/vaccinated mice failed to demonstrate a significant increase in IFN-gamma, TNF-alpha, or nitric oxide synthase mRNA at the time of challenge infection when compared with vaccinated controls, but did, however, display significantly suppressed Th2 cytokine mRNA production. |
| 6272 | 7722322 | Exposure to supernatant fluids (SNs) from Ag stimulated spleen cells of i.d., but not i.v. or i.m., immunized mice activated inflammatory M phi for in vitro killing of schistosome larvae, through a mechanism dependent on both IFN gamma and TNF-alpha. |
| 6273 | 7722322 | No evidence was observed for the preferential induction of the M phi activating Th1 cytokines IFN-gamma and IL-2 in i.d. immunized mice, nor did spleen cells from nonprotected animals produce higher levels of the Th2 associated cytokines IL-4 and IL-10, which are known to prevent M phi activation. |
| 6274 | 7890377 | Levels of tumor necrosis factor (TNF) and gamma interferon (IFN-gamma) in serum were, respectively, 10- and 50-fold higher in LPS-potentiated mice injected with 15 LD50s of TSST-1 than in mice given H135A. |
| 6275 | 7890377 | Levels of tumor necrosis factor (TNF) and gamma interferon (IFN-gamma) in serum were, respectively, 10- and 50-fold higher in LPS-potentiated mice injected with 15 LD50s of TSST-1 than in mice given H135A. |
| 6276 | 7890377 | Mice injected with only TSST-1 did not have elevated levels of TNF or IFN-gamma in serum, while H135A plus LPS or LPS alone elicited identical, yet very low, levels of TNF and IFN-gamma. |
| 6277 | 7890377 | Mice injected with only TSST-1 did not have elevated levels of TNF or IFN-gamma in serum, while H135A plus LPS or LPS alone elicited identical, yet very low, levels of TNF and IFN-gamma. |
| 6278 | 7697918 | We studied the production of TNF-alpha in spleens and bladders of mice after intravesical BCG or BCG/interferon-gamma (IFN-gamma) instillation. |
| 6279 | 7697918 | We studied the production of TNF-alpha in spleens and bladders of mice after intravesical BCG or BCG/interferon-gamma (IFN-gamma) instillation. |
| 6280 | 7697918 | Significant change of TNF-alpha mRNA expression of spleens and bladders of C3H/He mice was observed after intravesical BCG instillation, although intravesical IFN-gamma therapy 3 days after BCG instillation to maintain the activated state of monocyte/macrophage lineage cells did not show a significant change of TNF-alpha mRNA, compared with that of BCG therapy alone. |
| 6281 | 7697918 | Significant change of TNF-alpha mRNA expression of spleens and bladders of C3H/He mice was observed after intravesical BCG instillation, although intravesical IFN-gamma therapy 3 days after BCG instillation to maintain the activated state of monocyte/macrophage lineage cells did not show a significant change of TNF-alpha mRNA, compared with that of BCG therapy alone. |
| 6282 | 7537831 | Japanese national references of IL-2 and TNF alpha were calibrated by collaboration with related companies and NIH Japan and the concluded results are obtained as follows. |
| 6283 | 7882559 | This study concerns the production of IL-1 beta, IL-2, IL-4, IL-6, IL-8, IL-10, tumour necrosis factor-alpha (TNF-alpha), interferon-gamma (IFN-gamma) and soluble ICAM-1 (sICAM-1) throughout the six weekly instillations which comprise a therapeutic course. |
| 6284 | 7882559 | This study concerns the production of IL-1 beta, IL-2, IL-4, IL-6, IL-8, IL-10, tumour necrosis factor-alpha (TNF-alpha), interferon-gamma (IFN-gamma) and soluble ICAM-1 (sICAM-1) throughout the six weekly instillations which comprise a therapeutic course. |
| 6285 | 7882559 | Sequential instillations of BCG induced secretion of IL-1 beta, IL-2, IL-6, IL-8, IL-10, TNF-alpha, IFN-gamma and sICAM-1 into urine. |
| 6286 | 7882559 | Sequential instillations of BCG induced secretion of IL-1 beta, IL-2, IL-6, IL-8, IL-10, TNF-alpha, IFN-gamma and sICAM-1 into urine. |
| 6287 | 7882559 | IL-6, IL-8 and IL-10) could be detected after the first instillation, whilst others (e.g. |
| 6288 | 7882559 | IL-6, IL-8 and IL-10) could be detected after the first instillation, whilst others (e.g. |
| 6289 | 7882559 | IL-2 and IFN-gamma) were not detected until after the third or fourth instillation. |
| 6290 | 7882559 | IL-2 and IFN-gamma) were not detected until after the third or fourth instillation. |
| 6291 | 7868226 | Cells from humans, either BCG vaccinated or from countries where leprosy is endemic, were stimulated in vitro with a number of mycobacterial antigens--whole M. leprae, M. leprae cell walls, purified protein derivative of M. tuberculosis, and Mycobacterium bovis BCG--and tested for proliferation and production of interleukin-6, tumor necrosis factor alpha, and gamma interferon. |
| 6292 | 7705395 | Interleukin-12 is required for interferon-gamma production and lethality in lipopolysaccharide-induced shock in mice. |
| 6293 | 7705395 | Interleukin-12 is required for interferon-gamma production and lethality in lipopolysaccharide-induced shock in mice. |
| 6294 | 7705395 | Interleukin-12 is required for interferon-gamma production and lethality in lipopolysaccharide-induced shock in mice. |
| 6295 | 7705395 | Several cytokines, in particular tumor necrosis factor-alpha (TNF-alpha) and interferon-gamma (IFN-gamma), have been shown to be responsible for pathological reactions which may lead to shock and death observed in infection with Gram-negative bacteria and in response to endotoxins (lipopolysaccharides, LPS). |
| 6296 | 7705395 | Several cytokines, in particular tumor necrosis factor-alpha (TNF-alpha) and interferon-gamma (IFN-gamma), have been shown to be responsible for pathological reactions which may lead to shock and death observed in infection with Gram-negative bacteria and in response to endotoxins (lipopolysaccharides, LPS). |
| 6297 | 7705395 | Several cytokines, in particular tumor necrosis factor-alpha (TNF-alpha) and interferon-gamma (IFN-gamma), have been shown to be responsible for pathological reactions which may lead to shock and death observed in infection with Gram-negative bacteria and in response to endotoxins (lipopolysaccharides, LPS). |
| 6298 | 7705395 | In response to low doses (1 microgram/mouse) of LPS, BCG-primed mice produce interleukin-12 (IL-12) which controls IFN-gamma production, as demonstrated by the ability of neutralizing anti-IL-12 antibodies to suppress IFN-gamma production. |
| 6299 | 7705395 | In response to low doses (1 microgram/mouse) of LPS, BCG-primed mice produce interleukin-12 (IL-12) which controls IFN-gamma production, as demonstrated by the ability of neutralizing anti-IL-12 antibodies to suppress IFN-gamma production. |
| 6300 | 7705395 | In response to low doses (1 microgram/mouse) of LPS, BCG-primed mice produce interleukin-12 (IL-12) which controls IFN-gamma production, as demonstrated by the ability of neutralizing anti-IL-12 antibodies to suppress IFN-gamma production. |
| 6301 | 7705395 | However, the concentration of the biologically active IL-12 p70 heterodimer is similar in the serum of both BCG-primed or unprimed mice, reaching levels of 1-3 ng/ml at 3-6 h after LPS injection, whereas IFN-gamma production was observed only in BCG-primed mice. |
| 6302 | 7705395 | However, the concentration of the biologically active IL-12 p70 heterodimer is similar in the serum of both BCG-primed or unprimed mice, reaching levels of 1-3 ng/ml at 3-6 h after LPS injection, whereas IFN-gamma production was observed only in BCG-primed mice. |
| 6303 | 7705395 | However, the concentration of the biologically active IL-12 p70 heterodimer is similar in the serum of both BCG-primed or unprimed mice, reaching levels of 1-3 ng/ml at 3-6 h after LPS injection, whereas IFN-gamma production was observed only in BCG-primed mice. |
| 6304 | 7705395 | The priming effect of BCG on IFN-gamma production appears to be mostly due to its ability to increase TNF-alpha production, which acts as cofactor with LPS-induced IL-12 in inducing IFN-gamma production, as shown by the ability of injection of TNF-alpha and LPS (1 microgram/mouse), but not LPS alone, to induce IFN-gamma production. |
| 6305 | 7705395 | The priming effect of BCG on IFN-gamma production appears to be mostly due to its ability to increase TNF-alpha production, which acts as cofactor with LPS-induced IL-12 in inducing IFN-gamma production, as shown by the ability of injection of TNF-alpha and LPS (1 microgram/mouse), but not LPS alone, to induce IFN-gamma production. |
| 6306 | 7705395 | The priming effect of BCG on IFN-gamma production appears to be mostly due to its ability to increase TNF-alpha production, which acts as cofactor with LPS-induced IL-12 in inducing IFN-gamma production, as shown by the ability of injection of TNF-alpha and LPS (1 microgram/mouse), but not LPS alone, to induce IFN-gamma production. |
| 6307 | 7705395 | However, in addition to TNF-alpha, other LPS-induced cofactor(s) are required in cooperation with IL-12 to induce optimal IFN-gamma production, because co-injection of TNF-alpha and IL-12, sufficient to induce serum concentrations of both cytokines higher and more persistent than those obtained by injection of LPS, was not sufficient to induce IFN-gamma production in vivo. |
| 6308 | 7705395 | However, in addition to TNF-alpha, other LPS-induced cofactor(s) are required in cooperation with IL-12 to induce optimal IFN-gamma production, because co-injection of TNF-alpha and IL-12, sufficient to induce serum concentrations of both cytokines higher and more persistent than those obtained by injection of LPS, was not sufficient to induce IFN-gamma production in vivo. |
| 6309 | 7705395 | However, in addition to TNF-alpha, other LPS-induced cofactor(s) are required in cooperation with IL-12 to induce optimal IFN-gamma production, because co-injection of TNF-alpha and IL-12, sufficient to induce serum concentrations of both cytokines higher and more persistent than those obtained by injection of LPS, was not sufficient to induce IFN-gamma production in vivo. |
| 6310 | 7705395 | Thus, IL-12 is required for IFN-gamma production and lethality in an endotoxic shock model in mice. |
| 6311 | 7705395 | Thus, IL-12 is required for IFN-gamma production and lethality in an endotoxic shock model in mice. |
| 6312 | 7705395 | Thus, IL-12 is required for IFN-gamma production and lethality in an endotoxic shock model in mice. |
| 6313 | 7532543 | CD34+ HPC can be mobilized into the peripheral blood by in vivo administration of granulocyte-colony-stimulating factor. |
| 6314 | 7532543 | The aim of the current study was to determine whether functional dendritic cells could be elicited and grown in vitro from CD34+ HPC derived from bone marrow or granulocyte-colony-stimulating factor-mobilized peripheral blood. |
| 6315 | 7532543 | Culture of CD34+ HPC with granulocyte-macrophage-colony-stimulating factor and tumor necrosis factor alpha yielded a heterogeneous cell population containing cells with typical dendritic morphology. |
| 6316 | 7532543 | Phenotypic studies demonstrated a loss of the CD34 molecule over 1 week and an increase in cells expressing surface markers associated with dendritic cells, CD1a, CD80 (B7/BB1), CD4, CD14, HLA-DR, and CD64 (Fc gamma RI). |
| 6317 | 7532543 | Function was validated in experiments showing that cultured cells could stimulate proliferation of allogeneic CD4+ and CD8+ T lymphocytes. |
| 6318 | 7532543 | The derivation and expansion of dendritic cells from cultured bone marrow or granulocyte-colony-stimulating factor-mobilized CD34+ HPC may provide adequate numbers for testing of dendritic cells in clinical studies, such as vaccine and T cell therapy trials. |
| 6319 | 7882382 | These cytokines include interleukins IL-1 beta, IL-2, IL-4, IL-6, IL-8, IL-10, tumour necrosis factor alpha (TNF alpha), interferon gamma (IFN gamma) and also soluble intercellular adhesion molecule ICAM-1. |
| 6320 | 7544769 | We describe immunopathological consequences of this tendency, including a putative role for agalactosyl IgG, and review evidence for involvement of changes in the endocrine system, brought about not only by the cytokine-hypothalamus-pituitary-adrenal axis, but also by direct actions on peripheral endocrine organs of excess levels of cytokines such as TNF alpha, TGF beta and IL-6. |
| 6321 | 21556495 | In an attempt to study the possible role of cytokines in this system, we tested the effect of neutralizing antibodies to TNF-alpha and IFN-gamma on the therapeutic effect. |
| 6322 | 21556495 | In an attempt to study the possible role of cytokines in this system, we tested the effect of neutralizing antibodies to TNF-alpha and IFN-gamma on the therapeutic effect. |
| 6323 | 21556495 | Anti-TNF-alpha but not anti IFN-gamma antibody treatment augmented the immunotherapeutic effectiveness of immune PEC mediated ADI. |
| 6324 | 21556495 | Anti-TNF-alpha but not anti IFN-gamma antibody treatment augmented the immunotherapeutic effectiveness of immune PEC mediated ADI. |
| 6325 | 8574153 | PBMC from HIV-infected patients (asymptomatic, age 22-36, symptomatic, age 30-59 and pediatric, < 2 years old) were co-cultured with PHA-stimulated PBMC from uninfected individuals in medium containing IL-2 and PAI. |
| 6326 | 8574153 | PBMC from HIV-infected patients (asymptomatic, age 22-36, symptomatic, age 30-59 and pediatric, < 2 years old) were co-cultured with PHA-stimulated PBMC from uninfected individuals in medium containing IL-2 and PAI. |
| 6327 | 8574153 | HIV-p24 ag and cytokine profiles (IL-1 beta, IL-2, IL-4, IFN-gamma and TNF-alpha) were determined on supernatants on day 14. |
| 6328 | 8574153 | HIV-p24 ag and cytokine profiles (IL-1 beta, IL-2, IL-4, IFN-gamma and TNF-alpha) were determined on supernatants on day 14. |
| 6329 | 8574153 | Peripheral blood samples from each patient were evaluated at the beginning of the experiment as to total CD3, total CD19, CD3/CD4, CD3/CD8, CD16/CD56, CD8/HLA-DR and CD8/CD38 markers through flow cytometry. |
| 6330 | 8574153 | Peripheral blood samples from each patient were evaluated at the beginning of the experiment as to total CD3, total CD19, CD3/CD4, CD3/CD8, CD16/CD56, CD8/HLA-DR and CD8/CD38 markers through flow cytometry. |
| 6331 | 8574153 | PAI was able to induce the production of IFN-gamma and TNF-alpha while that of IL-4 and IL-1 beta was reduced. |
| 6332 | 8574153 | PAI was able to induce the production of IFN-gamma and TNF-alpha while that of IL-4 and IL-1 beta was reduced. |
| 6333 | 8574153 | The predominant cell type detected in the blood samples of the studied subjects were CD8+, CD8+/CD38+ or CD8+/HLA-DR+. |
| 6334 | 8574153 | The predominant cell type detected in the blood samples of the studied subjects were CD8+, CD8+/CD38+ or CD8+/HLA-DR+. |
| 6335 | 7983727 | Local expression of tumor necrosis factor alpha and interleukin-2 correlates with protection against corneal scarring after ocular challenge of vaccinated mice with herpes simplex virus type 1. |
| 6336 | 7983727 | Local expression of tumor necrosis factor alpha and interleukin-2 correlates with protection against corneal scarring after ocular challenge of vaccinated mice with herpes simplex virus type 1. |
| 6337 | 7983727 | Local expression of tumor necrosis factor alpha and interleukin-2 correlates with protection against corneal scarring after ocular challenge of vaccinated mice with herpes simplex virus type 1. |
| 6338 | 7983727 | Infiltration into the cornea of CD4+ T cells, CD8+ T cells, macrophages, and cells containing various lymphokines was monitored on days 0, 1, 3, 7, and 10 postchallenge by immunocytochemistry of corneal sections. |
| 6339 | 7983727 | Infiltration into the cornea of CD4+ T cells, CD8+ T cells, macrophages, and cells containing various lymphokines was monitored on days 0, 1, 3, 7, and 10 postchallenge by immunocytochemistry of corneal sections. |
| 6340 | 7983727 | Infiltration into the cornea of CD4+ T cells, CD8+ T cells, macrophages, and cells containing various lymphokines was monitored on days 0, 1, 3, 7, and 10 postchallenge by immunocytochemistry of corneal sections. |
| 6341 | 7983727 | In response to the ocular challenge, these mice developed high local levels of infiltrating CD4+ T cells and cells containing interleukin-2 (IL-2), IL-4, IL-6, or tumor necrosis factor alpha (TNF-alpha). |
| 6342 | 7983727 | In response to the ocular challenge, these mice developed high local levels of infiltrating CD4+ T cells and cells containing interleukin-2 (IL-2), IL-4, IL-6, or tumor necrosis factor alpha (TNF-alpha). |
| 6343 | 7983727 | In response to the ocular challenge, these mice developed high local levels of infiltrating CD4+ T cells and cells containing interleukin-2 (IL-2), IL-4, IL-6, or tumor necrosis factor alpha (TNF-alpha). |
| 6344 | 7983727 | In contrast, only low levels of infiltrating CD8+ T cells were found, and gamma interferon (IFN-gamma)-containing cells were not present until day 10. gE-vaccinated mice developed neutralizing antibody titers in serum almost as high as those of the KOS-vaccinated mice (> 1:320). |
| 6345 | 7983727 | In contrast, only low levels of infiltrating CD8+ T cells were found, and gamma interferon (IFN-gamma)-containing cells were not present until day 10. gE-vaccinated mice developed neutralizing antibody titers in serum almost as high as those of the KOS-vaccinated mice (> 1:320). |
| 6346 | 7983727 | In contrast, only low levels of infiltrating CD8+ T cells were found, and gamma interferon (IFN-gamma)-containing cells were not present until day 10. gE-vaccinated mice developed neutralizing antibody titers in serum almost as high as those of the KOS-vaccinated mice (> 1:320). |
| 6347 | 7983727 | Compared with KOS-vaccinated mice, the gE-vaccinated mice had a similar pattern of IFN-gamma, but a delay in the appearance of CD4+ T cells, CD8+ T cells, and IL-4-, IL-6-, and TNF-alpha-containing cells. |
| 6348 | 7983727 | Compared with KOS-vaccinated mice, the gE-vaccinated mice had a similar pattern of IFN-gamma, but a delay in the appearance of CD4+ T cells, CD8+ T cells, and IL-4-, IL-6-, and TNF-alpha-containing cells. |
| 6349 | 7983727 | Compared with KOS-vaccinated mice, the gE-vaccinated mice had a similar pattern of IFN-gamma, but a delay in the appearance of CD4+ T cells, CD8+ T cells, and IL-4-, IL-6-, and TNF-alpha-containing cells. |
| 6350 | 7716458 | Direct effector functions of cytotoxic CD8+ lymphocytes directly depend on local periparasitic gamma-interferon- and TNF alpha-concentrations. |
| 6351 | 7716458 | Immunological aberrance occurs if locally (cerebral) synthesized Il-10 and Il-6 induce anergistic immunosuppression. |
| 6352 | 7716458 | An experimental vaccine in the mouse demonstrated primary dependence of a protective immune response on CD8+ and CD4+ (Th) cells. |
| 6353 | 7551237 | Induction of enhanced cytokine secretion has been found to involve IFN-alpha/beta, IFN-gamma, TNF-alpha, TNF-beta, IL-1, IL-6, and the 40 kDa chain of IL-12. |
| 6354 | 8001028 | Productive immunity to murine and human parasites is associated with the development of a type I T cell response (interferon-gamma-producing) while type II responses (interleukin-4-producing) suppress the development of delayed-type hypersensitivity (DTH) and the elimination of the parasite. |
| 6355 | 8001028 | Productive immunity to murine and human parasites is associated with the development of a type I T cell response (interferon-gamma-producing) while type II responses (interleukin-4-producing) suppress the development of delayed-type hypersensitivity (DTH) and the elimination of the parasite. |
| 6356 | 8001028 | Productive immunity to murine and human parasites is associated with the development of a type I T cell response (interferon-gamma-producing) while type II responses (interleukin-4-producing) suppress the development of delayed-type hypersensitivity (DTH) and the elimination of the parasite. |
| 6357 | 8001028 | Intravesical growth of MB49 results in the host-derived expression of mRNA for both interleukin-4 (IL-4) (TH2) and interferon gamma (IFN gamma) (TH1), as well as tumor necrosis factor alpha (TNF alpha) expression of indeterminate origin. |
| 6358 | 8001028 | Intravesical growth of MB49 results in the host-derived expression of mRNA for both interleukin-4 (IL-4) (TH2) and interferon gamma (IFN gamma) (TH1), as well as tumor necrosis factor alpha (TNF alpha) expression of indeterminate origin. |
| 6359 | 8001028 | Intravesical growth of MB49 results in the host-derived expression of mRNA for both interleukin-4 (IL-4) (TH2) and interferon gamma (IFN gamma) (TH1), as well as tumor necrosis factor alpha (TNF alpha) expression of indeterminate origin. |
| 6360 | 8001028 | Intravesical instillation of bacillus Calmette-Guérin (BCG), highly effective in eliminating bladder tumors clinically and in experimental systems, results in IFN gamma and TNF alpha mRNa production in the bladder wall, but no IL-4. |
| 6361 | 8001028 | Intravesical instillation of bacillus Calmette-Guérin (BCG), highly effective in eliminating bladder tumors clinically and in experimental systems, results in IFN gamma and TNF alpha mRNa production in the bladder wall, but no IL-4. |
| 6362 | 8001028 | Intravesical instillation of bacillus Calmette-Guérin (BCG), highly effective in eliminating bladder tumors clinically and in experimental systems, results in IFN gamma and TNF alpha mRNa production in the bladder wall, but no IL-4. |
| 6363 | 8001028 | Following BCG treatment of intravesical MB49, the number bladders expressing IL-4 mRNA decreases, while IFN gamma and TNF alpha expression remains constant. |
| 6364 | 8001028 | Following BCG treatment of intravesical MB49, the number bladders expressing IL-4 mRNA decreases, while IFN gamma and TNF alpha expression remains constant. |
| 6365 | 8001028 | Following BCG treatment of intravesical MB49, the number bladders expressing IL-4 mRNA decreases, while IFN gamma and TNF alpha expression remains constant. |
| 6366 | 7960112 | Pulmonary immunity to Pseudomonas aeruginosa in intestinally immunized rats roles of alveolar macrophages, tumor necrosis factor alpha, and interleukin-1 alpha. |
| 6367 | 7960112 | Pulmonary immunity to Pseudomonas aeruginosa in intestinally immunized rats roles of alveolar macrophages, tumor necrosis factor alpha, and interleukin-1 alpha. |
| 6368 | 7960112 | Pulmonary immunity to Pseudomonas aeruginosa in intestinally immunized rats roles of alveolar macrophages, tumor necrosis factor alpha, and interleukin-1 alpha. |
| 6369 | 7960112 | Pulmonary immunity to Pseudomonas aeruginosa in intestinally immunized rats roles of alveolar macrophages, tumor necrosis factor alpha, and interleukin-1 alpha. |
| 6370 | 7960112 | Pulmonary immunity to Pseudomonas aeruginosa in intestinally immunized rats roles of alveolar macrophages, tumor necrosis factor alpha, and interleukin-1 alpha. |
| 6371 | 7960112 | The aims of this study were to assess the role played by alveolar macrophages, tumor necrosis factor alpha (TNF-alpha), and interleukin-1 alpha (IL-1 alpha) in pulmonary immunity against Pseudomonas aeruginosa in animals that have been immunized via the gut-associated lymphoid tissue. |
| 6372 | 7960112 | The aims of this study were to assess the role played by alveolar macrophages, tumor necrosis factor alpha (TNF-alpha), and interleukin-1 alpha (IL-1 alpha) in pulmonary immunity against Pseudomonas aeruginosa in animals that have been immunized via the gut-associated lymphoid tissue. |
| 6373 | 7960112 | The aims of this study were to assess the role played by alveolar macrophages, tumor necrosis factor alpha (TNF-alpha), and interleukin-1 alpha (IL-1 alpha) in pulmonary immunity against Pseudomonas aeruginosa in animals that have been immunized via the gut-associated lymphoid tissue. |
| 6374 | 7960112 | The aims of this study were to assess the role played by alveolar macrophages, tumor necrosis factor alpha (TNF-alpha), and interleukin-1 alpha (IL-1 alpha) in pulmonary immunity against Pseudomonas aeruginosa in animals that have been immunized via the gut-associated lymphoid tissue. |
| 6375 | 7960112 | The aims of this study were to assess the role played by alveolar macrophages, tumor necrosis factor alpha (TNF-alpha), and interleukin-1 alpha (IL-1 alpha) in pulmonary immunity against Pseudomonas aeruginosa in animals that have been immunized via the gut-associated lymphoid tissue. |
| 6376 | 7960112 | Following intra-Peyer's patch immunization and subsequent intratracheal challenge with live bacteria, significantly enhanced bacterial clearance from the lungs correlated with an increase in bronchoalveolar neutrophils, increased recruitment and phagocytic activity of alveolar macrophages, and accelerated production of TNF-alpha in the bronchoalveolar space, while levels of IL-1 alpha remained low. |
| 6377 | 7960112 | Following intra-Peyer's patch immunization and subsequent intratracheal challenge with live bacteria, significantly enhanced bacterial clearance from the lungs correlated with an increase in bronchoalveolar neutrophils, increased recruitment and phagocytic activity of alveolar macrophages, and accelerated production of TNF-alpha in the bronchoalveolar space, while levels of IL-1 alpha remained low. |
| 6378 | 7960112 | Following intra-Peyer's patch immunization and subsequent intratracheal challenge with live bacteria, significantly enhanced bacterial clearance from the lungs correlated with an increase in bronchoalveolar neutrophils, increased recruitment and phagocytic activity of alveolar macrophages, and accelerated production of TNF-alpha in the bronchoalveolar space, while levels of IL-1 alpha remained low. |
| 6379 | 7960112 | Following intra-Peyer's patch immunization and subsequent intratracheal challenge with live bacteria, significantly enhanced bacterial clearance from the lungs correlated with an increase in bronchoalveolar neutrophils, increased recruitment and phagocytic activity of alveolar macrophages, and accelerated production of TNF-alpha in the bronchoalveolar space, while levels of IL-1 alpha remained low. |
| 6380 | 7960112 | Following intra-Peyer's patch immunization and subsequent intratracheal challenge with live bacteria, significantly enhanced bacterial clearance from the lungs correlated with an increase in bronchoalveolar neutrophils, increased recruitment and phagocytic activity of alveolar macrophages, and accelerated production of TNF-alpha in the bronchoalveolar space, while levels of IL-1 alpha remained low. |
| 6381 | 7960112 | In acutely infected nonimmune animals, bronchoalveolar concentrations of soluble IL-1 alpha and TNF-alpha increased until the time of death. |
| 6382 | 7960112 | In acutely infected nonimmune animals, bronchoalveolar concentrations of soluble IL-1 alpha and TNF-alpha increased until the time of death. |
| 6383 | 7960112 | In acutely infected nonimmune animals, bronchoalveolar concentrations of soluble IL-1 alpha and TNF-alpha increased until the time of death. |
| 6384 | 7960112 | In acutely infected nonimmune animals, bronchoalveolar concentrations of soluble IL-1 alpha and TNF-alpha increased until the time of death. |
| 6385 | 7960112 | In acutely infected nonimmune animals, bronchoalveolar concentrations of soluble IL-1 alpha and TNF-alpha increased until the time of death. |
| 6386 | 7960112 | Levels of soluble IL-1 alpha and TNF-alpha in nonimmune rats increased consistently following infection until the time of death, thus implicating these cytokines in the pathogenesis of acute P. aeruginosa pneumonia. |
| 6387 | 7960112 | Levels of soluble IL-1 alpha and TNF-alpha in nonimmune rats increased consistently following infection until the time of death, thus implicating these cytokines in the pathogenesis of acute P. aeruginosa pneumonia. |
| 6388 | 7960112 | Levels of soluble IL-1 alpha and TNF-alpha in nonimmune rats increased consistently following infection until the time of death, thus implicating these cytokines in the pathogenesis of acute P. aeruginosa pneumonia. |
| 6389 | 7960112 | Levels of soluble IL-1 alpha and TNF-alpha in nonimmune rats increased consistently following infection until the time of death, thus implicating these cytokines in the pathogenesis of acute P. aeruginosa pneumonia. |
| 6390 | 7960112 | Levels of soluble IL-1 alpha and TNF-alpha in nonimmune rats increased consistently following infection until the time of death, thus implicating these cytokines in the pathogenesis of acute P. aeruginosa pneumonia. |
| 6391 | 7537721 | L. major induced the production of two competing cytokines in infected macrophages: (1) the parasite activated the gene for tumor necrosis factor (TNF), and production of TNF protein was enhanced by the presence of interferon-gamma (IFN-gamma). |
| 6392 | 7537721 | L. major induced the production of two competing cytokines in infected macrophages: (1) the parasite activated the gene for tumor necrosis factor (TNF), and production of TNF protein was enhanced by the presence of interferon-gamma (IFN-gamma). |
| 6393 | 7537721 | L. major induced the production of two competing cytokines in infected macrophages: (1) the parasite activated the gene for tumor necrosis factor (TNF), and production of TNF protein was enhanced by the presence of interferon-gamma (IFN-gamma). |
| 6394 | 7537721 | TNF then acted as a autocrine signal to amplify IFN-gamma-induced production of NO; and (2) the parasite upregulated production of transforming growth factor-beta (TGF-beta), which blocked IFN-gamma-induced production of NO. |
| 6395 | 7537721 | TNF then acted as a autocrine signal to amplify IFN-gamma-induced production of NO; and (2) the parasite upregulated production of transforming growth factor-beta (TGF-beta), which blocked IFN-gamma-induced production of NO. |
| 6396 | 7537721 | TNF then acted as a autocrine signal to amplify IFN-gamma-induced production of NO; and (2) the parasite upregulated production of transforming growth factor-beta (TGF-beta), which blocked IFN-gamma-induced production of NO. |
| 6397 | 7537721 | Whether parasite-induced TNF (parasite destruction) or TGF-beta (parasite survival) prevailed depended upon the presence and quantity of IFN-gamma at the time of infection. |
| 6398 | 7537721 | Whether parasite-induced TNF (parasite destruction) or TGF-beta (parasite survival) prevailed depended upon the presence and quantity of IFN-gamma at the time of infection. |
| 6399 | 7537721 | Whether parasite-induced TNF (parasite destruction) or TGF-beta (parasite survival) prevailed depended upon the presence and quantity of IFN-gamma at the time of infection. |
| 6400 | 7525727 | A similar, although less dramatic, increase in two other macrophage-activating cytokines, TNF-alpha and IL-2, also was observed. |
| 6401 | 7525727 | A similar, although less dramatic, increase in two other macrophage-activating cytokines, TNF-alpha and IL-2, also was observed. |
| 6402 | 7525727 | In contrast, although the Th2 cytokines IL-4, IL-5, IL-10, and IL-13 were elevated in challenged vaccinated animals, only IL-10 and IL-13 showed increases that were significant with respect to the mRNA levels observed in challenged controls. |
| 6403 | 7525727 | In contrast, although the Th2 cytokines IL-4, IL-5, IL-10, and IL-13 were elevated in challenged vaccinated animals, only IL-10 and IL-13 showed increases that were significant with respect to the mRNA levels observed in challenged controls. |
| 6404 | 7525727 | Neutralization of IFN-gamma reduced immunity in vaccinated animals and resulted in decreased IFN-gamma, IL-2, IL-10, TNF-alpha, and IL-12 p40 but markedly increased IL-4, IL-5, and IL-13 mRNA expression and serum IgE levels. |
| 6405 | 7525727 | Neutralization of IFN-gamma reduced immunity in vaccinated animals and resulted in decreased IFN-gamma, IL-2, IL-10, TNF-alpha, and IL-12 p40 but markedly increased IL-4, IL-5, and IL-13 mRNA expression and serum IgE levels. |
| 6406 | 7525727 | Furthermore, the observation that the down-regulatory cytokines IL-4, IL-10, and IL-13 are induced together with IFN-gamma may provide an explanation for the failure of this vaccine to provide complete protection. |
| 6407 | 7525727 | Furthermore, the observation that the down-regulatory cytokines IL-4, IL-10, and IL-13 are induced together with IFN-gamma may provide an explanation for the failure of this vaccine to provide complete protection. |
| 6408 | 7930610 | Pooled mouse sera were analyzed by ELISA at various times after immunization for IL-1 alpha, IL-2, IL-3, IL-4, IL-5, IL-6, IL-10, IFN-gamma, and TNF-alpha. |
| 6409 | 7930610 | In naive mice, vaccine alone induced low levels of IL-3 and IL-5 only; vaccine plus alum induced a low IL-6 response as well. |
| 6410 | 7930610 | The MF59-based adjuvants significantly increased the IL-5 and IL-6 levels, whereas Quil A LTC induced strong IFN-gamma and measurable IL-2 responses, in addition to moderate IL-5 and IL-6. |
| 6411 | 7930610 | In previously infected mice, MF59 and MF59/MTP-PE were capable of generating IFN-gamma responses, as well as IL-5 and IL-6. |
| 6412 | 7954527 | Tumor necrosis factor alpha (TNF alpha) and interleukin-1 beta (IL-1 beta) were detected at markedly high levels at 24 h, and interferon gamma (IFN gamma) was detected at 120 h. |
| 6413 | 7954527 | IL-2 and macrophage-colony-stimulating factor were not detected. |
| 6414 | 7839726 | Moreover, only 45-69 lipopeptide induces the secretion of cytokines such as IL-1, IL-6 and TNF-alpha by peritoneal macrophages. |
| 6415 | 7523268 | Administration of whole-cell diphtheria and tetanus toxoids and pertussis vaccine adsorbed (DTP vaccine) caused marked depression in the expression of mRNA for isozymes of cytochrome P-450 in the livers of endotoxin-responsive and nonresponsive mice. |
| 6416 | 7523268 | The levels of expression of mRNA for a polycyclic aromatic hydrocarbon-inducible (CYP1A2) and an ethanol-inducible (CYP2E1) form of P-450 were reduced by 70% to 80% 8 to 12 hr after vaccination or Bordetella pertussis endotoxin administration. |
| 6417 | 7523268 | These effects are preceded by marked increases (threefold to sixfold) in mRNA expression for interleukin-6, interleukin-1 and tumor necrosis factor in both strains of mice, with maximal increases 1 to 2 hr after injection. |
| 6418 | 7523268 | The finding of increased cytokine mRNA in the livers of mice injected with vaccine supports a role for cytokines as mediators of the decreased levels of cytochrome P-450. |
| 6419 | 7523268 | The temporal relationship of the increased cytokine mRNA expression, increased nitric oxide synthase and decreased expression of P-450 mRNAs suggests a mechanism by which cytokines mediate the induction of nitric oxide synthase, which increases nitric oxide and decreases the activities of some cytochromes P-450. |
| 6420 | 8063416 | PBMC and Mphi from all these donor groups secreted increased levels of tumor necrosis factor alpha, interleukin-1 beta, and interleukin-6 in response to stimulation with formalin-killed spherules (FKS), as measured by enzyme-linked immunosorbent assays. |
| 6421 | 8063416 | PBMC and Mphi from all these donor groups secreted increased levels of tumor necrosis factor alpha, interleukin-1 beta, and interleukin-6 in response to stimulation with formalin-killed spherules (FKS), as measured by enzyme-linked immunosorbent assays. |
| 6422 | 8063416 | Viable C. immitis spherules also stimulated PBMC and Mphi from healthy subjects and patients to secrete tumor necrosis factor alpha, interleukin-1 beta, and interleukin-6, although at levels lower than those induced by FKS. |
| 6423 | 8063416 | Viable C. immitis spherules also stimulated PBMC and Mphi from healthy subjects and patients to secrete tumor necrosis factor alpha, interleukin-1 beta, and interleukin-6, although at levels lower than those induced by FKS. |
| 6424 | 7998414 | Liposomal LPS also induced more active accumulation of IFN-gamma in human peripheral blood mononuclear cells and less active accumulation of monokines, contributing to the realization of the toxic properties of endotoxin (IL-1 alpha, TNF-alpha, IL-6 and GM-CSF). |
| 6425 | 7621248 | The transduced cells expressed the cytokine gene, secreted biologically active gamma IFN, and exhibited enhanced expression of MHC class I and class II (HLA-DR), and ICAM-1 surface antigens. |
| 6426 | 7621248 | Lymphocyte cultures that displayed increases in cytotoxicity after stimulation with the gamma IFN-transduced melanoma cells also exhibited enhanced expression or induction of one or more of the following lymphokines: IL-4, IL-1 alpha, IL-1 beta, gamma IFN, and TNF-alpha. |
| 6427 | 7522168 | Response of interleukin-6-deficient mice to tumor necrosis factor-induced metabolic changes and lethality. |
| 6428 | 7522168 | Response of interleukin-6-deficient mice to tumor necrosis factor-induced metabolic changes and lethality. |
| 6429 | 7522168 | Response of interleukin-6-deficient mice to tumor necrosis factor-induced metabolic changes and lethality. |
| 6430 | 7522168 | Response of interleukin-6-deficient mice to tumor necrosis factor-induced metabolic changes and lethality. |
| 6431 | 7522168 | Response of interleukin-6-deficient mice to tumor necrosis factor-induced metabolic changes and lethality. |
| 6432 | 7522168 | Response of interleukin-6-deficient mice to tumor necrosis factor-induced metabolic changes and lethality. |
| 6433 | 7522168 | Response of interleukin-6-deficient mice to tumor necrosis factor-induced metabolic changes and lethality. |
| 6434 | 7522168 | Whether interleukin (IL)-6 contributes to tumor necrosis factor (TNF)-induced lethal shock or whether, on the contrary, it is part of a protective feedback system, remains unresolved. |
| 6435 | 7522168 | Whether interleukin (IL)-6 contributes to tumor necrosis factor (TNF)-induced lethal shock or whether, on the contrary, it is part of a protective feedback system, remains unresolved. |
| 6436 | 7522168 | Whether interleukin (IL)-6 contributes to tumor necrosis factor (TNF)-induced lethal shock or whether, on the contrary, it is part of a protective feedback system, remains unresolved. |
| 6437 | 7522168 | Whether interleukin (IL)-6 contributes to tumor necrosis factor (TNF)-induced lethal shock or whether, on the contrary, it is part of a protective feedback system, remains unresolved. |
| 6438 | 7522168 | Whether interleukin (IL)-6 contributes to tumor necrosis factor (TNF)-induced lethal shock or whether, on the contrary, it is part of a protective feedback system, remains unresolved. |
| 6439 | 7522168 | Whether interleukin (IL)-6 contributes to tumor necrosis factor (TNF)-induced lethal shock or whether, on the contrary, it is part of a protective feedback system, remains unresolved. |
| 6440 | 7522168 | Whether interleukin (IL)-6 contributes to tumor necrosis factor (TNF)-induced lethal shock or whether, on the contrary, it is part of a protective feedback system, remains unresolved. |
| 6441 | 7522168 | We have tested the susceptibility of these to TNF-induced metabolic changes and lethality in different models, and compared the results with those obtained with IL-6+/+ wild-type mice. |
| 6442 | 7522168 | We have tested the susceptibility of these to TNF-induced metabolic changes and lethality in different models, and compared the results with those obtained with IL-6+/+ wild-type mice. |
| 6443 | 7522168 | We have tested the susceptibility of these to TNF-induced metabolic changes and lethality in different models, and compared the results with those obtained with IL-6+/+ wild-type mice. |
| 6444 | 7522168 | We have tested the susceptibility of these to TNF-induced metabolic changes and lethality in different models, and compared the results with those obtained with IL-6+/+ wild-type mice. |
| 6445 | 7522168 | We have tested the susceptibility of these to TNF-induced metabolic changes and lethality in different models, and compared the results with those obtained with IL-6+/+ wild-type mice. |
| 6446 | 7522168 | We have tested the susceptibility of these to TNF-induced metabolic changes and lethality in different models, and compared the results with those obtained with IL-6+/+ wild-type mice. |
| 6447 | 7522168 | We have tested the susceptibility of these to TNF-induced metabolic changes and lethality in different models, and compared the results with those obtained with IL-6+/+ wild-type mice. |
| 6448 | 7522168 | Furthermore, IL-6(0/0) mice could be equally well desensitized (by IL-1) to TNF/GalN-induced lethality and tolerized to TNF-induced shock as IL-6+/+ mice. |
| 6449 | 7522168 | Furthermore, IL-6(0/0) mice could be equally well desensitized (by IL-1) to TNF/GalN-induced lethality and tolerized to TNF-induced shock as IL-6+/+ mice. |
| 6450 | 7522168 | Furthermore, IL-6(0/0) mice could be equally well desensitized (by IL-1) to TNF/GalN-induced lethality and tolerized to TNF-induced shock as IL-6+/+ mice. |
| 6451 | 7522168 | Furthermore, IL-6(0/0) mice could be equally well desensitized (by IL-1) to TNF/GalN-induced lethality and tolerized to TNF-induced shock as IL-6+/+ mice. |
| 6452 | 7522168 | Furthermore, IL-6(0/0) mice could be equally well desensitized (by IL-1) to TNF/GalN-induced lethality and tolerized to TNF-induced shock as IL-6+/+ mice. |
| 6453 | 7522168 | Furthermore, IL-6(0/0) mice could be equally well desensitized (by IL-1) to TNF/GalN-induced lethality and tolerized to TNF-induced shock as IL-6+/+ mice. |
| 6454 | 7522168 | Furthermore, IL-6(0/0) mice could be equally well desensitized (by IL-1) to TNF/GalN-induced lethality and tolerized to TNF-induced shock as IL-6+/+ mice. |
| 6455 | 7522168 | We also observed that, in response to turpentine, TNF or IL-1, IL-6(0/0) mice produced significantly less acute phase proteins (APP) than IL-6+/+ mice. |
| 6456 | 7522168 | We also observed that, in response to turpentine, TNF or IL-1, IL-6(0/0) mice produced significantly less acute phase proteins (APP) than IL-6+/+ mice. |
| 6457 | 7522168 | We also observed that, in response to turpentine, TNF or IL-1, IL-6(0/0) mice produced significantly less acute phase proteins (APP) than IL-6+/+ mice. |
| 6458 | 7522168 | We also observed that, in response to turpentine, TNF or IL-1, IL-6(0/0) mice produced significantly less acute phase proteins (APP) than IL-6+/+ mice. |
| 6459 | 7522168 | We also observed that, in response to turpentine, TNF or IL-1, IL-6(0/0) mice produced significantly less acute phase proteins (APP) than IL-6+/+ mice. |
| 6460 | 7522168 | We also observed that, in response to turpentine, TNF or IL-1, IL-6(0/0) mice produced significantly less acute phase proteins (APP) than IL-6+/+ mice. |
| 6461 | 7522168 | We also observed that, in response to turpentine, TNF or IL-1, IL-6(0/0) mice produced significantly less acute phase proteins (APP) than IL-6+/+ mice. |
| 6462 | 7522168 | In IL-6(0/0) mice, less corticosterone was induced by TNF than in the control mice, while the response to adrenocorticotropic hormone was the same. |
| 6463 | 7522168 | In IL-6(0/0) mice, less corticosterone was induced by TNF than in the control mice, while the response to adrenocorticotropic hormone was the same. |
| 6464 | 7522168 | In IL-6(0/0) mice, less corticosterone was induced by TNF than in the control mice, while the response to adrenocorticotropic hormone was the same. |
| 6465 | 7522168 | In IL-6(0/0) mice, less corticosterone was induced by TNF than in the control mice, while the response to adrenocorticotropic hormone was the same. |
| 6466 | 7522168 | In IL-6(0/0) mice, less corticosterone was induced by TNF than in the control mice, while the response to adrenocorticotropic hormone was the same. |
| 6467 | 7522168 | In IL-6(0/0) mice, less corticosterone was induced by TNF than in the control mice, while the response to adrenocorticotropic hormone was the same. |
| 6468 | 7522168 | In IL-6(0/0) mice, less corticosterone was induced by TNF than in the control mice, while the response to adrenocorticotropic hormone was the same. |
| 6469 | 7522168 | The results indicate that IL-6 is not contributing in a major way to the pathogenesis leading to TNF-induced shock, and that neither IL-6 nor the APP studied are essential for a protective feedback system. |
| 6470 | 7522168 | The results indicate that IL-6 is not contributing in a major way to the pathogenesis leading to TNF-induced shock, and that neither IL-6 nor the APP studied are essential for a protective feedback system. |
| 6471 | 7522168 | The results indicate that IL-6 is not contributing in a major way to the pathogenesis leading to TNF-induced shock, and that neither IL-6 nor the APP studied are essential for a protective feedback system. |
| 6472 | 7522168 | The results indicate that IL-6 is not contributing in a major way to the pathogenesis leading to TNF-induced shock, and that neither IL-6 nor the APP studied are essential for a protective feedback system. |
| 6473 | 7522168 | The results indicate that IL-6 is not contributing in a major way to the pathogenesis leading to TNF-induced shock, and that neither IL-6 nor the APP studied are essential for a protective feedback system. |
| 6474 | 7522168 | The results indicate that IL-6 is not contributing in a major way to the pathogenesis leading to TNF-induced shock, and that neither IL-6 nor the APP studied are essential for a protective feedback system. |
| 6475 | 7522168 | The results indicate that IL-6 is not contributing in a major way to the pathogenesis leading to TNF-induced shock, and that neither IL-6 nor the APP studied are essential for a protective feedback system. |
| 6476 | 7520417 | OspA and OspB also induced the production of high levels (40 to 150 ng/ml) of IFN-gamma in cultures of macrophages incubated with interleukin-2 (IL-2)-elicited cells from normal (T and NK cells) and scid (NK cells) mice but not in macrophages or IL-2-elicited cells cultured individually. |
| 6477 | 7520417 | OspA and OspB also induced the production of high levels (40 to 150 ng/ml) of IFN-gamma in cultures of macrophages incubated with interleukin-2 (IL-2)-elicited cells from normal (T and NK cells) and scid (NK cells) mice but not in macrophages or IL-2-elicited cells cultured individually. |
| 6478 | 7520417 | Reverse transcriptase rapid PCR demonstrated that OspA and sonicated B. burgdorferi stimulated production of several inflammatory cytokines in macrophage cultures, including IL-1, IL-6, IL-12, IFN-beta, and tumor necrosis factor alpha. |
| 6479 | 7520417 | Reverse transcriptase rapid PCR demonstrated that OspA and sonicated B. burgdorferi stimulated production of several inflammatory cytokines in macrophage cultures, including IL-1, IL-6, IL-12, IFN-beta, and tumor necrosis factor alpha. |
| 6480 | 7520417 | As tumor necrosis factor alpha, IFN-beta, and IL-12 are potent activators of IFN-gamma production by T and NK cells, their presence in these cocultures could be responsible for the IFN-gamma production. |
| 6481 | 7520417 | As tumor necrosis factor alpha, IFN-beta, and IL-12 are potent activators of IFN-gamma production by T and NK cells, their presence in these cocultures could be responsible for the IFN-gamma production. |
| 6482 | 8056039 | Two patterns of cytokine synthesis were induced by TT: (i) T lymphocytes expressed a number of lymphokines (interleukin (IL)-2, IL-3, IL-4, IL-10, interferon (IFN)-gamma and tumor necrosis factor (TNF)-beta), each with distinct kinetics of synthesis. |
| 6483 | 8056039 | Two patterns of cytokine synthesis were induced by TT: (i) T lymphocytes expressed a number of lymphokines (interleukin (IL)-2, IL-3, IL-4, IL-10, interferon (IFN)-gamma and tumor necrosis factor (TNF)-beta), each with distinct kinetics of synthesis. |
| 6484 | 8056039 | Cells producing IL-2, IFN-gamma and particularly TNF-beta dominated this in vitro response. |
| 6485 | 8056039 | Cells producing IL-2, IFN-gamma and particularly TNF-beta dominated this in vitro response. |
| 6486 | 8056039 | The addition of IL-2 to the cultures caused a fourfold increase and a kinetics shift in the production of TNF-beta, which peaked already at 24 h. |
| 6487 | 8056039 | The addition of IL-2 to the cultures caused a fourfold increase and a kinetics shift in the production of TNF-beta, which peaked already at 24 h. |
| 6488 | 8056039 | Exogenously added IL-2 also caused a five- to tenfold increase in the number of IL-2 and IFN-gamma producers but no apparent change in the kinetics of intracellular lymphokine appearance. |
| 6489 | 8056039 | Exogenously added IL-2 also caused a five- to tenfold increase in the number of IL-2 and IFN-gamma producers but no apparent change in the kinetics of intracellular lymphokine appearance. |
| 6490 | 8056039 | (ii) The cytokines IL-1 alpha, IL-1 beta, IL-6 and TNF-alpha were produced by monocytes. |
| 6491 | 8056039 | (ii) The cytokines IL-1 alpha, IL-1 beta, IL-6 and TNF-alpha were produced by monocytes. |
| 6492 | 7997190 | Our results show that all T cells reactive with bacteria produce interferon-gamma (IFN-gamma) and tumor necrosis factor-alpha (TNF-alpha), but no interleukin (IL)-4 and no or very little IL-2 and IL-10 and, thus, belong to the Th1 subset, while T cells reactive with tetanus toxoid or Anisakis belong to the Th0 subset with production of IFN-gamma, IL-2, IL-4, IL-10 and TNF-alpha. |
| 6493 | 7992547 | [Thymosin alpha-1 and hybrid proteins consisting of tumor necrosis factor-alpha and thymosin alpha-1 enhance the efficacy of vaccination against the causative agent of plague]. |
| 6494 | 7526573 | Characterization of binding and TNF-alpha-inducing ability of chitosans on monocytes: the involvement of CD14. |
| 6495 | 7526573 | Characterization of binding and TNF-alpha-inducing ability of chitosans on monocytes: the involvement of CD14. |
| 6496 | 7526573 | Characterization of binding and TNF-alpha-inducing ability of chitosans on monocytes: the involvement of CD14. |
| 6497 | 7526573 | Monoclonal antibodies against CD14 inhibited TNF-alpha production from monocytes stimulated with neutral-soluble chitosans. |
| 6498 | 7526573 | Monoclonal antibodies against CD14 inhibited TNF-alpha production from monocytes stimulated with neutral-soluble chitosans. |
| 6499 | 7526573 | Monoclonal antibodies against CD14 inhibited TNF-alpha production from monocytes stimulated with neutral-soluble chitosans. |
| 6500 | 7526573 | LPS-binding protein (LBP) enhanced the chitosan-induced TNF-alpha production only to a minor degree, suggesting that serum proteins other than LBP play an important role in the stimulatory effect. |
| 6501 | 7526573 | LPS-binding protein (LBP) enhanced the chitosan-induced TNF-alpha production only to a minor degree, suggesting that serum proteins other than LBP play an important role in the stimulatory effect. |
| 6502 | 7526573 | LPS-binding protein (LBP) enhanced the chitosan-induced TNF-alpha production only to a minor degree, suggesting that serum proteins other than LBP play an important role in the stimulatory effect. |
| 6503 | 7515909 | We have previously described the APO-1 (CD95) cell surface molecule, a novel member of the nerve growth factor/TNF receptor superfamily, identical with the Fas Ag. |
| 6504 | 8205557 | Bacillus Calmette-Guérin potentiates monocyte responses to lipopolysaccharide-induced tumor necrosis factor and interleukin-1, but not interleukin-6 in bladder cancer patients. |
| 6505 | 8205557 | Bacillus Calmette-Guérin potentiates monocyte responses to lipopolysaccharide-induced tumor necrosis factor and interleukin-1, but not interleukin-6 in bladder cancer patients. |
| 6506 | 8205557 | Bacillus Calmette-Guérin potentiates monocyte responses to lipopolysaccharide-induced tumor necrosis factor and interleukin-1, but not interleukin-6 in bladder cancer patients. |
| 6507 | 8205557 | Bacillus Calmette-Guérin potentiates monocyte responses to lipopolysaccharide-induced tumor necrosis factor and interleukin-1, but not interleukin-6 in bladder cancer patients. |
| 6508 | 8205557 | Bacillus Calmette-Guérin potentiates monocyte responses to lipopolysaccharide-induced tumor necrosis factor and interleukin-1, but not interleukin-6 in bladder cancer patients. |
| 6509 | 8205557 | Blood was drawn 2 h after the last instillation, and monocytes were isolated (5 x 10(6) cells/ml) and treated, or not, with lipopolysaccharide (LPS) (20 microgram/ml) for tumor necrosis factor alpha (TNF alpha), interleukin-1 alpha (IL-1 alpha) and interleukin-6 (IL-6) release. |
| 6510 | 8205557 | Blood was drawn 2 h after the last instillation, and monocytes were isolated (5 x 10(6) cells/ml) and treated, or not, with lipopolysaccharide (LPS) (20 microgram/ml) for tumor necrosis factor alpha (TNF alpha), interleukin-1 alpha (IL-1 alpha) and interleukin-6 (IL-6) release. |
| 6511 | 8205557 | Blood was drawn 2 h after the last instillation, and monocytes were isolated (5 x 10(6) cells/ml) and treated, or not, with lipopolysaccharide (LPS) (20 microgram/ml) for tumor necrosis factor alpha (TNF alpha), interleukin-1 alpha (IL-1 alpha) and interleukin-6 (IL-6) release. |
| 6512 | 8205557 | Blood was drawn 2 h after the last instillation, and monocytes were isolated (5 x 10(6) cells/ml) and treated, or not, with lipopolysaccharide (LPS) (20 microgram/ml) for tumor necrosis factor alpha (TNF alpha), interleukin-1 alpha (IL-1 alpha) and interleukin-6 (IL-6) release. |
| 6513 | 8205557 | Blood was drawn 2 h after the last instillation, and monocytes were isolated (5 x 10(6) cells/ml) and treated, or not, with lipopolysaccharide (LPS) (20 microgram/ml) for tumor necrosis factor alpha (TNF alpha), interleukin-1 alpha (IL-1 alpha) and interleukin-6 (IL-6) release. |
| 6514 | 8205557 | Our results clearly show that, after 18 h incubation, macrophages from BCG-treated bladder cancer patients produced from 2.8- to 1.9-fold and from 2.0- to 1.3-fold greater amounts of TNF alpha and IL-1 alpha respectively, compared to macrophages from healthy controls, 5-fold higher than bladder cancer patients not treated with BCG. |
| 6515 | 8205557 | Our results clearly show that, after 18 h incubation, macrophages from BCG-treated bladder cancer patients produced from 2.8- to 1.9-fold and from 2.0- to 1.3-fold greater amounts of TNF alpha and IL-1 alpha respectively, compared to macrophages from healthy controls, 5-fold higher than bladder cancer patients not treated with BCG. |
| 6516 | 8205557 | Our results clearly show that, after 18 h incubation, macrophages from BCG-treated bladder cancer patients produced from 2.8- to 1.9-fold and from 2.0- to 1.3-fold greater amounts of TNF alpha and IL-1 alpha respectively, compared to macrophages from healthy controls, 5-fold higher than bladder cancer patients not treated with BCG. |
| 6517 | 8205557 | Our results clearly show that, after 18 h incubation, macrophages from BCG-treated bladder cancer patients produced from 2.8- to 1.9-fold and from 2.0- to 1.3-fold greater amounts of TNF alpha and IL-1 alpha respectively, compared to macrophages from healthy controls, 5-fold higher than bladder cancer patients not treated with BCG. |
| 6518 | 8205557 | Our results clearly show that, after 18 h incubation, macrophages from BCG-treated bladder cancer patients produced from 2.8- to 1.9-fold and from 2.0- to 1.3-fold greater amounts of TNF alpha and IL-1 alpha respectively, compared to macrophages from healthy controls, 5-fold higher than bladder cancer patients not treated with BCG. |
| 6519 | 8205557 | In another set of experiments macrophages (5 x 10(6) cells/ml) from healthy subjects were pretreated, or not, with BCG (100 micrograms/ml) overnight and treated, or not, with LPS 20 microgram/ml alone and in combination with interleukin-1 receptor antagonist (IL-1ra) 250 ng/ml. |
| 6520 | 8205557 | In another set of experiments macrophages (5 x 10(6) cells/ml) from healthy subjects were pretreated, or not, with BCG (100 micrograms/ml) overnight and treated, or not, with LPS 20 microgram/ml alone and in combination with interleukin-1 receptor antagonist (IL-1ra) 250 ng/ml. |
| 6521 | 8205557 | In another set of experiments macrophages (5 x 10(6) cells/ml) from healthy subjects were pretreated, or not, with BCG (100 micrograms/ml) overnight and treated, or not, with LPS 20 microgram/ml alone and in combination with interleukin-1 receptor antagonist (IL-1ra) 250 ng/ml. |
| 6522 | 8205557 | In another set of experiments macrophages (5 x 10(6) cells/ml) from healthy subjects were pretreated, or not, with BCG (100 micrograms/ml) overnight and treated, or not, with LPS 20 microgram/ml alone and in combination with interleukin-1 receptor antagonist (IL-1ra) 250 ng/ml. |
| 6523 | 8205557 | In another set of experiments macrophages (5 x 10(6) cells/ml) from healthy subjects were pretreated, or not, with BCG (100 micrograms/ml) overnight and treated, or not, with LPS 20 microgram/ml alone and in combination with interleukin-1 receptor antagonist (IL-1ra) 250 ng/ml. |
| 6524 | 8205557 | The addition of IL-1ra (250 ng/ml) to BCG was not effective, while when IL-1ra was added to BCG plus LPS only a partial inhibition of IL-1 alpha release was found (9.83 ng/ml), compared to BCG plus LPS without IL-1ra (13.71 ng/ml). |
| 6525 | 8205557 | The addition of IL-1ra (250 ng/ml) to BCG was not effective, while when IL-1ra was added to BCG plus LPS only a partial inhibition of IL-1 alpha release was found (9.83 ng/ml), compared to BCG plus LPS without IL-1ra (13.71 ng/ml). |
| 6526 | 8205557 | The addition of IL-1ra (250 ng/ml) to BCG was not effective, while when IL-1ra was added to BCG plus LPS only a partial inhibition of IL-1 alpha release was found (9.83 ng/ml), compared to BCG plus LPS without IL-1ra (13.71 ng/ml). |
| 6527 | 8205557 | The addition of IL-1ra (250 ng/ml) to BCG was not effective, while when IL-1ra was added to BCG plus LPS only a partial inhibition of IL-1 alpha release was found (9.83 ng/ml), compared to BCG plus LPS without IL-1ra (13.71 ng/ml). |
| 6528 | 8205557 | The addition of IL-1ra (250 ng/ml) to BCG was not effective, while when IL-1ra was added to BCG plus LPS only a partial inhibition of IL-1 alpha release was found (9.83 ng/ml), compared to BCG plus LPS without IL-1ra (13.71 ng/ml). |
| 6529 | 8205557 | The priming effect of BCG exerted on LPS-stimulated monocyte production of TNF alpha and IL-1 alpha from bladder cancer patients led us to study the possible modulation of fibrinogen and C-reactive protein in the serum of BCG-treated cancer patients. |
| 6530 | 8205557 | The priming effect of BCG exerted on LPS-stimulated monocyte production of TNF alpha and IL-1 alpha from bladder cancer patients led us to study the possible modulation of fibrinogen and C-reactive protein in the serum of BCG-treated cancer patients. |
| 6531 | 8205557 | The priming effect of BCG exerted on LPS-stimulated monocyte production of TNF alpha and IL-1 alpha from bladder cancer patients led us to study the possible modulation of fibrinogen and C-reactive protein in the serum of BCG-treated cancer patients. |
| 6532 | 8205557 | The priming effect of BCG exerted on LPS-stimulated monocyte production of TNF alpha and IL-1 alpha from bladder cancer patients led us to study the possible modulation of fibrinogen and C-reactive protein in the serum of BCG-treated cancer patients. |
| 6533 | 8205557 | The priming effect of BCG exerted on LPS-stimulated monocyte production of TNF alpha and IL-1 alpha from bladder cancer patients led us to study the possible modulation of fibrinogen and C-reactive protein in the serum of BCG-treated cancer patients. |
| 6534 | 8205557 | We conclude that the beneficial immunotherapeutic effects of BCG in bladder cancer patients are related to its capacity to prime macrophages to enhance the release of TNF alpha and IL-1 alpha, but not IL-6 in response to physiological secondary stimuli, or through the direct stimulation of BCG on IL-1 alpha or TNF alpha, which are directly involved in the killing of cancer cells. |
| 6535 | 8205557 | We conclude that the beneficial immunotherapeutic effects of BCG in bladder cancer patients are related to its capacity to prime macrophages to enhance the release of TNF alpha and IL-1 alpha, but not IL-6 in response to physiological secondary stimuli, or through the direct stimulation of BCG on IL-1 alpha or TNF alpha, which are directly involved in the killing of cancer cells. |
| 6536 | 8205557 | We conclude that the beneficial immunotherapeutic effects of BCG in bladder cancer patients are related to its capacity to prime macrophages to enhance the release of TNF alpha and IL-1 alpha, but not IL-6 in response to physiological secondary stimuli, or through the direct stimulation of BCG on IL-1 alpha or TNF alpha, which are directly involved in the killing of cancer cells. |
| 6537 | 8205557 | We conclude that the beneficial immunotherapeutic effects of BCG in bladder cancer patients are related to its capacity to prime macrophages to enhance the release of TNF alpha and IL-1 alpha, but not IL-6 in response to physiological secondary stimuli, or through the direct stimulation of BCG on IL-1 alpha or TNF alpha, which are directly involved in the killing of cancer cells. |
| 6538 | 8205557 | We conclude that the beneficial immunotherapeutic effects of BCG in bladder cancer patients are related to its capacity to prime macrophages to enhance the release of TNF alpha and IL-1 alpha, but not IL-6 in response to physiological secondary stimuli, or through the direct stimulation of BCG on IL-1 alpha or TNF alpha, which are directly involved in the killing of cancer cells. |
| 6539 | 7927991 | The mediators produced by monocytes and macrophages (TNF, IL-1) are known to exert a protective effect when given early at the beginning of infection. |
| 6540 | 8170078 | [A study of the mechanism of action of BCG against transitional cell carcinoma of the bladder--the change of TNF-alpha and IL-2 in the serum and urine]. |
| 6541 | 8170078 | [A study of the mechanism of action of BCG against transitional cell carcinoma of the bladder--the change of TNF-alpha and IL-2 in the serum and urine]. |
| 6542 | 8170078 | [A study of the mechanism of action of BCG against transitional cell carcinoma of the bladder--the change of TNF-alpha and IL-2 in the serum and urine]. |
| 6543 | 8170078 | To study the mechanism of action of BCG against transitional cell carcinoma of the bladder from the immunological standpoint, we observed time-course changes in the serum and urine levels of tumor necrosis factor (TNF-alpha) and interleukin-2 (IL-2) before and after an intravesical BCG instillation in 16 patients with superficialis transitional cell carcinoma. |
| 6544 | 8170078 | To study the mechanism of action of BCG against transitional cell carcinoma of the bladder from the immunological standpoint, we observed time-course changes in the serum and urine levels of tumor necrosis factor (TNF-alpha) and interleukin-2 (IL-2) before and after an intravesical BCG instillation in 16 patients with superficialis transitional cell carcinoma. |
| 6545 | 8170078 | To study the mechanism of action of BCG against transitional cell carcinoma of the bladder from the immunological standpoint, we observed time-course changes in the serum and urine levels of tumor necrosis factor (TNF-alpha) and interleukin-2 (IL-2) before and after an intravesical BCG instillation in 16 patients with superficialis transitional cell carcinoma. |
| 6546 | 8170078 | Thus, the present study failed to demonstrate the involvement of a direct action of TNF-alpha, activation of immunological cells by IL-2 or its direct action as an anti-tumor effect of intravesical instillation of BCG. |
| 6547 | 8170078 | Thus, the present study failed to demonstrate the involvement of a direct action of TNF-alpha, activation of immunological cells by IL-2 or its direct action as an anti-tumor effect of intravesical instillation of BCG. |
| 6548 | 8170078 | Thus, the present study failed to demonstrate the involvement of a direct action of TNF-alpha, activation of immunological cells by IL-2 or its direct action as an anti-tumor effect of intravesical instillation of BCG. |
| 6549 | 8126987 | As for the cytokines, interleukin-2, granulocyte macrophage-colony stimulating factor, and tumor necrosis factor have very strong antimycobacterial activity. |
| 6550 | 8116114 | Detection of urinary interleukin-2, interleukin-2 receptor, and tumor necrosis factor levels in patients with superficial bladder tumors after intravesical BCG immunotherapy. |
| 6551 | 8113740 | Modulation of antiviral immune responses by exogenous cytokines: effects of tumour necrosis factor-alpha, interleukin-1 alpha, interleukin-2 and interferon-gamma on the immunogenicity of an inactivated rabies vaccine. |
| 6552 | 8113740 | Modulation of antiviral immune responses by exogenous cytokines: effects of tumour necrosis factor-alpha, interleukin-1 alpha, interleukin-2 and interferon-gamma on the immunogenicity of an inactivated rabies vaccine. |
| 6553 | 8113740 | We investigated the effects of tumour necrosis factor-alpha (TNF-alpha), interleukin-1 alpha (IL-1 alpha), interleukin-2 (IL-2) and interferon-gamma (IFN-gamma) on the immune response elicited by inactivated rabies virus vaccine in a mouse model. |
| 6554 | 8113740 | We investigated the effects of tumour necrosis factor-alpha (TNF-alpha), interleukin-1 alpha (IL-1 alpha), interleukin-2 (IL-2) and interferon-gamma (IFN-gamma) on the immune response elicited by inactivated rabies virus vaccine in a mouse model. |
| 6555 | 8113740 | A single dose of 1.3 ng TNF-alpha or IL-1 alpha, when injected shortly before vaccination, only marginally stimulated resistance to challenge infection (four- and seven-fold, respectively) without enhancing virus neutralizing antibody (VNAb) responses. |
| 6556 | 8113740 | A single dose of 1.3 ng TNF-alpha or IL-1 alpha, when injected shortly before vaccination, only marginally stimulated resistance to challenge infection (four- and seven-fold, respectively) without enhancing virus neutralizing antibody (VNAb) responses. |
| 6557 | 8113740 | In contrast, a single injection of 10(3) units of IFN-gamma or five daily injections of 1.6 micrograms IL-2 increased vaccine dilutions protecting 50% of mice (PD50 values) 77- to 50-fold, respectively, with a concomitant enhancement of VNAb. |
| 6558 | 8113740 | In contrast, a single injection of 10(3) units of IFN-gamma or five daily injections of 1.6 micrograms IL-2 increased vaccine dilutions protecting 50% of mice (PD50 values) 77- to 50-fold, respectively, with a concomitant enhancement of VNAb. |
| 6559 | 8113740 | At a 1:10,000 dilution of a standard inactivated rabies vaccine preparation both IFN-gamma and IL-2 increased protective immunity without enhancing VNAb responses; in non-vaccinated animals this treatment had no effect on resistance to challenge. |
| 6560 | 8113740 | At a 1:10,000 dilution of a standard inactivated rabies vaccine preparation both IFN-gamma and IL-2 increased protective immunity without enhancing VNAb responses; in non-vaccinated animals this treatment had no effect on resistance to challenge. |
| 6561 | 8113740 | Combined administration of IFN-gamma and IL-2 synergistically enhanced VNAb responses. |
| 6562 | 8113740 | Combined administration of IFN-gamma and IL-2 synergistically enhanced VNAb responses. |
| 6563 | 7958061 | A complex pattern of tumour infiltrating cells has been observed in TNF-producing tumours consisting of macrophages, CD4+ and CD8+ T cells. |
| 6564 | 7958061 | For tumour suppression macrophages and CD8+ T cells are needed whereas CD4+ T cells seem to reflect innocent bystander cells. |
| 6565 | 7865356 | An increasing body of work utilizing recombinant versions of interleukin-1, -2, -3, -6, -12, gamma-interferon, tumor necrosis factor, and granulocyte-monocyte-colony stimulating factor has shown that cytokines do have vaccine adjuvant activity. |
| 6566 | 16843333 | The in vitro production of interleukin-1 and interleukin-6 from whole blood was suppressed by fish oil supplementation, however, production of tumor necrosis factor alpha was not significantly altered. |
| 6567 | 16843333 | Fish oil supplementation may therefore provide a non-pharmacological approach of attenuating several of the responses associated with injury and infection and this may be related to reduced cytokine (IL-1 and IL-6) production. |
| 6568 | 8230540 | We found that none of the cytokines interleukin-1, interleukin-2, interferon-gamma, tumor necrosis factor alpha, lymphotoxin, or BCG alone were cytotoxic against the bladder carcinoma cell lines. |
| 6569 | 8288319 | IL-1 and tumour necrosis factor-alpha (TNF-alpha) remained undetectable in both instances. |
| 6570 | 8288319 | IL-1 and tumour necrosis factor-alpha (TNF-alpha) remained undetectable in both instances. |
| 6571 | 8288319 | Spleen cells taken at intervals after infection and cultured with brucella antigens produced high titres of IL-6, IL-1 and TNF-alpha. |
| 6572 | 8288319 | Spleen cells taken at intervals after infection and cultured with brucella antigens produced high titres of IL-6, IL-1 and TNF-alpha. |
| 6573 | 8288319 | Of the characteristically T-cell-derived lymphokines, interferon-gamma (IFN-gamma) production rose 2 weeks after infection, peaking at 6 weeks, while IL-2 was not detected until 6 weeks post-infection. |
| 6574 | 8288319 | Of the characteristically T-cell-derived lymphokines, interferon-gamma (IFN-gamma) production rose 2 weeks after infection, peaking at 6 weeks, while IL-2 was not detected until 6 weeks post-infection. |
| 6575 | 8288319 | Granulocyte-macrophage colony-stimulating factor (GM-CSF) was produced in substantial amounts, but IL-3 production was minimal. |
| 6576 | 8288319 | Granulocyte-macrophage colony-stimulating factor (GM-CSF) was produced in substantial amounts, but IL-3 production was minimal. |
| 6577 | 8288319 | In contrast, spleen cells from mice immunized with SBP produced IL-2 but failed to produce IFN-gamma. |
| 6578 | 8288319 | In contrast, spleen cells from mice immunized with SBP produced IL-2 but failed to produce IFN-gamma. |
| 6579 | 8242663 | Interleukin-4 plus tumor necrosis factor alpha augments the antigenicity of melanoma cells. |
| 6580 | 8242663 | Interleukin-4 plus tumor necrosis factor alpha augments the antigenicity of melanoma cells. |
| 6581 | 8242663 | Interleukin-4 plus tumor necrosis factor alpha augments the antigenicity of melanoma cells. |
| 6582 | 8242663 | Interleukin-4 plus tumor necrosis factor alpha augments the antigenicity of melanoma cells. |
| 6583 | 8242663 | Interleukin-4 plus tumor necrosis factor alpha augments the antigenicity of melanoma cells. |
| 6584 | 8242663 | Interleukin-4 plus tumor necrosis factor alpha augments the antigenicity of melanoma cells. |
| 6585 | 8242663 | We previously reported that interleukin 4 (IL-4) and either tumor necrosis factor alpha (TNF) or interferon gamma (IFN) synergistically inhibit melanoma cell growth and induce cell differentiation. |
| 6586 | 8242663 | We previously reported that interleukin 4 (IL-4) and either tumor necrosis factor alpha (TNF) or interferon gamma (IFN) synergistically inhibit melanoma cell growth and induce cell differentiation. |
| 6587 | 8242663 | We previously reported that interleukin 4 (IL-4) and either tumor necrosis factor alpha (TNF) or interferon gamma (IFN) synergistically inhibit melanoma cell growth and induce cell differentiation. |
| 6588 | 8242663 | We previously reported that interleukin 4 (IL-4) and either tumor necrosis factor alpha (TNF) or interferon gamma (IFN) synergistically inhibit melanoma cell growth and induce cell differentiation. |
| 6589 | 8242663 | We previously reported that interleukin 4 (IL-4) and either tumor necrosis factor alpha (TNF) or interferon gamma (IFN) synergistically inhibit melanoma cell growth and induce cell differentiation. |
| 6590 | 8242663 | We previously reported that interleukin 4 (IL-4) and either tumor necrosis factor alpha (TNF) or interferon gamma (IFN) synergistically inhibit melanoma cell growth and induce cell differentiation. |
| 6591 | 8242663 | In the present study we used various combinations of IL-4, IFN and TNF to enhance the antigenicity of melanoma cells. |
| 6592 | 8242663 | In the present study we used various combinations of IL-4, IFN and TNF to enhance the antigenicity of melanoma cells. |
| 6593 | 8242663 | In the present study we used various combinations of IL-4, IFN and TNF to enhance the antigenicity of melanoma cells. |
| 6594 | 8242663 | In the present study we used various combinations of IL-4, IFN and TNF to enhance the antigenicity of melanoma cells. |
| 6595 | 8242663 | In the present study we used various combinations of IL-4, IFN and TNF to enhance the antigenicity of melanoma cells. |
| 6596 | 8242663 | In the present study we used various combinations of IL-4, IFN and TNF to enhance the antigenicity of melanoma cells. |
| 6597 | 8242663 | IL-4 plus TNF significantly increased the ability of melanoma cells to stimulate cytotoxic T cells (CTL) and act as targets of these CTL; IL-4 plus IFN was somewhat less effective, while TNF plus IFN was not as effective. |
| 6598 | 8242663 | IL-4 plus TNF significantly increased the ability of melanoma cells to stimulate cytotoxic T cells (CTL) and act as targets of these CTL; IL-4 plus IFN was somewhat less effective, while TNF plus IFN was not as effective. |
| 6599 | 8242663 | IL-4 plus TNF significantly increased the ability of melanoma cells to stimulate cytotoxic T cells (CTL) and act as targets of these CTL; IL-4 plus IFN was somewhat less effective, while TNF plus IFN was not as effective. |
| 6600 | 8242663 | IL-4 plus TNF significantly increased the ability of melanoma cells to stimulate cytotoxic T cells (CTL) and act as targets of these CTL; IL-4 plus IFN was somewhat less effective, while TNF plus IFN was not as effective. |
| 6601 | 8242663 | IL-4 plus TNF significantly increased the ability of melanoma cells to stimulate cytotoxic T cells (CTL) and act as targets of these CTL; IL-4 plus IFN was somewhat less effective, while TNF plus IFN was not as effective. |
| 6602 | 8242663 | IL-4 plus TNF significantly increased the ability of melanoma cells to stimulate cytotoxic T cells (CTL) and act as targets of these CTL; IL-4 plus IFN was somewhat less effective, while TNF plus IFN was not as effective. |
| 6603 | 8242663 | IL-4 plus TNF also increased the expression of HLA class I and HLA-DR antigens on melanoma cells. |
| 6604 | 8242663 | IL-4 plus TNF also increased the expression of HLA class I and HLA-DR antigens on melanoma cells. |
| 6605 | 8242663 | IL-4 plus TNF also increased the expression of HLA class I and HLA-DR antigens on melanoma cells. |
| 6606 | 8242663 | IL-4 plus TNF also increased the expression of HLA class I and HLA-DR antigens on melanoma cells. |
| 6607 | 8242663 | IL-4 plus TNF also increased the expression of HLA class I and HLA-DR antigens on melanoma cells. |
| 6608 | 8242663 | IL-4 plus TNF also increased the expression of HLA class I and HLA-DR antigens on melanoma cells. |
| 6609 | 8242663 | These preclinical results suggest that the immune response to melanoma whole-cell vaccines might be enhanced by pretreating vaccine cells with IL-4 plus TNF. |
| 6610 | 8242663 | These preclinical results suggest that the immune response to melanoma whole-cell vaccines might be enhanced by pretreating vaccine cells with IL-4 plus TNF. |
| 6611 | 8242663 | These preclinical results suggest that the immune response to melanoma whole-cell vaccines might be enhanced by pretreating vaccine cells with IL-4 plus TNF. |
| 6612 | 8242663 | These preclinical results suggest that the immune response to melanoma whole-cell vaccines might be enhanced by pretreating vaccine cells with IL-4 plus TNF. |
| 6613 | 8242663 | These preclinical results suggest that the immune response to melanoma whole-cell vaccines might be enhanced by pretreating vaccine cells with IL-4 plus TNF. |
| 6614 | 8242663 | These preclinical results suggest that the immune response to melanoma whole-cell vaccines might be enhanced by pretreating vaccine cells with IL-4 plus TNF. |
| 6615 | 7906131 | Enhancement of HIV-1 gene expression was observed with supernatants from CD4+ CTL clones and with supernatants from a subset of CD8+ CTL clones. |
| 6616 | 7906131 | CD4+ and CD8+ CTLs that released TNF-alpha on antigen stimulation were also shown to express a biologically active 26-kDa transmembrane form of TNF-alpha, which was sufficient to induce upregulation of HIV-1 gene expression in chronically infected T cells placed in direct contact with the CTLs. |
| 6617 | 7906131 | Supernatants from antigen-activated, vaccine-induced CD4+ and CD8+ CTLs also caused upregulation of HIV-1 gene expression in chronically infected promonocytic cells. |
| 6618 | 7906131 | A subset of CD8+ CTL clones also produced a soluble factor(s) that inhibited HIV-1 replication in acutely infected autologous CD4+ blasts. |
| 6619 | 8406812 | Cytochrome P-450 (P-450) levels were inhibited more than 50% at 7 days following a single injection of PT mixed with either vaccine. |
| 6620 | 8406812 | Cytochrome P-450 (P-450) levels were inhibited more than 50% at 7 days following a single injection of PT mixed with either vaccine. |
| 6621 | 8406812 | Alterations of P-450 levels were accompanied by increased activities of quinone reductase but not with changes in plasma interleukin-6 or tumor necrosis factor levels. |
| 6622 | 8406812 | Alterations of P-450 levels were accompanied by increased activities of quinone reductase but not with changes in plasma interleukin-6 or tumor necrosis factor levels. |
| 6623 | 8406812 | Endotoxin or preparations containing endotoxin caused alterations in hepatic drug metabolism within 24 h, concomitant with increased interleukin-6 and tumor necrosis factor levels, but these effects had resolved by 1 week. |
| 6624 | 8406812 | Endotoxin or preparations containing endotoxin caused alterations in hepatic drug metabolism within 24 h, concomitant with increased interleukin-6 and tumor necrosis factor levels, but these effects had resolved by 1 week. |
| 6625 | 8359905 | OspA and OspB also stimulated the production of IL-6 and tumor necrosis factor alpha by bone marrow-derived macrophages from BALB/c and C3H/HeJ mice. |
| 6626 | 8142603 | Data suggest that although the EIA kits that were evaluated for human IL-1 alpha, IFN-gamma, and TNF-beta failed, the EIA kits for IL-1 beta, IL-2, IL-4, IL-6, and TNF-alpha, the bioassays and RT-PCR assays for each of the cytokines were successful in detection and most likely quantitation of the non-human primate cytokine homologues. |
| 6627 | 7692655 | In the treatment of advanced renal cell carcinoma, cytokines such as interferons, interleukin-2, tumor necrosis factor and immune therapy with autologous tumor cells and tumor cell vaccines have been tested on a large scale. |
| 6628 | 7692655 | In the treatment of advanced renal cell carcinoma, cytokines such as interferons, interleukin-2, tumor necrosis factor and immune therapy with autologous tumor cells and tumor cell vaccines have been tested on a large scale. |
| 6629 | 7692655 | Immunotherapy with interferons, interleukin-2, tumor necrosis factor, autologous tumor cells or tumor cell vaccines has to be regarded as experimental. |
| 6630 | 7692655 | Immunotherapy with interferons, interleukin-2, tumor necrosis factor, autologous tumor cells or tumor cell vaccines has to be regarded as experimental. |
| 6631 | 8357078 | No detectable fluctuations were observed in circulating levels of tumor necrosis factor, interferon-gamma, or interleukin-6 during the course of this study. |
| 6632 | 8244448 | IL-1, TNF-alpha and IL-2 production by peritoneal and spleen cells from Schistosoma mansoni infected mice and its potentiation by preimmunization with schistosomal antigens and immunostimulants. |
| 6633 | 8244448 | IL-1, TNF-alpha and IL-2 production by peritoneal and spleen cells from Schistosoma mansoni infected mice and its potentiation by preimmunization with schistosomal antigens and immunostimulants. |
| 6634 | 8244448 | Peritoneal and spleen macrophages from immunostimulant treated and/or immunized animals showed a significant increase in LPS triggered TNF-alpha production, as compared to non-treated controls. |
| 6635 | 8244448 | Peritoneal and spleen macrophages from immunostimulant treated and/or immunized animals showed a significant increase in LPS triggered TNF-alpha production, as compared to non-treated controls. |
| 6636 | 8319241 | The results were compared with the cytotoxicity exerted by lymphokine-activated killer (LAK) cells generated by interleukin-2 (IL-2) and interferon gamma (IFN gamma). |
| 6637 | 8319241 | BCG-stimulated PBMC showed a cytotoxic potential against BT-A and BT-B comparable to that of IFN gamma-generated LAK cells, but this did not reach the level of IL-2-generated LAK cells. |
| 6638 | 8319241 | We could demonstrate the presence of the cytokines IFN gamma, IL-2, tumour necrosis factor alpha (TNF alpha) and TNF beta in the supernatants harvested during the generation of BAK cells. |
| 6639 | 8319241 | The cells effective in BCG-activated killing of bladder tumour cells could be localized within the CD8+/CD56+ lymphocyte subset. |
| 6640 | 8319241 | Our findings imply that the activation by BCG of CD8+/CD56+ killer cells might be an important antitumoral mechanism during BCG therapy against superficial urothelial bladder cancer. |
| 6641 | 7690109 | Effects of bacillus of Calmette-Guerin, Candida albicans and human recombinant interferon-gamma on RNA metabolism and on in vitro release of tumor necrosis factor-alpha by human monocytes/macrophages. |
| 6642 | 8486931 | Characterization of human tumor cell lines transduced with the cDNA encoding either tumor necrosis factor alpha (TNF-a) or interleukin-2 (IL-2). |
| 6643 | 8486931 | Characterization of human tumor cell lines transduced with the cDNA encoding either tumor necrosis factor alpha (TNF-a) or interleukin-2 (IL-2). |
| 6644 | 8486931 | Characterization of human tumor cell lines transduced with the cDNA encoding either tumor necrosis factor alpha (TNF-a) or interleukin-2 (IL-2). |
| 6645 | 8486931 | The tumor cell lines were transduced using retroviruses encoding neomycin phosphotransferase and either human tumor necrosis factor alpha (TNF-alpha) or interleukin-2 (IL-2). |
| 6646 | 8486931 | The tumor cell lines were transduced using retroviruses encoding neomycin phosphotransferase and either human tumor necrosis factor alpha (TNF-alpha) or interleukin-2 (IL-2). |
| 6647 | 8486931 | The tumor cell lines were transduced using retroviruses encoding neomycin phosphotransferase and either human tumor necrosis factor alpha (TNF-alpha) or interleukin-2 (IL-2). |
| 6648 | 8486931 | The amount of specific cytokine produced per 10(5) transduced tumor cells in 24 h ranged from 0.2 ng to 5.8 ng of TNF-alpha for the TNF transduced lines and from 0.1 ng to 3.6 ng of IL-2 for the IL-2 transduced tumor cell lines. |
| 6649 | 8486931 | The amount of specific cytokine produced per 10(5) transduced tumor cells in 24 h ranged from 0.2 ng to 5.8 ng of TNF-alpha for the TNF transduced lines and from 0.1 ng to 3.6 ng of IL-2 for the IL-2 transduced tumor cell lines. |
| 6650 | 8486931 | The amount of specific cytokine produced per 10(5) transduced tumor cells in 24 h ranged from 0.2 ng to 5.8 ng of TNF-alpha for the TNF transduced lines and from 0.1 ng to 3.6 ng of IL-2 for the IL-2 transduced tumor cell lines. |
| 6651 | 8519092 | There was no change in the proportion of PBMC that were CD4+ T cells, CD8+ T cells, NK cells, or B cells as analyzed by flow cytometry. |
| 6652 | 8519092 | Analysis for cytokines after vaccination showed spontaneous production of high levels of IL-4 (vaccinees 99 +/- 23; controls 5.6 +/- 5.6 ng/ml, P = 0.031) and TNF alpha (vaccinees 140 +/- 45; controls 42 +/- 14 pg/ml, P = 0.072) accompanied by low levels of IFN-gamma (vaccinees 1.3 +/- 0.6; controls 14.3 +/- 10.1 U/ml), IL-1 alpha (vaccinees 111 +/- 22; controls 442 +/- 107 pg/ml, P = 0.0001), and PGE2 (vaccinees 75 +/- 39; controls 300 +/- 72 pg/ml, P = 0.048). |
| 6653 | 8519092 | Increased amounts of IL-4 were also produced after stimulation with PHA (vaccinees 140 +/- 25; controls 40 +/- 40 ng/ml, P = 0.013) while levels of IFN-gamma and soluble IL-2 receptor were similar to controls and levels of IL-1 alpha (vaccinees 443 +/- 67; controls 792 +/- 118 pg/ml, P = 0.026) remained low. |
| 6654 | 8378590 | No correlation was found between the effect of BCG on the development of lesions induced by L. major and the amounts of IFN gamma, IL5 and TNF produced after in vitro antigenic challenge of either draining lymph node or spleen cells, the antigenic challenge being either live BCG or live L. major. |
| 6655 | 7684167 | In the past, cytokines such as interferons, IL-2, and TNF have been tested on a large scale in the treatment of advanced renal cell carcinoma. |
| 6656 | 7684167 | The combination of IFN-alpha and IL-2 by subcutaneous administration appears to provide results similar to those of other treatment modalities with lower morbidity. |
| 6657 | 7681081 | Ag presentation to these T cell clones was enhanced by pretreatment of THP-1 cells with IFN-gamma but not TNF-alpha. |
| 6658 | 7679048 | The potential of tumor cells (J558L) engineered to produce one of 5 different cytokines (interleukin 2, interleukin 4, interleukin 7, tumor necrosis factor, or gamma-interferon) to give rise to systemic immunity protective against a contralateral challenge with the parental cells was analyzed. |
| 6659 | 8094096 | We also detected cytokines in the skin lesions: (1) interleukin-1 alpha and tumor necrosis factor alpha were strongly positive in all patients with acute Kawasaki disease, (2) interleukin-2 and interferon gamma were weakly or partially positive, (3) no cytokines were detected in the convalescent phase, and (4) the amounts of cytokines at the site of BCG vaccine inoculations were larger than those at the site of the polymorphous exanthem. |
| 6660 | 8094096 | We also detected cytokines in the skin lesions: (1) interleukin-1 alpha and tumor necrosis factor alpha were strongly positive in all patients with acute Kawasaki disease, (2) interleukin-2 and interferon gamma were weakly or partially positive, (3) no cytokines were detected in the convalescent phase, and (4) the amounts of cytokines at the site of BCG vaccine inoculations were larger than those at the site of the polymorphous exanthem. |
| 6661 | 8094096 | These findings suggest that CD4+ T lymphocytes and CD13+ macrophages are activated and interleukin-1 alpha and tumor necrosis factor alpha may be involved in the pathogenesis of the inflammation of acute Kawasaki disease. |
| 6662 | 8094096 | These findings suggest that CD4+ T lymphocytes and CD13+ macrophages are activated and interleukin-1 alpha and tumor necrosis factor alpha may be involved in the pathogenesis of the inflammation of acute Kawasaki disease. |
| 6663 | 8514204 | Expression of the cytokines interleukin-1, interleukin-6 and tumor necrosis factor, the cell adhesion molecules ICAM-1 and LFA-3 and the class II major histocompatibility molecule HLA-DR by monocytes from the elderly and young subjects was similar. |
| 6664 | 8418196 | The parasite GPI moiety, free or associated with protein, induces tumor necrosis factor and interleukin 1 production by macrophages and regulates glucose metabolism in adipocytes. |
| 6665 | 8279092 | A 24-h treatment of T24 cells with BCG resulted in a tenfold higher secretion of interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF alpha) when compared with T24 cells treated with Escherichia coli, Streptococcus faecalis or a cell wall preparation of Nocardia rubra (N-CWS). |
| 6666 | 8279092 | A 24-h treatment of T24 cells with BCG resulted in a tenfold higher secretion of interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF alpha) when compared with T24 cells treated with Escherichia coli, Streptococcus faecalis or a cell wall preparation of Nocardia rubra (N-CWS). |
| 6667 | 8279092 | A 24-h treatment of T24 cells with BCG resulted in a tenfold higher secretion of interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF alpha) when compared with T24 cells treated with Escherichia coli, Streptococcus faecalis or a cell wall preparation of Nocardia rubra (N-CWS). |
| 6668 | 8279092 | No secretion of IL-1 beta and IL-2 was detected. |
| 6669 | 8279092 | No secretion of IL-1 beta and IL-2 was detected. |
| 6670 | 8279092 | No secretion of IL-1 beta and IL-2 was detected. |
| 6671 | 8279092 | Pre-exposing T24 cells to BCG for various periods of time indicated that a minimum exposure time of 0.5-1 h was required to upregulate IL-6 and TNF alpha production. |
| 6672 | 8279092 | Pre-exposing T24 cells to BCG for various periods of time indicated that a minimum exposure time of 0.5-1 h was required to upregulate IL-6 and TNF alpha production. |
| 6673 | 8279092 | Pre-exposing T24 cells to BCG for various periods of time indicated that a minimum exposure time of 0.5-1 h was required to upregulate IL-6 and TNF alpha production. |
| 6674 | 8279092 | The amounts of these cytokines secreted in the presence of BCG-conditioned medium did not differ significantly from the constitutively secreted amounts, excluding an effect of products possibly secreted by BCG on the upregulation of IL-6 and TNF alpha. |
| 6675 | 8279092 | The amounts of these cytokines secreted in the presence of BCG-conditioned medium did not differ significantly from the constitutively secreted amounts, excluding an effect of products possibly secreted by BCG on the upregulation of IL-6 and TNF alpha. |
| 6676 | 8279092 | The amounts of these cytokines secreted in the presence of BCG-conditioned medium did not differ significantly from the constitutively secreted amounts, excluding an effect of products possibly secreted by BCG on the upregulation of IL-6 and TNF alpha. |
| 6677 | 8171765 | Albumin and the cytokines interleukin (IL)1 beta, IL2, IL6, and tumor necrosis factor alpha (TNF alpha) were determined in urine from 20 patients treated with 6 weekly intravesical BCG instillations, collected prior to each instillation and 2, 4, 6, 8, 12, and 24 h thereafter. |
| 6678 | 8171765 | Albumin and the cytokines interleukin (IL)1 beta, IL2, IL6, and tumor necrosis factor alpha (TNF alpha) were determined in urine from 20 patients treated with 6 weekly intravesical BCG instillations, collected prior to each instillation and 2, 4, 6, 8, 12, and 24 h thereafter. |
| 6679 | 8171765 | A significant correlation between albumin and concentration of the cytokines IL1 beta, IL2, IL6, and TNF alpha was found (P < 0.01), correlation coefficients (r) being 0.56, 0.56, 0.67, and 0.71 (n = 418), respectively. |
| 6680 | 8171765 | A significant correlation between albumin and concentration of the cytokines IL1 beta, IL2, IL6, and TNF alpha was found (P < 0.01), correlation coefficients (r) being 0.56, 0.56, 0.67, and 0.71 (n = 418), respectively. |
| 6681 | 7513036 | MBV's effect on interleukin-2 (IL-2) production, plasma interferon (IFN) and tumor necrosis factor (TNF) levels was monitored. |
| 6682 | 7513036 | In general there was little correlation between IL-2 and IFN levels or with the response to therapy. |
| 6683 | 1363824 | Role of T cells, TNF alpha and IFN gamma in recall of immunity to oral challenge with virulent salmonellae in mice vaccinated with live attenuated aro- Salmonella vaccines. |
| 6684 | 1363824 | Role of T cells, TNF alpha and IFN gamma in recall of immunity to oral challenge with virulent salmonellae in mice vaccinated with live attenuated aro- Salmonella vaccines. |
| 6685 | 1363824 | Role of T cells, TNF alpha and IFN gamma in recall of immunity to oral challenge with virulent salmonellae in mice vaccinated with live attenuated aro- Salmonella vaccines. |
| 6686 | 1363824 | BALB/c mice immunized with SL3261 and later subjected to in vivo depletion of both CD4+ and CD8+ T cells had impaired recall of immunity to oral challenge with the virulent S. typhimurium C5, with increased mortality and higher bacterial loads in the reticuloendothelial system (RES). |
| 6687 | 1363824 | BALB/c mice immunized with SL3261 and later subjected to in vivo depletion of both CD4+ and CD8+ T cells had impaired recall of immunity to oral challenge with the virulent S. typhimurium C5, with increased mortality and higher bacterial loads in the reticuloendothelial system (RES). |
| 6688 | 1363824 | BALB/c mice immunized with SL3261 and later subjected to in vivo depletion of both CD4+ and CD8+ T cells had impaired recall of immunity to oral challenge with the virulent S. typhimurium C5, with increased mortality and higher bacterial loads in the reticuloendothelial system (RES). |
| 6689 | 1363824 | Surprisingly, IFN gamma was detectable in sera of both controls and T cell-depleted mice on day 8 of the secondary infection, as well as in sera of anti-TNF alpha-treated mice on day 6 of infection. |
| 6690 | 1363824 | Surprisingly, IFN gamma was detectable in sera of both controls and T cell-depleted mice on day 8 of the secondary infection, as well as in sera of anti-TNF alpha-treated mice on day 6 of infection. |
| 6691 | 1363824 | Surprisingly, IFN gamma was detectable in sera of both controls and T cell-depleted mice on day 8 of the secondary infection, as well as in sera of anti-TNF alpha-treated mice on day 6 of infection. |
| 6692 | 1363824 | The results indicate that T cells, IFN gamma and TNF alpha are all important in the specific recall of immunity to virulent salmonellae conferred by immunization with live vaccines, with the effect of T cell and IFN gamma depletion (marked macrophage infiltration) being qualitatively very different from that of TNF alpha neutralization (no mononuclear infiltrate or granuloma formation). |
| 6693 | 1363824 | The results indicate that T cells, IFN gamma and TNF alpha are all important in the specific recall of immunity to virulent salmonellae conferred by immunization with live vaccines, with the effect of T cell and IFN gamma depletion (marked macrophage infiltration) being qualitatively very different from that of TNF alpha neutralization (no mononuclear infiltrate or granuloma formation). |
| 6694 | 1363824 | The results indicate that T cells, IFN gamma and TNF alpha are all important in the specific recall of immunity to virulent salmonellae conferred by immunization with live vaccines, with the effect of T cell and IFN gamma depletion (marked macrophage infiltration) being qualitatively very different from that of TNF alpha neutralization (no mononuclear infiltrate or granuloma formation). |
| 6695 | 1401929 | To examine the regulation of cytokine synthesis during murine listeriosis, we have monitored IFN-gamma, TNF-alpha, and IL-1 beta mRNA levels in the spleens of C57B1/6 mice after the i.v. infusion of virulent and nonvirulent preparations of Listeria monocytogenes (LM). |
| 6696 | 1401929 | To examine the regulation of cytokine synthesis during murine listeriosis, we have monitored IFN-gamma, TNF-alpha, and IL-1 beta mRNA levels in the spleens of C57B1/6 mice after the i.v. infusion of virulent and nonvirulent preparations of Listeria monocytogenes (LM). |
| 6697 | 1401929 | Messenger RNA coding for TNF, IL-1, or IFN did not become detectable until approximately 12 to 15 h after the infusion of virulent LM. |
| 6698 | 1401929 | Messenger RNA coding for TNF, IL-1, or IFN did not become detectable until approximately 12 to 15 h after the infusion of virulent LM. |
| 6699 | 1500188 | Furthermore, cytochrome P-450 levels were decreased 30 to 40% 24 h after DTP vaccine administration in both R and NR mice, while after LPS administration they were decreased 30% in R mice and less than 10% in NR mice. |
| 6700 | 1500188 | Levels of tumor necrosis factor and interleukin-6 in plasma of R mice were markedly increased after DTP and LPS treatment, while NR mice had reduced increases. |
| 6701 | 1388844 | Progress has been made in understanding the anti-parasitic properties of tumor necrosis factor-alpha, interferon-gamma and nitric oxide, in defining the parasite toxins that induce tumor necrosis factor-alpha production, and in exploring the role of cytokines and adhesion molecules in the pathogenesis of cerebral malaria. |
| 6702 | 1351088 | Production of transmembrane and secreted forms of tumor necrosis factor (TNF)-alpha by HIV-1-specific CD4+ cytolytic T lymphocyte clones. |
| 6703 | 1351088 | Production of transmembrane and secreted forms of tumor necrosis factor (TNF)-alpha by HIV-1-specific CD4+ cytolytic T lymphocyte clones. |
| 6704 | 1351088 | Production of transmembrane and secreted forms of tumor necrosis factor (TNF)-alpha by HIV-1-specific CD4+ cytolytic T lymphocyte clones. |
| 6705 | 1351088 | Production of transmembrane and secreted forms of tumor necrosis factor (TNF)-alpha by HIV-1-specific CD4+ cytolytic T lymphocyte clones. |
| 6706 | 1351088 | Production of transmembrane and secreted forms of tumor necrosis factor (TNF)-alpha by HIV-1-specific CD4+ cytolytic T lymphocyte clones. |
| 6707 | 1351088 | Production of transmembrane and secreted forms of tumor necrosis factor (TNF)-alpha by HIV-1-specific CD4+ cytolytic T lymphocyte clones. |
| 6708 | 1351088 | Production of transmembrane and secreted forms of tumor necrosis factor (TNF)-alpha by HIV-1-specific CD4+ cytolytic T lymphocyte clones. |
| 6709 | 1351088 | Candidate AIDS vaccines consisting of recombinant forms of the HIV-1 envelope glycoprotein induce, in seronegative human volunteers, an env-specific T cell response that includes CD4+, MHC class II-restricted CTL capable of lysing HIV-1-infected target cells. |
| 6710 | 1351088 | Candidate AIDS vaccines consisting of recombinant forms of the HIV-1 envelope glycoprotein induce, in seronegative human volunteers, an env-specific T cell response that includes CD4+, MHC class II-restricted CTL capable of lysing HIV-1-infected target cells. |
| 6711 | 1351088 | Candidate AIDS vaccines consisting of recombinant forms of the HIV-1 envelope glycoprotein induce, in seronegative human volunteers, an env-specific T cell response that includes CD4+, MHC class II-restricted CTL capable of lysing HIV-1-infected target cells. |
| 6712 | 1351088 | Candidate AIDS vaccines consisting of recombinant forms of the HIV-1 envelope glycoprotein induce, in seronegative human volunteers, an env-specific T cell response that includes CD4+, MHC class II-restricted CTL capable of lysing HIV-1-infected target cells. |
| 6713 | 1351088 | Candidate AIDS vaccines consisting of recombinant forms of the HIV-1 envelope glycoprotein induce, in seronegative human volunteers, an env-specific T cell response that includes CD4+, MHC class II-restricted CTL capable of lysing HIV-1-infected target cells. |
| 6714 | 1351088 | Candidate AIDS vaccines consisting of recombinant forms of the HIV-1 envelope glycoprotein induce, in seronegative human volunteers, an env-specific T cell response that includes CD4+, MHC class II-restricted CTL capable of lysing HIV-1-infected target cells. |
| 6715 | 1351088 | Candidate AIDS vaccines consisting of recombinant forms of the HIV-1 envelope glycoprotein induce, in seronegative human volunteers, an env-specific T cell response that includes CD4+, MHC class II-restricted CTL capable of lysing HIV-1-infected target cells. |
| 6716 | 1351088 | In this study, we have analyzed the production of the cytokines TNF-alpha and lymphotoxin (LT) by a set of env-specific CD4+ human CTL clones. |
| 6717 | 1351088 | In this study, we have analyzed the production of the cytokines TNF-alpha and lymphotoxin (LT) by a set of env-specific CD4+ human CTL clones. |
| 6718 | 1351088 | In this study, we have analyzed the production of the cytokines TNF-alpha and lymphotoxin (LT) by a set of env-specific CD4+ human CTL clones. |
| 6719 | 1351088 | In this study, we have analyzed the production of the cytokines TNF-alpha and lymphotoxin (LT) by a set of env-specific CD4+ human CTL clones. |
| 6720 | 1351088 | In this study, we have analyzed the production of the cytokines TNF-alpha and lymphotoxin (LT) by a set of env-specific CD4+ human CTL clones. |
| 6721 | 1351088 | In this study, we have analyzed the production of the cytokines TNF-alpha and lymphotoxin (LT) by a set of env-specific CD4+ human CTL clones. |
| 6722 | 1351088 | In this study, we have analyzed the production of the cytokines TNF-alpha and lymphotoxin (LT) by a set of env-specific CD4+ human CTL clones. |
| 6723 | 1351088 | TNF-alpha and LT are of interest because of their potential role in target cell destruction by CD4+ CTL. |
| 6724 | 1351088 | TNF-alpha and LT are of interest because of their potential role in target cell destruction by CD4+ CTL. |
| 6725 | 1351088 | TNF-alpha and LT are of interest because of their potential role in target cell destruction by CD4+ CTL. |
| 6726 | 1351088 | TNF-alpha and LT are of interest because of their potential role in target cell destruction by CD4+ CTL. |
| 6727 | 1351088 | TNF-alpha and LT are of interest because of their potential role in target cell destruction by CD4+ CTL. |
| 6728 | 1351088 | TNF-alpha and LT are of interest because of their potential role in target cell destruction by CD4+ CTL. |
| 6729 | 1351088 | TNF-alpha and LT are of interest because of their potential role in target cell destruction by CD4+ CTL. |
| 6730 | 1351088 | We found that, upon interaction with target cells expressing env epitopes in the context of the appropriate MHC class II molecules, CD4+ CTL released TNF-alpha with kinetics that were rapid, compared with other cytokines, and that were generally similar to the kinetics of target cell destruction. |
| 6731 | 1351088 | We found that, upon interaction with target cells expressing env epitopes in the context of the appropriate MHC class II molecules, CD4+ CTL released TNF-alpha with kinetics that were rapid, compared with other cytokines, and that were generally similar to the kinetics of target cell destruction. |
| 6732 | 1351088 | We found that, upon interaction with target cells expressing env epitopes in the context of the appropriate MHC class II molecules, CD4+ CTL released TNF-alpha with kinetics that were rapid, compared with other cytokines, and that were generally similar to the kinetics of target cell destruction. |
| 6733 | 1351088 | We found that, upon interaction with target cells expressing env epitopes in the context of the appropriate MHC class II molecules, CD4+ CTL released TNF-alpha with kinetics that were rapid, compared with other cytokines, and that were generally similar to the kinetics of target cell destruction. |
| 6734 | 1351088 | We found that, upon interaction with target cells expressing env epitopes in the context of the appropriate MHC class II molecules, CD4+ CTL released TNF-alpha with kinetics that were rapid, compared with other cytokines, and that were generally similar to the kinetics of target cell destruction. |
| 6735 | 1351088 | We found that, upon interaction with target cells expressing env epitopes in the context of the appropriate MHC class II molecules, CD4+ CTL released TNF-alpha with kinetics that were rapid, compared with other cytokines, and that were generally similar to the kinetics of target cell destruction. |
| 6736 | 1351088 | We found that, upon interaction with target cells expressing env epitopes in the context of the appropriate MHC class II molecules, CD4+ CTL released TNF-alpha with kinetics that were rapid, compared with other cytokines, and that were generally similar to the kinetics of target cell destruction. |
| 6737 | 1351088 | A novel flow cytometric assay was used to show that physiologic activation of CD4+ CTL with target APC induced expression by the CTL of cell surface forms of TNF-alpha. |
| 6738 | 1351088 | A novel flow cytometric assay was used to show that physiologic activation of CD4+ CTL with target APC induced expression by the CTL of cell surface forms of TNF-alpha. |
| 6739 | 1351088 | A novel flow cytometric assay was used to show that physiologic activation of CD4+ CTL with target APC induced expression by the CTL of cell surface forms of TNF-alpha. |
| 6740 | 1351088 | A novel flow cytometric assay was used to show that physiologic activation of CD4+ CTL with target APC induced expression by the CTL of cell surface forms of TNF-alpha. |
| 6741 | 1351088 | A novel flow cytometric assay was used to show that physiologic activation of CD4+ CTL with target APC induced expression by the CTL of cell surface forms of TNF-alpha. |
| 6742 | 1351088 | A novel flow cytometric assay was used to show that physiologic activation of CD4+ CTL with target APC induced expression by the CTL of cell surface forms of TNF-alpha. |
| 6743 | 1351088 | A novel flow cytometric assay was used to show that physiologic activation of CD4+ CTL with target APC induced expression by the CTL of cell surface forms of TNF-alpha. |
| 6744 | 1351088 | For a subset of CD4+ CTL, we found that treatment of CTL with cyclosporin A inhibited Ag-induced production of both transmembrane and secreted forms of TNF-alpha but had no effect on cytolysis. |
| 6745 | 1351088 | For a subset of CD4+ CTL, we found that treatment of CTL with cyclosporin A inhibited Ag-induced production of both transmembrane and secreted forms of TNF-alpha but had no effect on cytolysis. |
| 6746 | 1351088 | For a subset of CD4+ CTL, we found that treatment of CTL with cyclosporin A inhibited Ag-induced production of both transmembrane and secreted forms of TNF-alpha but had no effect on cytolysis. |
| 6747 | 1351088 | For a subset of CD4+ CTL, we found that treatment of CTL with cyclosporin A inhibited Ag-induced production of both transmembrane and secreted forms of TNF-alpha but had no effect on cytolysis. |
| 6748 | 1351088 | For a subset of CD4+ CTL, we found that treatment of CTL with cyclosporin A inhibited Ag-induced production of both transmembrane and secreted forms of TNF-alpha but had no effect on cytolysis. |
| 6749 | 1351088 | For a subset of CD4+ CTL, we found that treatment of CTL with cyclosporin A inhibited Ag-induced production of both transmembrane and secreted forms of TNF-alpha but had no effect on cytolysis. |
| 6750 | 1351088 | For a subset of CD4+ CTL, we found that treatment of CTL with cyclosporin A inhibited Ag-induced production of both transmembrane and secreted forms of TNF-alpha but had no effect on cytolysis. |
| 6751 | 1351088 | Thus, although transmembrane and secreted TNF-alpha produced by HIV-1-specific CD4+ CTL may have important effects in vivo, the rapid destruction of target APC by the set of CD4+ CTL clones described here occurs through a TNF-alpha-independent mechanism. |
| 6752 | 1351088 | Thus, although transmembrane and secreted TNF-alpha produced by HIV-1-specific CD4+ CTL may have important effects in vivo, the rapid destruction of target APC by the set of CD4+ CTL clones described here occurs through a TNF-alpha-independent mechanism. |
| 6753 | 1351088 | Thus, although transmembrane and secreted TNF-alpha produced by HIV-1-specific CD4+ CTL may have important effects in vivo, the rapid destruction of target APC by the set of CD4+ CTL clones described here occurs through a TNF-alpha-independent mechanism. |
| 6754 | 1351088 | Thus, although transmembrane and secreted TNF-alpha produced by HIV-1-specific CD4+ CTL may have important effects in vivo, the rapid destruction of target APC by the set of CD4+ CTL clones described here occurs through a TNF-alpha-independent mechanism. |
| 6755 | 1351088 | Thus, although transmembrane and secreted TNF-alpha produced by HIV-1-specific CD4+ CTL may have important effects in vivo, the rapid destruction of target APC by the set of CD4+ CTL clones described here occurs through a TNF-alpha-independent mechanism. |
| 6756 | 1351088 | Thus, although transmembrane and secreted TNF-alpha produced by HIV-1-specific CD4+ CTL may have important effects in vivo, the rapid destruction of target APC by the set of CD4+ CTL clones described here occurs through a TNF-alpha-independent mechanism. |
| 6757 | 1351088 | Thus, although transmembrane and secreted TNF-alpha produced by HIV-1-specific CD4+ CTL may have important effects in vivo, the rapid destruction of target APC by the set of CD4+ CTL clones described here occurs through a TNF-alpha-independent mechanism. |
| 6758 | 1548064 | Compared with LPS derived from Escherichia coli, B. abortus LPS was 10,000-fold less potent in eliciting fever in rabbits, 268-fold less potent in killing D-galactosamine-sensitized mice, and 1,400-fold and 400-fold less potent in inducing interleukin-1 beta and tumor necrosis factor alpha production, respectively. |
| 6759 | 1727868 | The antiidiotopic antibodies, however, did not stimulate endotoxin-associated bioactivities, such as induction of TNF and IL-1. |
| 6760 | 1540977 | Induction of urinary interleukin-1 (IL-1), IL-2, IL-6, and tumour necrosis factor during intravesical immunotherapy with bacillus Calmette-Guérin in superficial bladder cancer. |
| 6761 | 1540977 | Induction of urinary interleukin-1 (IL-1), IL-2, IL-6, and tumour necrosis factor during intravesical immunotherapy with bacillus Calmette-Guérin in superficial bladder cancer. |
| 6762 | 1540977 | Induction of urinary interleukin-1 (IL-1), IL-2, IL-6, and tumour necrosis factor during intravesical immunotherapy with bacillus Calmette-Guérin in superficial bladder cancer. |
| 6763 | 1540977 | Induction of urinary interleukin-1 (IL-1), IL-2, IL-6, and tumour necrosis factor during intravesical immunotherapy with bacillus Calmette-Guérin in superficial bladder cancer. |
| 6764 | 1540977 | Induction of urinary interleukin-1 (IL-1), IL-2, IL-6, and tumour necrosis factor during intravesical immunotherapy with bacillus Calmette-Guérin in superficial bladder cancer. |
| 6765 | 1540977 | To study the local immunological effects of intravesical bacillus Calmette-Guérin (BCG) therapy in superficial bladder cancer patients, the production of interleukin-1 (IL-1), IL-2, IL-6, tumour necrosis factor alpha (TNF alpha), and interferon gamma (IFN gamma) was investigated in the urine. |
| 6766 | 1540977 | To study the local immunological effects of intravesical bacillus Calmette-Guérin (BCG) therapy in superficial bladder cancer patients, the production of interleukin-1 (IL-1), IL-2, IL-6, tumour necrosis factor alpha (TNF alpha), and interferon gamma (IFN gamma) was investigated in the urine. |
| 6767 | 1540977 | To study the local immunological effects of intravesical bacillus Calmette-Guérin (BCG) therapy in superficial bladder cancer patients, the production of interleukin-1 (IL-1), IL-2, IL-6, tumour necrosis factor alpha (TNF alpha), and interferon gamma (IFN gamma) was investigated in the urine. |
| 6768 | 1540977 | To study the local immunological effects of intravesical bacillus Calmette-Guérin (BCG) therapy in superficial bladder cancer patients, the production of interleukin-1 (IL-1), IL-2, IL-6, tumour necrosis factor alpha (TNF alpha), and interferon gamma (IFN gamma) was investigated in the urine. |
| 6769 | 1540977 | To study the local immunological effects of intravesical bacillus Calmette-Guérin (BCG) therapy in superficial bladder cancer patients, the production of interleukin-1 (IL-1), IL-2, IL-6, tumour necrosis factor alpha (TNF alpha), and interferon gamma (IFN gamma) was investigated in the urine. |
| 6770 | 1540977 | Like IL-2, TNF alpha was only detected after repeated BCG instillations. |
| 6771 | 1540977 | Like IL-2, TNF alpha was only detected after repeated BCG instillations. |
| 6772 | 1540977 | Like IL-2, TNF alpha was only detected after repeated BCG instillations. |
| 6773 | 1540977 | Like IL-2, TNF alpha was only detected after repeated BCG instillations. |
| 6774 | 1540977 | Like IL-2, TNF alpha was only detected after repeated BCG instillations. |
| 6775 | 1540977 | With respect to the occurrence of the cytokines during the first 24 h after the BCG instillation, TNF, IL-2, and IL-6 were detectable 2 h after the instillation. |
| 6776 | 1540977 | With respect to the occurrence of the cytokines during the first 24 h after the BCG instillation, TNF, IL-2, and IL-6 were detectable 2 h after the instillation. |
| 6777 | 1540977 | With respect to the occurrence of the cytokines during the first 24 h after the BCG instillation, TNF, IL-2, and IL-6 were detectable 2 h after the instillation. |
| 6778 | 1540977 | With respect to the occurrence of the cytokines during the first 24 h after the BCG instillation, TNF, IL-2, and IL-6 were detectable 2 h after the instillation. |
| 6779 | 1540977 | With respect to the occurrence of the cytokines during the first 24 h after the BCG instillation, TNF, IL-2, and IL-6 were detectable 2 h after the instillation. |
| 6780 | 1540977 | Generally IL-2 was not detectable in the 8-h samples, whereas IL-1 and IL-6 were present up to 8 h after instillation of BCG. |
| 6781 | 1540977 | Generally IL-2 was not detectable in the 8-h samples, whereas IL-1 and IL-6 were present up to 8 h after instillation of BCG. |
| 6782 | 1540977 | Generally IL-2 was not detectable in the 8-h samples, whereas IL-1 and IL-6 were present up to 8 h after instillation of BCG. |
| 6783 | 1540977 | Generally IL-2 was not detectable in the 8-h samples, whereas IL-1 and IL-6 were present up to 8 h after instillation of BCG. |
| 6784 | 1540977 | Generally IL-2 was not detectable in the 8-h samples, whereas IL-1 and IL-6 were present up to 8 h after instillation of BCG. |
| 6785 | 1540977 | The presence of TNF was found less frequently than the presence of IL-1, IL-2, and IL-6. |
| 6786 | 1540977 | The presence of TNF was found less frequently than the presence of IL-1, IL-2, and IL-6. |
| 6787 | 1540977 | The presence of TNF was found less frequently than the presence of IL-1, IL-2, and IL-6. |
| 6788 | 1540977 | The presence of TNF was found less frequently than the presence of IL-1, IL-2, and IL-6. |
| 6789 | 1540977 | The presence of TNF was found less frequently than the presence of IL-1, IL-2, and IL-6. |
| 6790 | 1540977 | The presence of IL-1, IL-6, and TNF alpha might suggest activation of macrophages by intravesically administered BCG, although production by other cell types cannot be excluded. |
| 6791 | 1540977 | The presence of IL-1, IL-6, and TNF alpha might suggest activation of macrophages by intravesically administered BCG, although production by other cell types cannot be excluded. |
| 6792 | 1540977 | The presence of IL-1, IL-6, and TNF alpha might suggest activation of macrophages by intravesically administered BCG, although production by other cell types cannot be excluded. |
| 6793 | 1540977 | The presence of IL-1, IL-6, and TNF alpha might suggest activation of macrophages by intravesically administered BCG, although production by other cell types cannot be excluded. |
| 6794 | 1540977 | The presence of IL-1, IL-6, and TNF alpha might suggest activation of macrophages by intravesically administered BCG, although production by other cell types cannot be excluded. |
| 6795 | 1465054 | Monocytes fail to elicit adequate help for T cell proliferation despite normal production of Il-1 and Il-6, but they produce elevated amounts of TNF alpha. |
| 6796 | 1426672 | In monocytes/macrophages, lipopeptide stimulate the secretion of IL-1, IL-6, tumor necrosis factor (TNF) and nitrogen oxide (NO); they also induce tumor cytotoxicity. |
| 6797 | 1810454 | The cytokines IL1, IL2, IL6 and TNF alpha were also increased after BCG instillations. |
| 6798 | 1909711 | Francisella tularensis-induced in vitro gamma interferon, tumor necrosis factor alpha, and interleukin 2 responses appear within 2 weeks of tularemia vaccination in human beings. |
| 6799 | 1909711 | Francisella tularensis-induced in vitro gamma interferon, tumor necrosis factor alpha, and interleukin 2 responses appear within 2 weeks of tularemia vaccination in human beings. |
| 6800 | 1909711 | Francisella tularensis-induced in vitro gamma interferon, tumor necrosis factor alpha, and interleukin 2 responses appear within 2 weeks of tularemia vaccination in human beings. |
| 6801 | 1909711 | Positive in vitro T-cell responses in the form of lymphocyte proliferation and lymphokine interleukin 2 (IL-2) and gamma interferon (IFN-gamma) secretion are found in memory immunity. |
| 6802 | 1909711 | Positive in vitro T-cell responses in the form of lymphocyte proliferation and lymphokine interleukin 2 (IL-2) and gamma interferon (IFN-gamma) secretion are found in memory immunity. |
| 6803 | 1909711 | Positive in vitro T-cell responses in the form of lymphocyte proliferation and lymphokine interleukin 2 (IL-2) and gamma interferon (IFN-gamma) secretion are found in memory immunity. |
| 6804 | 1909711 | Positive reactions, i.e., responses exceeding those on day 0, were reached on day 10 with regard to the whole blood culture DNA synthesis response and IL-2 and IFN-gamma secretion and on day 14 with regard to the mononuclear cell DNA synthesis response and tumor necrosis factor alpha (TNF-alpha) secretion. |
| 6805 | 1909711 | Positive reactions, i.e., responses exceeding those on day 0, were reached on day 10 with regard to the whole blood culture DNA synthesis response and IL-2 and IFN-gamma secretion and on day 14 with regard to the mononuclear cell DNA synthesis response and tumor necrosis factor alpha (TNF-alpha) secretion. |
| 6806 | 1909711 | Positive reactions, i.e., responses exceeding those on day 0, were reached on day 10 with regard to the whole blood culture DNA synthesis response and IL-2 and IFN-gamma secretion and on day 14 with regard to the mononuclear cell DNA synthesis response and tumor necrosis factor alpha (TNF-alpha) secretion. |
| 6807 | 1909711 | If it is shown later that specific T cells produce it, the TNF-alpha response and the negative IL-4 finding may speak for the importance of the Th1-like pattern in immunity to F. tularensis. |
| 6808 | 1909711 | If it is shown later that specific T cells produce it, the TNF-alpha response and the negative IL-4 finding may speak for the importance of the Th1-like pattern in immunity to F. tularensis. |
| 6809 | 1909711 | If it is shown later that specific T cells produce it, the TNF-alpha response and the negative IL-4 finding may speak for the importance of the Th1-like pattern in immunity to F. tularensis. |
| 6810 | 2017199 | --is stimulated by PRFs such as interferon-gamma, IL-1, TNF, GM-CSF and IL-4. |
| 6811 | 2017199 | The activation and expansion of T-lymphocytes requires IL-1, IL-2, IL-4, interferon-gamma, IL-6 and probably IL-7. |
| 6812 | 2017199 | Likewise, the activation and expansion of B-lymphocytes is regulated by PRFs such as IL-1, IL-2, IL-4, IL-5, IL-6, IL-7 and interferon-gamma. |
| 6813 | 2017199 | Antibody class is critically influenced by particular PRFs, e.g. interferon-gamma regulates IgG2a; IL-4, IgE and IgG1; IL-5 and TGF-beta, IgA. |
| 6814 | 2017199 | The recruitment and enhanced production and function of granulocytic and phagocytic cells involves a number of T-lymphocyte PRFs including GM-CSF, IL-3, IL-5, IL-4, and IL-6. |
| 6815 | 2017199 | IL-3 induces a mastocytosis and IL-5 an eosinophilia. |
| 6816 | 1993354 | An investigation was undertaken to determine whether a recombinant gp160 envelope protein, which is currently being evaluated as a vaccine for AIDS, induces or modulates the production of tumour necrosis factor-alpha (TNF-alpha) or interleukin-1 beta (IL-1 beta). |
| 6817 | 1993354 | An investigation was undertaken to determine whether a recombinant gp160 envelope protein, which is currently being evaluated as a vaccine for AIDS, induces or modulates the production of tumour necrosis factor-alpha (TNF-alpha) or interleukin-1 beta (IL-1 beta). |
| 6818 | 1993354 | An investigation was undertaken to determine whether a recombinant gp160 envelope protein, which is currently being evaluated as a vaccine for AIDS, induces or modulates the production of tumour necrosis factor-alpha (TNF-alpha) or interleukin-1 beta (IL-1 beta). |
| 6819 | 1993354 | Incubation of monocytes from healthy, HIV-seronegative persons with 0.0001-1.0 micrograms of the recombinant vaccine did not result in the secretion of TNF-alpha or IL-1 beta, nor did the recombinant product augment or suppress monokine production by lipopolysaccharide (LPS) stimulated monocytes. |
| 6820 | 1993354 | Incubation of monocytes from healthy, HIV-seronegative persons with 0.0001-1.0 micrograms of the recombinant vaccine did not result in the secretion of TNF-alpha or IL-1 beta, nor did the recombinant product augment or suppress monokine production by lipopolysaccharide (LPS) stimulated monocytes. |
| 6821 | 1993354 | Incubation of monocytes from healthy, HIV-seronegative persons with 0.0001-1.0 micrograms of the recombinant vaccine did not result in the secretion of TNF-alpha or IL-1 beta, nor did the recombinant product augment or suppress monokine production by lipopolysaccharide (LPS) stimulated monocytes. |
| 6822 | 1993354 | The vaccine was also without a stimulatory or modulatory effect upon TNF-alpha or IL-1 beta secretion by monocytes from a patient with the AIDS-related complex (ARC) and from the monocytic THP-1 cell line. |
| 6823 | 1993354 | The vaccine was also without a stimulatory or modulatory effect upon TNF-alpha or IL-1 beta secretion by monocytes from a patient with the AIDS-related complex (ARC) and from the monocytic THP-1 cell line. |
| 6824 | 1993354 | The vaccine was also without a stimulatory or modulatory effect upon TNF-alpha or IL-1 beta secretion by monocytes from a patient with the AIDS-related complex (ARC) and from the monocytic THP-1 cell line. |
| 6825 | 2123823 | Mycobacterium-specific T cells from both BALB/c and B10.D2 mice produced interleukin-2 and no interleukin-4. |
| 6826 | 2123823 | This suggests that tumor necrosis factor, in addition to gamma interferon, may be involved in resistance to L. major and that interleukin-4 may inhibit the leishmanicidal activity of tumor necrosis factor and/or gamma interferon. |
| 6827 | 1701805 | The empirical evidence that IFN alpha exerts clinically significant anti-tumor effects against melanoma is reviewed, and evolving status of adjuvant trials of IFN alpha and gamma is noted. |
| 6828 | 1701805 | Regional therapy by the intralesional route has yielded enhanced activity for a range of biologics, including bacillus Calmette-Guerin (BCG), IL-2, and tumor necrosis factor (TNF). |
| 6829 | 2247306 | Frequent regression of tumors and subjective improvement by vaccine therapy of patients may be explained by: a) infection of tumor cells by the virus and so enhancing their immunogenicity, b) activation of cells of the immune system, increased production of interferons, tumor necrosis factor-alpha and other cytokines, c) increased production of ACTH and beta endorphin by monocytes and lymphocytes resulting in an improvement in the general well-being. |
| 6830 | 2193171 | Elevations of cytokines interleukin-1, interleukin-2 and tumor necrosis factor in the urine of patients after intravesical bacillus Calmette-Guerin immunotherapy. |
| 6831 | 2193171 | Elevations of cytokines interleukin-1, interleukin-2 and tumor necrosis factor in the urine of patients after intravesical bacillus Calmette-Guerin immunotherapy. |
| 6832 | 2193171 | Elevations of cytokines interleukin-1, interleukin-2 and tumor necrosis factor in the urine of patients after intravesical bacillus Calmette-Guerin immunotherapy. |
| 6833 | 2193171 | In an attempt to elucidate further the immunological mechanisms responsible for the effectiveness of intravesical bacillus Calmette-Guerin in the therapy of superficial urothelial bladder cancer, a prospective study was performed in which the urine of patients was examined before and after 6 intravesical instillations of bacillus Calmette-Guerin for the presence of the cytokines interleukin-1, interleukin-2 and tumor necrosis factor-alpha. |
| 6834 | 2193171 | In an attempt to elucidate further the immunological mechanisms responsible for the effectiveness of intravesical bacillus Calmette-Guerin in the therapy of superficial urothelial bladder cancer, a prospective study was performed in which the urine of patients was examined before and after 6 intravesical instillations of bacillus Calmette-Guerin for the presence of the cytokines interleukin-1, interleukin-2 and tumor necrosis factor-alpha. |
| 6835 | 2193171 | In an attempt to elucidate further the immunological mechanisms responsible for the effectiveness of intravesical bacillus Calmette-Guerin in the therapy of superficial urothelial bladder cancer, a prospective study was performed in which the urine of patients was examined before and after 6 intravesical instillations of bacillus Calmette-Guerin for the presence of the cytokines interleukin-1, interleukin-2 and tumor necrosis factor-alpha. |
| 6836 | 2193171 | Urinary titers of interleukin-1, interleukin-2 and tumor necrosis factor increased significantly after bacillus Calmette-Guerin instillation but showed inter-individual differences. |
| 6837 | 2193171 | Urinary titers of interleukin-1, interleukin-2 and tumor necrosis factor increased significantly after bacillus Calmette-Guerin instillation but showed inter-individual differences. |
| 6838 | 2193171 | Urinary titers of interleukin-1, interleukin-2 and tumor necrosis factor increased significantly after bacillus Calmette-Guerin instillation but showed inter-individual differences. |
| 6839 | 2104221 | Detection of urinary TNF, IL 1, and IL 2 after local BCG immunotherapy for bladder carcinoma. |
| 6840 | 2104221 | Detection of urinary TNF, IL 1, and IL 2 after local BCG immunotherapy for bladder carcinoma. |
| 6841 | 2104221 | Detection of urinary TNF, IL 1, and IL 2 after local BCG immunotherapy for bladder carcinoma. |
| 6842 | 2104221 | In an attempt to monitor the immunological effects of this therapy, we analyzed the urine of patients following the sixth intravessical instillation, to show the presence of the monokines TNF and IL 1 and the lymphokine IL 2. |
| 6843 | 2104221 | In an attempt to monitor the immunological effects of this therapy, we analyzed the urine of patients following the sixth intravessical instillation, to show the presence of the monokines TNF and IL 1 and the lymphokine IL 2. |
| 6844 | 2104221 | In an attempt to monitor the immunological effects of this therapy, we analyzed the urine of patients following the sixth intravessical instillation, to show the presence of the monokines TNF and IL 1 and the lymphokine IL 2. |
| 6845 | 2104221 | Within 24 hours following the instillation, all (n = 10) patients exhibited a strong increase in urinary cytokine secretion, which was significantly different from the control group (n = 10), with respect to TNF L929 biological assay (P less than 0.01), TNF sandwich-ELISA (P less than 0.01), IL 2 CTL 6 biological assay (P less than 0.05), IL 2 sandwich-ELISA (P less than 0.005), and IL 1 sandwich-ELISA (P less than 0.05), but not to the IL 1 fibroblast biological assay. |
| 6846 | 2104221 | Within 24 hours following the instillation, all (n = 10) patients exhibited a strong increase in urinary cytokine secretion, which was significantly different from the control group (n = 10), with respect to TNF L929 biological assay (P less than 0.01), TNF sandwich-ELISA (P less than 0.01), IL 2 CTL 6 biological assay (P less than 0.05), IL 2 sandwich-ELISA (P less than 0.005), and IL 1 sandwich-ELISA (P less than 0.05), but not to the IL 1 fibroblast biological assay. |
| 6847 | 2104221 | Within 24 hours following the instillation, all (n = 10) patients exhibited a strong increase in urinary cytokine secretion, which was significantly different from the control group (n = 10), with respect to TNF L929 biological assay (P less than 0.01), TNF sandwich-ELISA (P less than 0.01), IL 2 CTL 6 biological assay (P less than 0.05), IL 2 sandwich-ELISA (P less than 0.005), and IL 1 sandwich-ELISA (P less than 0.05), but not to the IL 1 fibroblast biological assay. |
| 6848 | 2327475 | Here, the authors studied the effect of endogenous TNF on LPS-induced hypotension and tissue injury and investigated the role of PAF in these responses. |
| 6849 | 1690777 | All but one of the clones were CD4+, CD5+, Th cells. |
| 6850 | 1690777 | One clone, 35, produced Il-2 and IFN-gamma and was designated a TH1 clone. |
| 6851 | 1690777 | IFN-gamma and TNF-alpha were essential to the killing mechanism whereas Il-1, Il-2, and Il-4 were not required. |
| 6852 | 2303746 | Production of monokines such as IL-1 and plasminogen activator, which affect APC capacity, was similar in the CD4 MO subsets. |
| 6853 | 2303746 | Production of monokines such as IL-1 and plasminogen activator, which affect APC capacity, was similar in the CD4 MO subsets. |
| 6854 | 2303746 | However, tumor necrosis factor (TNF) production (IFN gamma plus MDP-induced) of the CD4+ MO subset was slightly greater than that of the CD4- MO. |
| 6855 | 2303746 | However, tumor necrosis factor (TNF) production (IFN gamma plus MDP-induced) of the CD4+ MO subset was slightly greater than that of the CD4- MO. |
| 6856 | 2303746 | CD4- MO's lower APC capacity is not totally explained by their differential IL-1, TNF, or PGE2 production. |
| 6857 | 2303746 | CD4- MO's lower APC capacity is not totally explained by their differential IL-1, TNF, or PGE2 production. |
| 6858 | 2675486 | GLA-60, which is devoid of endotoxic activity, showed interleukin-1 (IL-1)-inducing activity and activation of murine macrophages comparable to those of LPS or compound 506. |
| 6859 | 2675486 | However, TNF- and CSF-inducing activities of these conjugates were lower than those of GLA-60. |
| 6860 | 2659724 | Pretreatment with recombinant murine tumor necrosis factor alpha/cachectin and murine interleukin 1 alpha protects mice from lethal bacterial infection. |
| 6861 | 2659724 | Pretreatment with recombinant murine tumor necrosis factor alpha/cachectin and murine interleukin 1 alpha protects mice from lethal bacterial infection. |
| 6862 | 2659724 | To test this hypothesis we pretreated the C3H/HeJ mouse with a combination of recombinant murine TNF/C-alpha and IL-1 alpha. |
| 6863 | 2659724 | To test this hypothesis we pretreated the C3H/HeJ mouse with a combination of recombinant murine TNF/C-alpha and IL-1 alpha. |
| 6864 | 2465739 | These drugs are living-BCG, OK-432, MY-1, WPG, interferon preparation (alpha, beta and gamma), TNF, IL-2, peplomycin, bleomycin and others. |
| 6865 | 2462667 | BRM administration group gained higher TNF and interferon (IFN) activity than control group. |
| 6866 | 3258889 | Sensitization and desensitization to lethal effects of tumor necrosis factor and IL-1. |
| 6867 | 3258889 | Sensitization and desensitization to lethal effects of tumor necrosis factor and IL-1. |
| 6868 | 3258889 | Sensitization and desensitization to lethal effects of tumor necrosis factor and IL-1. |
| 6869 | 3258889 | Sensitization and desensitization to lethal effects of tumor necrosis factor and IL-1. |
| 6870 | 3258889 | Sensitization and desensitization to lethal effects of tumor necrosis factor and IL-1. |
| 6871 | 3258889 | In contrast, treatment with sublethal doses of TNF or IL-1 themselves resulted in desensitization of the mice to the lethal effect of these cytokines: mice injected with TNF or IL-1 in the absence of Act D or GalN responded to a second injection of TNF or IL-1, this time together with Act D or GalN, by a significantly delayed death, or even survived. |
| 6872 | 3258889 | In contrast, treatment with sublethal doses of TNF or IL-1 themselves resulted in desensitization of the mice to the lethal effect of these cytokines: mice injected with TNF or IL-1 in the absence of Act D or GalN responded to a second injection of TNF or IL-1, this time together with Act D or GalN, by a significantly delayed death, or even survived. |
| 6873 | 3258889 | In contrast, treatment with sublethal doses of TNF or IL-1 themselves resulted in desensitization of the mice to the lethal effect of these cytokines: mice injected with TNF or IL-1 in the absence of Act D or GalN responded to a second injection of TNF or IL-1, this time together with Act D or GalN, by a significantly delayed death, or even survived. |
| 6874 | 3258889 | In contrast, treatment with sublethal doses of TNF or IL-1 themselves resulted in desensitization of the mice to the lethal effect of these cytokines: mice injected with TNF or IL-1 in the absence of Act D or GalN responded to a second injection of TNF or IL-1, this time together with Act D or GalN, by a significantly delayed death, or even survived. |
| 6875 | 3258889 | In contrast, treatment with sublethal doses of TNF or IL-1 themselves resulted in desensitization of the mice to the lethal effect of these cytokines: mice injected with TNF or IL-1 in the absence of Act D or GalN responded to a second injection of TNF or IL-1, this time together with Act D or GalN, by a significantly delayed death, or even survived. |
| 6876 | 3258889 | Injection of TNF or IL-1 at sublethal doses resulted also in hyporesponsiveness to the lethal effect of LPS on mice primed with bacillus Calmette-Guérin, an effect which most likely is mediated by TNF and IL-1 produced in those mice in response to the LPS. |
| 6877 | 3258889 | Injection of TNF or IL-1 at sublethal doses resulted also in hyporesponsiveness to the lethal effect of LPS on mice primed with bacillus Calmette-Guérin, an effect which most likely is mediated by TNF and IL-1 produced in those mice in response to the LPS. |
| 6878 | 3258889 | Injection of TNF or IL-1 at sublethal doses resulted also in hyporesponsiveness to the lethal effect of LPS on mice primed with bacillus Calmette-Guérin, an effect which most likely is mediated by TNF and IL-1 produced in those mice in response to the LPS. |
| 6879 | 3258889 | Injection of TNF or IL-1 at sublethal doses resulted also in hyporesponsiveness to the lethal effect of LPS on mice primed with bacillus Calmette-Guérin, an effect which most likely is mediated by TNF and IL-1 produced in those mice in response to the LPS. |
| 6880 | 3258889 | Injection of TNF or IL-1 at sublethal doses resulted also in hyporesponsiveness to the lethal effect of LPS on mice primed with bacillus Calmette-Guérin, an effect which most likely is mediated by TNF and IL-1 produced in those mice in response to the LPS. |
| 6881 | 3258889 | TNF and IL-1 in combination had an additive effect both in lethality and in desensitization of the mice. |
| 6882 | 3258889 | TNF and IL-1 in combination had an additive effect both in lethality and in desensitization of the mice. |
| 6883 | 3258889 | TNF and IL-1 in combination had an additive effect both in lethality and in desensitization of the mice. |
| 6884 | 3258889 | TNF and IL-1 in combination had an additive effect both in lethality and in desensitization of the mice. |
| 6885 | 3258889 | TNF and IL-1 in combination had an additive effect both in lethality and in desensitization of the mice. |
| 6886 | 3258889 | These findings suggest that some of the deleterious effects of TNF and IL-1 are modulated by antagonistic mechanisms; mechanisms which can be suppressed by sensitizing agents, specifically by agents inhibiting the synthesis of RNA or protein; but which, in the absence of such agents, are found to be augmented in response to TNF and IL-1, thus resulting in desensitization. |
| 6887 | 3258889 | These findings suggest that some of the deleterious effects of TNF and IL-1 are modulated by antagonistic mechanisms; mechanisms which can be suppressed by sensitizing agents, specifically by agents inhibiting the synthesis of RNA or protein; but which, in the absence of such agents, are found to be augmented in response to TNF and IL-1, thus resulting in desensitization. |
| 6888 | 3258889 | These findings suggest that some of the deleterious effects of TNF and IL-1 are modulated by antagonistic mechanisms; mechanisms which can be suppressed by sensitizing agents, specifically by agents inhibiting the synthesis of RNA or protein; but which, in the absence of such agents, are found to be augmented in response to TNF and IL-1, thus resulting in desensitization. |
| 6889 | 3258889 | These findings suggest that some of the deleterious effects of TNF and IL-1 are modulated by antagonistic mechanisms; mechanisms which can be suppressed by sensitizing agents, specifically by agents inhibiting the synthesis of RNA or protein; but which, in the absence of such agents, are found to be augmented in response to TNF and IL-1, thus resulting in desensitization. |
| 6890 | 3258889 | These findings suggest that some of the deleterious effects of TNF and IL-1 are modulated by antagonistic mechanisms; mechanisms which can be suppressed by sensitizing agents, specifically by agents inhibiting the synthesis of RNA or protein; but which, in the absence of such agents, are found to be augmented in response to TNF and IL-1, thus resulting in desensitization. |
| 6891 | 2439187 | In recent years, those substances that have attracted the greatest attention have included interferon (and, more recently, recombinant gamma interferon), bacillus Calmette-Guerin (BCG), tumor necrosis factor, prostaglandin synthetase inhibitors, and interleukin-2. |
| 6892 | 2435854 | In addition to the IFN production, forphenicinol increased production of LPS-induced tumor necrosis factor (TNF) in mice sensitized with BCG, and the dose of LPS required to induce TNF was reduced by the drug. |