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Gene Information
Gene symbol: CD28
Gene name: CD28 molecule
HGNC ID: 1653
Related Genes
Related Sentences
| # | PMID | Sentence |
| 1 | 1717561 | CD28 delivers a costimulatory signal involved in antigen-specific IL-2 production by human T cells. |
| 2 | 1717561 | CD4+ T cells require two signals to produce maximal amounts of IL-2, i.e., TCR occupancy and an unidentified APC-derived costimulus. |
| 3 | 1717561 | An agonistic anti-CD28 mAb, but not IL-1 and/or IL-6, stimulated T cell proliferation by tetanus toxoid-specific T cells cultured with Ag-pulsed, costimulation-deficient APC. |
| 4 | 1717561 | Furthermore, the ability of B cell tumor lines to provide costimulatory signals to purified T cells correlated well with expression of the CD28 ligand B7/BB-1. |
| 5 | 1717561 | Together, these results suggest that the two signals required for IL-2 production by CD4+ T cells can be transduced by the TCR and CD28. |
| 6 | 1717561 | CD28 delivers a costimulatory signal involved in antigen-specific IL-2 production by human T cells. |
| 7 | 1717561 | CD4+ T cells require two signals to produce maximal amounts of IL-2, i.e., TCR occupancy and an unidentified APC-derived costimulus. |
| 8 | 1717561 | An agonistic anti-CD28 mAb, but not IL-1 and/or IL-6, stimulated T cell proliferation by tetanus toxoid-specific T cells cultured with Ag-pulsed, costimulation-deficient APC. |
| 9 | 1717561 | Furthermore, the ability of B cell tumor lines to provide costimulatory signals to purified T cells correlated well with expression of the CD28 ligand B7/BB-1. |
| 10 | 1717561 | Together, these results suggest that the two signals required for IL-2 production by CD4+ T cells can be transduced by the TCR and CD28. |
| 11 | 1717561 | CD28 delivers a costimulatory signal involved in antigen-specific IL-2 production by human T cells. |
| 12 | 1717561 | CD4+ T cells require two signals to produce maximal amounts of IL-2, i.e., TCR occupancy and an unidentified APC-derived costimulus. |
| 13 | 1717561 | An agonistic anti-CD28 mAb, but not IL-1 and/or IL-6, stimulated T cell proliferation by tetanus toxoid-specific T cells cultured with Ag-pulsed, costimulation-deficient APC. |
| 14 | 1717561 | Furthermore, the ability of B cell tumor lines to provide costimulatory signals to purified T cells correlated well with expression of the CD28 ligand B7/BB-1. |
| 15 | 1717561 | Together, these results suggest that the two signals required for IL-2 production by CD4+ T cells can be transduced by the TCR and CD28. |
| 16 | 7541819 | Roles of CD40 ligand and B7-2 in established germinal centers. |
| 17 | 7541819 | We have compared the roles of CD40L and B7-2 in the initiation and maturation of humoral immunity by administering anti-CD40 ligand (L) or anti-B7-2 Ab during the early (days -1 to 3) or late (days 6-10) phases of primary responses to thymus-dependent (Td) and -independent (Ti) Ags. |
| 18 | 7541819 | Our findings suggest that the costimulatory roles of CD40:CD40L and B7-2:CD28/CTLA-4 differ in the GC; administration of anti-CD40L abrogates an established GC reaction, whereas Ab to B7-2 suppresses Ig hypermutation and entry into the B cell memory compartment. |
| 19 | 7541819 | Once B cells have entered the differentiation pathway to Ab production, neither CD40L nor B7-2 is necessary for their continued differentiation and persistence. |
| 20 | 7545119 | Tumor cells cotransfected with interleukin-7 and B7.1 genes induce CD25 and CD28 on tumor-infiltrating T lymphocytes and are strong vaccines. |
| 21 | 7545119 | In B7 transfected tumors, T cells were predominantly CD28+ and CD25-, while in IL-7 transfected tumors, T cells were mainly CD28- and CD25+. |
| 22 | 7545119 | In IL-7/B7 cotransfected tumors, the majority of T cells was CD28+ and CD25+. |
| 23 | 7545119 | Tumor cells cotransfected with interleukin-7 and B7.1 genes induce CD25 and CD28 on tumor-infiltrating T lymphocytes and are strong vaccines. |
| 24 | 7545119 | In B7 transfected tumors, T cells were predominantly CD28+ and CD25-, while in IL-7 transfected tumors, T cells were mainly CD28- and CD25+. |
| 25 | 7545119 | In IL-7/B7 cotransfected tumors, the majority of T cells was CD28+ and CD25+. |
| 26 | 7545119 | Tumor cells cotransfected with interleukin-7 and B7.1 genes induce CD25 and CD28 on tumor-infiltrating T lymphocytes and are strong vaccines. |
| 27 | 7545119 | In B7 transfected tumors, T cells were predominantly CD28+ and CD25-, while in IL-7 transfected tumors, T cells were mainly CD28- and CD25+. |
| 28 | 7545119 | In IL-7/B7 cotransfected tumors, the majority of T cells was CD28+ and CD25+. |
| 29 | 7620165 | We investigated the production of cytokines by highly purified T helper cells from B-cell chronic lymphocytic leukemia (B-CLL) patients stimulated by different activation pathways, and we studied the influence of various accessory cell populations on the pattern of the secretion of cytokines, including interleukin (IL)-2, IL-4, interferon-gamma (IFN-gamma), and IL-10. |
| 30 | 7620165 | Neither a qualitative nor a quantitative difference in cytokine production and proliferative capacity was observed in CLL-derived purified T cells compared with normal individuals, when T cells were stimulated by different pathways, including CD3, CD2, and costimulation with CD28. |
| 31 | 7620165 | CLL cells as aAC caused a marked increase of IL-2, whereas IFN-gamma was only slightly induced and IL-4 was not influenced. |
| 32 | 7620165 | In contrast, in normal individuals addition of aAC, which predominantly consisted of monocytes, resulted in a significant increase of IFN-gamma and a reduction of IL-4 secretion. |
| 33 | 7620165 | On the other hand, purified monocytes from CLL patients and controls both induced IFN-gamma production and inhibited IL-4 secretion. |
| 34 | 7622182 | The outer surface lipoprotein A of Borrelia burgdorferi provides direct and indirect augmenting/co-stimulatory signals for the activation of CD4+ and CD8+ T cells. |
| 35 | 7622182 | Naive CD4+ and CD8+ T cells require two distinct signals to proliferate and to express effector functions [1]. |
| 36 | 7622182 | The major co-stimulatory molecules for CD4+ T cells seem to be B7 [3], B7.2 [4,5], and heat-stable antigen (HSA) [6]. |
| 37 | 7622182 | These molecules are expressed on a variety of naive and/or activated APC and bind to CD28 and CTLA-4 and possibly other, as yet undefined, TCRs [3,7]. |
| 38 | 7688125 | Although a number of candidate molecules have been identified that are capable of delivering a costimulatory signal, increasing evidence suggests that one such critical pathway involves the interaction of the T-cell surface antigen CD28 with its ligand B7, expressed on APCs. |
| 39 | 8566072 | Addition of a second or third co-stimulatory signal provided by recombinant IL-2, CD28 or both had no effect on the Ins(1,4,5)P3 formation of the patients' antigen-driven T cell lines. |
| 40 | 8639914 | Recent studies have shown that tumor cells genetically modified by transduction of B7-1, a natural ligand for the T-cell costimulatory molecules CD28 and CTLA-4, are rejected in syngeneic hosts. |
| 41 | 8639914 | The antileukemia immunity is CD8+ T-cell-dependent and B7/CD28-mediated, since in vivo treatment of mice with anti-CD8 monoclonal antibody or CTLA-4 Ig leads to abrogation of the specific antileukemia immune response. |
| 42 | 8639914 | Recent studies have shown that tumor cells genetically modified by transduction of B7-1, a natural ligand for the T-cell costimulatory molecules CD28 and CTLA-4, are rejected in syngeneic hosts. |
| 43 | 8639914 | The antileukemia immunity is CD8+ T-cell-dependent and B7/CD28-mediated, since in vivo treatment of mice with anti-CD8 monoclonal antibody or CTLA-4 Ig leads to abrogation of the specific antileukemia immune response. |
| 44 | 8943568 | CD4+ CD45RA+ T cells from adults respond to recall antigens after CD28 ligation. |
| 45 | 9079822 | The immunological response enhanced by B7-2 decreased below the level of mice immunized with the DNA vaccine in combination with CTLA4Ig, an inhibitor of the B7/CD28 co-stimulatory signal, suggesting that this signal is critical for the enhanced response induced by co-inoculation of the DNA vaccine and B7-2 expression plasmid. |
| 46 | 9079822 | This enhancement appeared to occur via an interferon-gamma (IFN-gamma)-dependent mechanism, as combined administration of the B7-2 plasmid and neutralizing anti-IFN-gamma antibody abrogated the virus-specific cell-mediated immunity. |
| 47 | 9097923 | All parameters of T cell activation were normal, including proliferation mediated by CD2, CD3-T cell receptor (TCR) complex, and CD28; acquisition of responsiveness to exogenous IL-2 and IL-4; activation of proteinkinase C (PKC) by phorbol ester and calcium influx by addition of ionomycin. |
| 48 | 9389737 | Effects of subcutaneous interleukin-2 therapy on CD4 subsets and in vitro cytokine production in HIV+ subjects. |
| 49 | 9389737 | HIV infection is characterized by the reduction of the CD4+, CD45RA+, CD26+, and CD28+ lymphocyte subsets and of the in vitro production of IL-2, IL-4, and interferon-gamma; on the contrary, chemokine production is usually increased. |
| 50 | 9389737 | The aim of this study was to define the effects of rIL-2 administration on CD4+, CD45RA+, CD45R0+, and CD26+ lymphocytes and on the in vitro production of IL-2, IL-4, IL-10, IFN-gamma, RANTES, and sCD30 in HIV+ patients. 10 HIV+ patients with CD4 cell counts between 200 and 500 cells/mm3 were treated with six cycles of subcutaneous recombinant IL-2 administration, in combination with zidovudine and didanosine. |
| 51 | 9389737 | At this time, the in vitro production of IL-2, IL-4, IFN-gamma, and sCD30 were significantly upregulated. |
| 52 | 9389737 | This expanded cell population recovered the ability to produce in vitro IL-2, IL-4, and IFN-gamma. |
| 53 | 9533542 | The production and functional testing of two new bispecific (bs) hybrid antibodies [Abs; bs Ab hemagglutinin-neuraminidase (HN) x CD3 and bs Ab HN x CD28] designed for cancer vaccine modification are described. |
| 54 | 9533542 | The bs Abs attached to tumor target cells were able to cross-link CTL effector cells and up-regulate T-cell activation markers on autologous cancer patient-derived CD4 and CD8 T lymphocytes. |
| 55 | 9570577 | T cell activation requires an antigen-specific signal through the TCR and a costimulatory signal, which can be mediated by B7-1 or B7-2 engagement of CD28. |
| 56 | 9570577 | To directly examine the activation state of myelin-reactive T cells in MS, the costimulation requirements necessary to activate myelin basic protein (MBP) or tetanus toxoid (TT)-reactive CD4 T cells were compared between normal controls and MS patients. |
| 57 | 9570577 | In marked contrast, T cells from patients with MS stimulated with MBP p85-99 in the absence of B7-1 or B7-2 signals expanded and proliferated. |
| 58 | 9570577 | Thus, MBP-reactive CD4 T cells in patients with MS are costimulation independent and have been previously activated in vivo. |
| 59 | 9570577 | These experiments provide further direct evidence for a role of activated MBP-specific CD4 T cells in the pathogenesis of MS. |
| 60 | 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. |
| 61 | 9573027 | In this study, we show that CD34(+)/CD86(+) cells can also present tetanus toxoid antigen to memory CD4(+) T cells. |
| 62 | 9573027 | CD34(+)/CD86(+) marrow cells cultured in granulocyte-macrophage colony-stimulating factor (GM-CSF)-generated macrophages. |
| 63 | 9573027 | In contrast, CD34(+)/CD86(-) cells cultured in GM-CSF generated a predominant population of granulocytes. |
| 64 | 9573027 | CD34(+)/CD86(+) cells cultured in GM-CSF plus tumor necrosis factor-alpha (TNF-alpha) generated almost exclusively CD1a+/CD83(+) dendritic cells. |
| 65 | 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. |
| 66 | 9573027 | In addition, CD34(+)/CD86(+) cells cultured in granulocyte colony-stimulating factor failed to generate CD15(+) granulocytes. |
| 67 | 9573027 | The ontogeny of dendritic cells was recapitulated by stimulation of CD34(+)/CD86(-) cells with TNF-alpha that induced expression of CD86. |
| 68 | 9573027 | Subsequent costimulation of CD86(+) cells with GM-CSF plus TNF-alpha lead to expression of CD83 and produced terminal dendritic cell differentiation. |
| 69 | 9645616 | LAG-3 has been proposed as an alternate ligand for HLA class II due to some sequence homology and similarities in exon-intron organization with CD4. |
| 70 | 9645616 | Unlike blockade of the CD28 receptor, however, LAG-3-Ig-mediated inhibition could not be reversed by exogenous IL-2 supplementation. |
| 71 | 9645616 | Cytofluorimetric analysis of the phenotype of cells exposed to LAG-3-Ig in MLR cultures revealed a decrease in IL-2 receptor expression (CD25) on CD4+ cells in all donors tested. |
| 72 | 9707601 | CTLA-4 blockade synergizes with tumor-derived granulocyte-macrophage colony-stimulating factor for treatment of an experimental mammary carcinoma. |
| 73 | 9707601 | CTLA-4 is a second B7 receptor expressed by T cells upon activation that, unlike CD28, appears to deliver an inhibitory signal to T cells. |
| 74 | 9707601 | In the present study, we report that the combination of both CTLA-4 blockade and a vaccine consisting of granulocyte-macrophage colony-stimulating factor-expressing SM1 cells resulted in regression of parental SM1 tumors, despite the ineffectiveness of either treatment alone. |
| 75 | 9707601 | This synergistic therapy resulted in long-lasting immunity to SM1 and depended on both CD4(+) and CD8(+) T cells. |
| 76 | 9707601 | Given that granulocyte-macrophage colony-stimulating factor promotes differentiation and activation of dendritic cells as well as enhances cross-priming of T cells to tumor-derived antigens and that SM1 is major histocompatibility complex class II-negative, our findings suggest that CTLA-4 blockade acts at the level of a host-derived antigen-presenting cell. |
| 77 | 9711781 | Maturation of human neonatal CD4+ and CD8+ T lymphocytes into Th1/Th2 effectors. |
| 78 | 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. |
| 79 | 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. |
| 80 | 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. |
| 81 | 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. |
| 82 | 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. |
| 83 | 9711781 | Unlike CD4+ T cells, neonatal CD8+ T cells strictly require exogenous IL-4 to develop into IL-4/IL-5 producers. |
| 84 | 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. |
| 85 | 9711781 | Maturation of human neonatal CD4+ and CD8+ T lymphocytes into Th1/Th2 effectors. |
| 86 | 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. |
| 87 | 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. |
| 88 | 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. |
| 89 | 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. |
| 90 | 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. |
| 91 | 9711781 | Unlike CD4+ T cells, neonatal CD8+ T cells strictly require exogenous IL-4 to develop into IL-4/IL-5 producers. |
| 92 | 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. |
| 93 | 9711781 | Maturation of human neonatal CD4+ and CD8+ T lymphocytes into Th1/Th2 effectors. |
| 94 | 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. |
| 95 | 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. |
| 96 | 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. |
| 97 | 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. |
| 98 | 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. |
| 99 | 9711781 | Unlike CD4+ T cells, neonatal CD8+ T cells strictly require exogenous IL-4 to develop into IL-4/IL-5 producers. |
| 100 | 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. |
| 101 | 9711781 | Maturation of human neonatal CD4+ and CD8+ T lymphocytes into Th1/Th2 effectors. |
| 102 | 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. |
| 103 | 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. |
| 104 | 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. |
| 105 | 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. |
| 106 | 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. |
| 107 | 9711781 | Unlike CD4+ T cells, neonatal CD8+ T cells strictly require exogenous IL-4 to develop into IL-4/IL-5 producers. |
| 108 | 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. |
| 109 | 9720647 | Here we describe that aging is associated with the emergence of an unusual CD4 T cell subset characterized by the loss of CD28 expression. |
| 110 | 9720647 | Despite the deficiency of CD28, these unusual T cells remain functionally active and produce high concentrations of interferon-gamma (IFN-gamma) and interleukin-2 (IL-2). |
| 111 | 9720647 | The loss of CD28 expression is correlated with a lack of CD40 ligand expression rendering these CD4 T cells incapable of promoting B cell differentiation and immunoglobulin secretion. |
| 112 | 9720647 | We propose that the emergence of CD28-deficient CD4 T cells in the elderly can partially explain age-specific aberrations in immune responsiveness. |
| 113 | 9720647 | Here we describe that aging is associated with the emergence of an unusual CD4 T cell subset characterized by the loss of CD28 expression. |
| 114 | 9720647 | Despite the deficiency of CD28, these unusual T cells remain functionally active and produce high concentrations of interferon-gamma (IFN-gamma) and interleukin-2 (IL-2). |
| 115 | 9720647 | The loss of CD28 expression is correlated with a lack of CD40 ligand expression rendering these CD4 T cells incapable of promoting B cell differentiation and immunoglobulin secretion. |
| 116 | 9720647 | We propose that the emergence of CD28-deficient CD4 T cells in the elderly can partially explain age-specific aberrations in immune responsiveness. |
| 117 | 9720647 | Here we describe that aging is associated with the emergence of an unusual CD4 T cell subset characterized by the loss of CD28 expression. |
| 118 | 9720647 | Despite the deficiency of CD28, these unusual T cells remain functionally active and produce high concentrations of interferon-gamma (IFN-gamma) and interleukin-2 (IL-2). |
| 119 | 9720647 | The loss of CD28 expression is correlated with a lack of CD40 ligand expression rendering these CD4 T cells incapable of promoting B cell differentiation and immunoglobulin secretion. |
| 120 | 9720647 | We propose that the emergence of CD28-deficient CD4 T cells in the elderly can partially explain age-specific aberrations in immune responsiveness. |
| 121 | 9720647 | Here we describe that aging is associated with the emergence of an unusual CD4 T cell subset characterized by the loss of CD28 expression. |
| 122 | 9720647 | Despite the deficiency of CD28, these unusual T cells remain functionally active and produce high concentrations of interferon-gamma (IFN-gamma) and interleukin-2 (IL-2). |
| 123 | 9720647 | The loss of CD28 expression is correlated with a lack of CD40 ligand expression rendering these CD4 T cells incapable of promoting B cell differentiation and immunoglobulin secretion. |
| 124 | 9720647 | We propose that the emergence of CD28-deficient CD4 T cells in the elderly can partially explain age-specific aberrations in immune responsiveness. |
| 125 | 9758406 | Although the roles played by the CD4+ population of T lymphocytes in immunodermatology were so far actively investigated, much less is known about the roles played in the skin by CD8+ cytolytic T lymphocytes (CTL). |
| 126 | 9758406 | Phenotypically, not only CD8+ CTL can be subdivided into CD8+ CD28+ CD11b- and CD8+ CD28- CD11b+ subsets, but also an up-to-now undetected CD8+ CD28- CD11b- subset does exist. |
| 127 | 9796737 | Such Ts cells express the CD8+CD28- phenotype and show the following characteristics: (a) antigen specificity and restriction by self MHC Class I molecules; (b) limited TCR V beta gene usage; (c) ability to inhibit antigen-specific, MHC Class II restricted, Th proliferative responses; and (d) capacity to downregulate and/or inhibit the upregulation by Th of CD40, CD80, and CD86 molecules on APCs. |
| 128 | 9844052 | Decreased CD4 and increased CD8 counts with T cell activation is associated with chronic helminth infection. |
| 129 | 9844052 | The main findings in the 'new' ETH group in comparison with the non-Ethiopian controls were: (i) decreased CD4 and increased CD8 lymphocyte counts; (ii) elevated levels of activated T cells (CD3, CD4 and CD8) expressing HLA-DR; (iii) decreased levels of 'naive' CD4+ cells (CD45RA+), with increased levels of 'memory' CD4+ cells (CD45RO+); (iv) decreased numbers of CD28+ CD8+ lymphocytes; (v) marked increase in lymphocyte apoptosis. |
| 130 | 9988453 | Some of the agents with the most potential include antagonists of the T-cell costimulatory molecule CD28, local stimulators of the Thl subset of cytokines such as the BCG vaccine and potentially, antagonists of the eotaxin chemokine receptor and agonists of the T-cell costimulatory molecule CTLA-4. |
| 131 | 10079108 | We coimmunized cDNA expression cassettes encoding the adhesion molecules intracellular adhesion molecule-1 (ICAM-1), lymphocyte function associated-3 (LFA-3), and vascular cell adhesion molecule-1 (VCAM-1) along with DNA immunogens, and we analyzed the resulting antigen-specific immune responses. |
| 132 | 10079108 | We observed that antigen-specific T-cell responses can be enhanced by the coexpression of DNA immunogen and adhesion molecules ICAM-1 and LFA-3. |
| 133 | 10079108 | Coexpression of ICAM-1 or LFA-3 molecules along with DNA immunogens resulted in a significant enhancement of T-helper cell proliferative responses. |
| 134 | 10079108 | Although VCAM-1 and ICAM-1 are similar in size, VCAM-1 coimmunization did not have any measurable effect on cell-mediated responses. |
| 135 | 10079108 | These results suggest that ICAM-1 and LFA-3 provide direct T-cell costimulation. |
| 136 | 10079108 | These observations are further supported by the finding that coinjection with ICAM-1 dramatically enhanced the level of interferon-gamma (IFN-gamma) and beta-chemokines macrophage inflammatory protein-1alpha (MIP-1alpha), MIP-1beta, and regulated on activation normal T-cell expression and secreted (RANTES) produced by stimulated T cells. |
| 137 | 10079108 | Through comparative studies, we observed that ICAM-1/LFA-1 T-cell costimulatory pathways are independent of CD86/CD28 pathways and that they may synergistically expand T-cell responses in vivo. |
| 138 | 10380709 | Cloning and sequence comparison of sheep CD28 and CTLA-4. |
| 139 | 10607491 | Both groups of VPLN cells were activated in vitro with anti-CD3 or anti-CD3/CD28 mAbs followed by expansion in IL-2. |
| 140 | 10607491 | Anti-CD3/CD28 activation resulted in greater expansion of CD4(+) T cells compared to anti-CD3. |
| 141 | 10607491 | After activation, VPLN cells were stimulated with irradiated autologous tumor targets and cytokines (IFN-gamma, GM-CSF, IL-10) released into the supernatants were measured 24 h later. |
| 142 | 10607491 | Anti-CD3/CD28-activated BCG-VPLN cells were found to have a greater release of IFN-gamma compared with that of WT-VPLN cells, which was not observed significantly with IL-10 or GM-CSF. |
| 143 | 10607491 | BCG resulted in increased VPLN cell yield as well as enhanced type 1 (IFN-gamma release) immune responses of VPLN cells to autologous tumor without upregulating type 2 (IL-10 release) responses. |
| 144 | 10607491 | Both groups of VPLN cells were activated in vitro with anti-CD3 or anti-CD3/CD28 mAbs followed by expansion in IL-2. |
| 145 | 10607491 | Anti-CD3/CD28 activation resulted in greater expansion of CD4(+) T cells compared to anti-CD3. |
| 146 | 10607491 | After activation, VPLN cells were stimulated with irradiated autologous tumor targets and cytokines (IFN-gamma, GM-CSF, IL-10) released into the supernatants were measured 24 h later. |
| 147 | 10607491 | Anti-CD3/CD28-activated BCG-VPLN cells were found to have a greater release of IFN-gamma compared with that of WT-VPLN cells, which was not observed significantly with IL-10 or GM-CSF. |
| 148 | 10607491 | BCG resulted in increased VPLN cell yield as well as enhanced type 1 (IFN-gamma release) immune responses of VPLN cells to autologous tumor without upregulating type 2 (IL-10 release) responses. |
| 149 | 10607491 | Both groups of VPLN cells were activated in vitro with anti-CD3 or anti-CD3/CD28 mAbs followed by expansion in IL-2. |
| 150 | 10607491 | Anti-CD3/CD28 activation resulted in greater expansion of CD4(+) T cells compared to anti-CD3. |
| 151 | 10607491 | After activation, VPLN cells were stimulated with irradiated autologous tumor targets and cytokines (IFN-gamma, GM-CSF, IL-10) released into the supernatants were measured 24 h later. |
| 152 | 10607491 | Anti-CD3/CD28-activated BCG-VPLN cells were found to have a greater release of IFN-gamma compared with that of WT-VPLN cells, which was not observed significantly with IL-10 or GM-CSF. |
| 153 | 10607491 | BCG resulted in increased VPLN cell yield as well as enhanced type 1 (IFN-gamma release) immune responses of VPLN cells to autologous tumor without upregulating type 2 (IL-10 release) responses. |
| 154 | 10607750 | However, upon re-stimulation with fresh APC and antigen, tolerized T(h)1 cells failed to proliferate or to produce T(h)1 cytokine message or secreted protein, had decreased expression of CD25, CD28 and B7 and increased expression of MHC class II molecules, and demonstrated an enhanced commitment to apoptosis. |
| 155 | 10640735 | Interaction between B7 on APC and CD28 on naive T cells is necessary for priming the T cells. |
| 156 | 10640735 | On the other hand, interaction between B7 on APC and CTLA-4 on activated T cells transduces a negative regulatory signal to the activated T cells. |
| 157 | 10652164 | Both the number of CD4+ and CD8+ T cells increased during the first week of therapy in parallel with a decline in plasma viraemia. |
| 158 | 10652164 | The majority of CD4+ T cells contributing to this expansion expressed CD28, CD45RO and Fas, whereas the expanded CD8+ T cells were predominantly CD28-, CD45RO+, CD38+, Fas+ and Fas+ (CD95). |
| 159 | 10655112 | T-cell co-stimulation delivered by the molecules B7-1 or B7-2 through CD28 has a positive effect on T-cell activation, whereas engagement of cytotoxic T-lymphocyte antigen 4 (CTLA-4) by these molecules inhibits activation. |
| 160 | 10655112 | The effects of B7-1 and B7-2 co-stimulation through CD28 depend on the strength of the signal delivered through the T-cell receptor (TCR) and the activation state of T cells during activation. |
| 161 | 10655112 | T-cell co-stimulation delivered by the molecules B7-1 or B7-2 through CD28 has a positive effect on T-cell activation, whereas engagement of cytotoxic T-lymphocyte antigen 4 (CTLA-4) by these molecules inhibits activation. |
| 162 | 10655112 | The effects of B7-1 and B7-2 co-stimulation through CD28 depend on the strength of the signal delivered through the T-cell receptor (TCR) and the activation state of T cells during activation. |
| 163 | 10816483 | Therefore, CD28(+) CD4(+) T cells are sufficient for clearance of avirulent Salmonella in naive hosts, whereas CD4(+) T cells and specific antibodies are required for protection from virulent Salmonella in immune hosts. |
| 164 | 10854153 | The rationale for this strategy is that T-cells need two signals before they can mount a cytotoxic response: the binding of the T-cell receptor (TCR) to an antigenic peptide presented on major histocompatibility complex (MHC) molecules and the binding of CD28 to B7-1. |
| 165 | 10888354 | The inhibition of CD4+ cell depletion was associated with maintaining the proliferative response of helper T-cells against SIV p27 in the previously nonpathogenic virus-inoculated animals following the pathogenic virus challenge. |
| 166 | 10888354 | Furthermore, the decline of CD28+ cells, the increase in CD95+ cells, and the enhancement of in vitro apoptosis in PBMC were inhibited in the non-pathogenic virus-inoculated animals. |
| 167 | 11106934 | Selection and characterization of MUC1-specific CD8+ T cells from MUC1 transgenic mice immunized with dendritic-carcinoma fusion cells. |
| 168 | 11106934 | Here we demonstrate that lymph node cells from MUC1.Tg mice immunized with the FC/MUC1 fusion cells proliferate in response to MUC1 antigen by a mechanism dependent on the function of CD4, major histocompatibility complex (MHC) class II, B7-1, B7-2, CD28, CD40 and CD40 ligand. |
| 169 | 11106934 | The findings demonstrate that stimulation of lymph node cells with MUC1 results in selection of MUC1-specific CD8+ T cells. |
| 170 | 11106934 | We show that the CD8+ T cells exhibit MUC1-specific cytotoxic T lymphocyte (CTL) activity by recognition of MUC1 peptides presented in the context of MHC class I molecules Kb and Db. |
| 171 | 11106934 | The MUC1-specific CD8+ T cells also exhibit antitumour activity against MUC1-positive metastases, but with no apparent reactivity against normal tissues. |
| 172 | 11106934 | These results indicate that immunization of MUC1.Tg mice with FC/MUC1 reverses immunological unresponsiveness to MUC1 by presentation of MUC1 peptides in the presence of costimulatory signals and generates MHC-restricted MUC1-specific CD8+ T cells. |
| 173 | 11120800 | CD28, the primary positive costimulatory receptor on T cells, has two identified ligands, B7-1 and B7-2. |
| 174 | 11120800 | Functional differences between B7-1 and B7-2 observed in vivo therefore may not reflect inherent differences in the interactions of CD28 with these ligands. |
| 175 | 11120800 | CD28, the primary positive costimulatory receptor on T cells, has two identified ligands, B7-1 and B7-2. |
| 176 | 11120800 | Functional differences between B7-1 and B7-2 observed in vivo therefore may not reflect inherent differences in the interactions of CD28 with these ligands. |
| 177 | 11282983 | Using mAb to trigger CD2 and CD28 co-stimulatory molecules, we found that such dual co-stimulation of LT-T induces profound and sustained responses including CD25 expression, IL-2 secretion and proliferation. |
| 178 | 11282983 | Blocking studies demonstrated that optimal proliferation was critically dependent on co-stimulation via CD2 and CD28 engaged by their ligands on the APC. |
| 179 | 11282983 | Using mAb to trigger CD2 and CD28 co-stimulatory molecules, we found that such dual co-stimulation of LT-T induces profound and sustained responses including CD25 expression, IL-2 secretion and proliferation. |
| 180 | 11282983 | Blocking studies demonstrated that optimal proliferation was critically dependent on co-stimulation via CD2 and CD28 engaged by their ligands on the APC. |
| 181 | 11283156 | B7-DC fails to bind the B7.1/2 receptors CD28 and cytotoxic T lymphocyte-associated antigen (CTLA)-4, but does bind PD-1, a receptor for B7-H1/PD-L1. |
| 182 | 11283156 | In particular, B7-DC strongly costimulates interferon gamma but not interleukin (IL)-4 or IL-10 production from isolated naive T cells. |
| 183 | 11300483 | Activation of these T cells was indicated by increased secretion of proinflammatory cytokines IFN-gamma, interleukin (IL)-12 and granulocyte/macrophage-colony stimulating factor, as well as specific tumor rejection and growth suppression in vaccinated CEA-transgenic mice after a lethal challenge with murine MC38 colon carcinoma cells. |
| 184 | 11300483 | These tumor cells were double transfected with CEA and the human epithelial cell adhesion molecule (Ep-CAM)/KSA and consequently served as a docking site for a recombinant antibody-IL2 fusion protein (KS1/4-IL2) recognizing KSA. |
| 185 | 11300483 | Importantly, the efficacy of the tumor-protective immune response was markedly increased by boosts with this antibody-IL2 fusion protein, resulting in more effective tumor rejection coupled with increased expression of costimulatory molecules B7.2/B7.2 and intercellular adhesion molecule 1 (ICAM-1) on dendritic cells and intensified release of proinflammatory cytokines IFN-gamma, IL-12, and granulocyte/macrophage-colony stimulating factor from T cells of successfully vaccinated CEA-transgenic C57BL/6J mice. |
| 186 | 11300483 | Increased T-cell activation mediated by boosts with KS1/4-IL2 fusion protein after tumor cell challenge was further indicated by expanded expression of T-cell activation markers CD25, CD28, CD69, and LFA-1. |
| 187 | 11300490 | For CFC, whole blood was incubated overnight with antigen in the presence of costimulatory antibodies to CD28 and CD49d. |
| 188 | 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. |
| 189 | 11300490 | Most responses were detected with both TNF-alpha and IFN-gamma, but one patient's KLH response was detected only with TNF-alpha. |
| 190 | 11390619 | Differential incorporation of CD45, CD80 (B7-1), CD86 (B7-2), and major histocompatibility complex class I and II molecules into human immunodeficiency virus type 1 virions and microvesicles: implications for viral pathogenesis and immune regulation. |
| 191 | 11390619 | Because T-cell receptor engagement of major histocompatibility complex (MHC) molecules in the absence of costimulation mediated via CD28 binding to CD80 (B7-1) or CD86 (B7-2) can lead to anergy or apoptosis, we determined whether HIV type 1 (HIV-1) virions incorporated MHC class I (MHC-I), MHC-II, CD80, or CD86. |
| 192 | 11390619 | HIV infection increased MHC-II expression on T- and B-cell lines, macrophages, and peripheral blood mononclear cells (PBMC) but did not significantly alter the expression of CD80 or CD86. |
| 193 | 11390619 | HIV virions derived from all MHC-II-positive cell types incorporated high levels of MHC-II, and both virions and microvesicles preferentially incorporated CD86 compared to CD80. |
| 194 | 11405550 | Anti-inflammatory cytokines in asthma and allergy: interleukin-10, interleukin-12, interferon-gamma. |
| 195 | 11405550 | Interleukin-10 (IL-10) is a cytokine derived from CD4+ T-helper type 2 (T(H2)) cells identified as a suppressor of cytokines from T-helper type 1(T(H1)) cells. |
| 196 | 11405550 | In this context, IL-12 and IFN-gamma production in asthma have been found to be decreased, and this may reduce their capacity to inhibit IgE synthesis and allergic inflammation. |
| 197 | 11405550 | Therapeutic modulation of T(H1)/T(H2) imbalance in asthma and allergy by mycobacterial vaccine, specific immunotherapy and cytoline-guanosine dinucleotide motif may lead to increases in IL-12 and IFN-gamma production. |
| 198 | 11405550 | Stimulation of IL-10 production by antigen-specific T-cells during immunotherapy may lead to anergy through inhibition of CD28-costimulatory molecule signalling by IL-10s anti-inflammatory effect on basophils, mast cells and eosinophils. |
| 199 | 11434720 | Specifically, anergy is characterized by lack of activation of lck, ZAP 70, Ras, ERK, JNK, AP-1, and NF-AT. |
| 200 | 11434720 | This second messenger upregulates the cyclin-dependent kinase (cdk) inhibitor p27kip1, sequestering cyclin D2-cdk4, and cyclin E/cdk2 complexes and preventing progression of T cells through the G1 restriction point of the cell cycle. |
| 201 | 11434720 | In contrast, costimulation through CD28 prevents p27kip1 accumulation by decreasing the levels of intracellular cAMP and promotes p27kip1 down-regulation due to direct degradation of the protein via the ubiquitin-proteasome pathway. |
| 202 | 11434720 | Subsequent autocrine action of IL-2 leads to further degradation of p27kip1 and entry into S phase. |
| 203 | 11446744 | The costimulatory pathway that includes CD80, CD86, CD28, and CTLA-4 plays a key role in regulating T cell activation and tolerance and is a promising therapeutic target. |
| 204 | 11446744 | We found that DeltaCD86 was able to inhibit the engagement of FcCTLA-4 but not of FcCD28 to CD80 and CD86 expressed on COS cells. |
| 205 | 11446744 | Coadministration of plasmid pDelta86 encoding for the extracellular domains of CD86 along with a plasmid encoding for the glycoprotein D (pgD) of herpes simplex virus-2 (a membrane-bound protein) by the im route in mice resulted in a strong inhibition of the cell-mediated immune response in the spleen and in draining lymph nodes. |
| 206 | 11485354 | Additionally, bromelain did not affect TCR and CD28-induced proliferation of highly purified CD4+ T cells, but did inhibit IL-2 production by these cells. |
| 207 | 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). |
| 208 | 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. |
| 209 | 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). |
| 210 | 11590187 | Vdelta2 cells had a phenotype typical of most alphabeta T cells in blood; i.e., they were CD5(+), CD28(+), and CD57(-). |
| 211 | 11590187 | In contrast, Vdelta1 cells tended to be CD5(-/dull), CD28(-), and CD57(+). |
| 212 | 11590187 | Vdelta2 cells had a phenotype typical of most alphabeta T cells in blood; i.e., they were CD5(+), CD28(+), and CD57(-). |
| 213 | 11590187 | In contrast, Vdelta1 cells tended to be CD5(-/dull), CD28(-), and CD57(+). |
| 214 | 11591784 | A dual-function DNA vaccine encoding carcinoembryonic antigen and CD40 ligand trimer induces T cell-mediated protective immunity against colon cancer in carcinoembryonic antigen-transgenic mice. |
| 215 | 11591784 | A carcinoembryonic Ag (CEA)-based DNA vaccine encoding both CEA and CD40 ligand trimer achieved effective tumor-protective immunity against murine colon carcinoma in CEA-transgenic mice by activating both naive T cells and dendritic cells. |
| 216 | 11591784 | Peripheral T cell tolerance to CEA was broken in a prophylactic model by this novel, dual-function DNA vaccine, whose efficacy was further enhanced by boosts with a recombinant Ab-IL-2 fusion protein (huKS1/4-IL-2). |
| 217 | 11591784 | Second, specific activation of dendritic cells was indicated by their marked up-regulation in expression of costimulatory molecules B7.1 (CD80), B7.2 (CD86), and ICAM-1. |
| 218 | 11591784 | Third, a decisive increase over control values was observed in both MHC class I Ag-restricted cytotoxicity of CTLs from successfully vaccinated mice and secretion of proinflammatory cytokines IFN-gamma and IL-12. |
| 219 | 11591784 | Fourth, activation of CTLs was augmented, as indicated by up-regulation of activity markers LFA-1, CD25, CD28, and CD69. |
| 220 | 11591784 | Taken together, these results suggest that a dual-function DNA vaccine encoding CEA and CD40 ligand trimer combined with tumor-targeted IL-2 may be a promising strategy for the rational development of DNA-based cancer vaccines for future clinical applications. |
| 221 | 11672905 | This vaccine, delivered by oral gavage with an attenuated strain of Salmonella typhimurium (SL7207), and boosted with an antibody-IL2 fusion protein, induced tumor-protective immunity mediated by MHC class I antigen-restricted CD8(+) T cells, resulting in eradication of subcutaneous tumors in 100% of mice and prevention of experimental pulmonary metastases in 75% of experimental animals. |
| 222 | 11672905 | Both CTL and antigen-presenting dendritic cells were activated as indicated by a decisive increase in their respective activation markers CD2, CD25, CD28 as well as CD48 and CD80. |
| 223 | 11711609 | The composition of the T-cell compartment was analyzed by flow cytometry and the sizes of three T-cell subsets, CD4(+) CD45RO(+) cells, CD4(+) CD28(null) cells, and CD8(+) CD28(null) cells, were determined. |
| 224 | 11711609 | The likelihood of successful vaccination declined with age and was independently correlated with the expansion of a particular T-cell subset, CD8(+) CD28(null) T cells. |
| 225 | 11711609 | The sizes of the CD4(+) CD45RO(+) memory T-cell and CD4(+) CD28(null) T-cell subsets had no effect on the ability to mount anti-influenza virus antibody responses. |
| 226 | 11711609 | Frequencies of CD8(+) CD28(null) T cells are useful biological markers of compromised immunocompetence, identifying individuals at risk for insufficient antibody responses. |
| 227 | 11711609 | The composition of the T-cell compartment was analyzed by flow cytometry and the sizes of three T-cell subsets, CD4(+) CD45RO(+) cells, CD4(+) CD28(null) cells, and CD8(+) CD28(null) cells, were determined. |
| 228 | 11711609 | The likelihood of successful vaccination declined with age and was independently correlated with the expansion of a particular T-cell subset, CD8(+) CD28(null) T cells. |
| 229 | 11711609 | The sizes of the CD4(+) CD45RO(+) memory T-cell and CD4(+) CD28(null) T-cell subsets had no effect on the ability to mount anti-influenza virus antibody responses. |
| 230 | 11711609 | Frequencies of CD8(+) CD28(null) T cells are useful biological markers of compromised immunocompetence, identifying individuals at risk for insufficient antibody responses. |
| 231 | 11711609 | The composition of the T-cell compartment was analyzed by flow cytometry and the sizes of three T-cell subsets, CD4(+) CD45RO(+) cells, CD4(+) CD28(null) cells, and CD8(+) CD28(null) cells, were determined. |
| 232 | 11711609 | The likelihood of successful vaccination declined with age and was independently correlated with the expansion of a particular T-cell subset, CD8(+) CD28(null) T cells. |
| 233 | 11711609 | The sizes of the CD4(+) CD45RO(+) memory T-cell and CD4(+) CD28(null) T-cell subsets had no effect on the ability to mount anti-influenza virus antibody responses. |
| 234 | 11711609 | Frequencies of CD8(+) CD28(null) T cells are useful biological markers of compromised immunocompetence, identifying individuals at risk for insufficient antibody responses. |
| 235 | 11711609 | The composition of the T-cell compartment was analyzed by flow cytometry and the sizes of three T-cell subsets, CD4(+) CD45RO(+) cells, CD4(+) CD28(null) cells, and CD8(+) CD28(null) cells, were determined. |
| 236 | 11711609 | The likelihood of successful vaccination declined with age and was independently correlated with the expansion of a particular T-cell subset, CD8(+) CD28(null) T cells. |
| 237 | 11711609 | The sizes of the CD4(+) CD45RO(+) memory T-cell and CD4(+) CD28(null) T-cell subsets had no effect on the ability to mount anti-influenza virus antibody responses. |
| 238 | 11711609 | Frequencies of CD8(+) CD28(null) T cells are useful biological markers of compromised immunocompetence, identifying individuals at risk for insufficient antibody responses. |
| 239 | 11751943 | Naive T cells are optimally delineated by their homogeneous CD95(low)CD28(high)beta(7) integrin(int) (CD4+) or CD95(low)CD28(int)CD11a(low) (CD8+) phenotypes. |
| 240 | 11751943 | CD4+ and CD8+ memory subsets were CD95(high), but otherwise phenotypically heterogeneous and included all IFN-gamma production, RM CMV-specific responses, effector site T cells, and demonstrated high in vivo proliferative activity ( approximately 10 times the naive subset). |
| 241 | 11797392 | Formation of tri-molecular complex among T cell antigen receptor(TCR), major histocompatibility complex(MHC) molecule, and antigen peptide produces signal 1 via TCR. |
| 242 | 11797392 | However, signal 2 is elicited by interaction between CD28 and its ligands(CD80 and CD86) and is antigen-independent. |
| 243 | 11797392 | Interestingly, cell surface expression of CD80 and CD86 on antigen-presenting cell(APC) is regulated by stimulus via CD40. |
| 244 | 11846457 | CD4+ nadirs were positively correlated with recent numbers of CD4+ T-cells (P < 0.001), memory cells (P < 0.001), and naïve CD4+ T-cells (P < 0.05) and CD4+ CD28+ T-lymphocytes (P < 0.05) and were negatively correlated with recent CD8+ T-lymphocyte counts (P < 0.05). |
| 245 | 11860706 | Cytotoxic T lymphocyte antigen 4 (CTLA-4 or CD152) is a strong negative regulator of T cell activity. |
| 246 | 11860706 | Like CD28 (a positive regulator) it binds to B7-1 and B7-2, and there is no known natural selective ligand. |
| 247 | 11860706 | However, a single amino acid substitution in B7-1 (W88 > A; denoted B7-1wa) abrogates binding to CD28 but not to CTLA-4. |
| 248 | 11860706 | Interferon-gamma and interleukin-4 were both depressed, arguing against a Th2 bias. |
| 249 | 11860706 | Cytotoxic T lymphocyte antigen 4 (CTLA-4 or CD152) is a strong negative regulator of T cell activity. |
| 250 | 11860706 | Like CD28 (a positive regulator) it binds to B7-1 and B7-2, and there is no known natural selective ligand. |
| 251 | 11860706 | However, a single amino acid substitution in B7-1 (W88 > A; denoted B7-1wa) abrogates binding to CD28 but not to CTLA-4. |
| 252 | 11860706 | Interferon-gamma and interleukin-4 were both depressed, arguing against a Th2 bias. |
| 253 | 11937526 | In vivo triggering through 4-1BB enables Th-independent priming of CTL in the presence of an intact CD28 costimulatory pathway. |
| 254 | 11937526 | Triggering of 4-1BB, a member of the TNFR family, through in vivo administration of agonistic anti-4-1BB Ab delivers a powerful costimulatory signal to CTL. |
| 255 | 11937526 | Accordingly, blockade of the CD28-costimulatory pathway abrogates the capacity of agonistic anti-4-1BB Ab to trigger Th-independent CTL immunity. |
| 256 | 11937526 | In conclusion, our data reveal that the 4-1BB-mediated survival signal is positioned downstream of Ag-specific TCR triggering and CD28-dependent costimulation of naive CTL. |
| 257 | 11937526 | In vivo triggering through 4-1BB enables Th-independent priming of CTL in the presence of an intact CD28 costimulatory pathway. |
| 258 | 11937526 | Triggering of 4-1BB, a member of the TNFR family, through in vivo administration of agonistic anti-4-1BB Ab delivers a powerful costimulatory signal to CTL. |
| 259 | 11937526 | Accordingly, blockade of the CD28-costimulatory pathway abrogates the capacity of agonistic anti-4-1BB Ab to trigger Th-independent CTL immunity. |
| 260 | 11937526 | In conclusion, our data reveal that the 4-1BB-mediated survival signal is positioned downstream of Ag-specific TCR triggering and CD28-dependent costimulation of naive CTL. |
| 261 | 11937526 | In vivo triggering through 4-1BB enables Th-independent priming of CTL in the presence of an intact CD28 costimulatory pathway. |
| 262 | 11937526 | Triggering of 4-1BB, a member of the TNFR family, through in vivo administration of agonistic anti-4-1BB Ab delivers a powerful costimulatory signal to CTL. |
| 263 | 11937526 | Accordingly, blockade of the CD28-costimulatory pathway abrogates the capacity of agonistic anti-4-1BB Ab to trigger Th-independent CTL immunity. |
| 264 | 11937526 | In conclusion, our data reveal that the 4-1BB-mediated survival signal is positioned downstream of Ag-specific TCR triggering and CD28-dependent costimulation of naive CTL. |
| 265 | 11964715 | IL-10 initiates anergy in T cells by blocking tyrosine phosphorylation of CD28 and inhibiting the CD28 co-stimulatory signal. |
| 266 | 11964715 | Restimulation in the presence of IL-2, IL-15 and possibly IL-12 leads to a T helper type 1 cytokine pattern (immunity:effective immunotherapy) and with IL-4 a T helper type 2 pattern (persistence of allergy:relapse). |
| 267 | 11990527 | Use of human CD3 monoclonal antibody for accurate CD4+ and CD8+ lymphocyte determinations in macaques: phenotypic characterization of the CD3- CD8+ cell subset. |
| 268 | 11990527 | Use of the CD2 monoclonal antibody as the T-cell marker resulted in underestimating CD4/CD8 ratios compared with using the CD3 mAb in pigtailed macaques. |
| 269 | 11990527 | Phenotypic characterization of this subset of CD3- CD8+ cells indicated that they are CD16+, CD45RA+, CD11b+, CD69+ and CD28-. |
| 270 | 12023394 | Lack of antibody production following immunization in old age: association with CD8(+)CD28(-) T cell clonal expansions and an imbalance in the production of Th1 and Th2 cytokines. |
| 271 | 12023394 | We now demonstrate the predominance of CD8(+)CD28(-) T cell clonal expansions in elderly persons who fail to produce specific Abs following influenza vaccination. |
| 272 | 12023394 | When isolated and put into culture, they are unable to proliferate, but produce IFN-gamma (but no IL-5) upon stimulation with anti-CD3 or autoantigen. |
| 273 | 12023394 | These autoreactive CD8(+) type 1 effector cells seem to trigger a Th1 polarization, as CD4(+) T cells from elderly persons without in vivo Ab production produce Th1, but only low amounts of Th2 cytokines upon in vitro stimulation with PHA. |
| 274 | 12023394 | Therefore, the increased occurrence of CD8(+)CD28(-) clonal expansions may be decisive for the development of immune deficiency in the elderly. |
| 275 | 12023394 | Lack of antibody production following immunization in old age: association with CD8(+)CD28(-) T cell clonal expansions and an imbalance in the production of Th1 and Th2 cytokines. |
| 276 | 12023394 | We now demonstrate the predominance of CD8(+)CD28(-) T cell clonal expansions in elderly persons who fail to produce specific Abs following influenza vaccination. |
| 277 | 12023394 | When isolated and put into culture, they are unable to proliferate, but produce IFN-gamma (but no IL-5) upon stimulation with anti-CD3 or autoantigen. |
| 278 | 12023394 | These autoreactive CD8(+) type 1 effector cells seem to trigger a Th1 polarization, as CD4(+) T cells from elderly persons without in vivo Ab production produce Th1, but only low amounts of Th2 cytokines upon in vitro stimulation with PHA. |
| 279 | 12023394 | Therefore, the increased occurrence of CD8(+)CD28(-) clonal expansions may be decisive for the development of immune deficiency in the elderly. |
| 280 | 12023394 | Lack of antibody production following immunization in old age: association with CD8(+)CD28(-) T cell clonal expansions and an imbalance in the production of Th1 and Th2 cytokines. |
| 281 | 12023394 | We now demonstrate the predominance of CD8(+)CD28(-) T cell clonal expansions in elderly persons who fail to produce specific Abs following influenza vaccination. |
| 282 | 12023394 | When isolated and put into culture, they are unable to proliferate, but produce IFN-gamma (but no IL-5) upon stimulation with anti-CD3 or autoantigen. |
| 283 | 12023394 | These autoreactive CD8(+) type 1 effector cells seem to trigger a Th1 polarization, as CD4(+) T cells from elderly persons without in vivo Ab production produce Th1, but only low amounts of Th2 cytokines upon in vitro stimulation with PHA. |
| 284 | 12023394 | Therefore, the increased occurrence of CD8(+)CD28(-) clonal expansions may be decisive for the development of immune deficiency in the elderly. |
| 285 | 12096029 | For this reason antiviral CD4(+) and CD8(+) T cell responses in CD28-deficient mice were studied using two different viruses [vesicular stomatitis virus and lymphocytic choriomeningitis virus (LCMV)]. |
| 286 | 12096029 | Most importantly, the present study reveals that CD28 generally is essential for the host to respond optimally over a broad set of conditions, and our results may imply that the relatively CD28 independent activation of LCMV-specific CD8(+) T cells may represent an extreme situation related to the non-cytolytic nature of this virus allowing the delivery of a uniquely strong and prolonged signal 1. |
| 287 | 12096029 | For this reason antiviral CD4(+) and CD8(+) T cell responses in CD28-deficient mice were studied using two different viruses [vesicular stomatitis virus and lymphocytic choriomeningitis virus (LCMV)]. |
| 288 | 12096029 | Most importantly, the present study reveals that CD28 generally is essential for the host to respond optimally over a broad set of conditions, and our results may imply that the relatively CD28 independent activation of LCMV-specific CD8(+) T cells may represent an extreme situation related to the non-cytolytic nature of this virus allowing the delivery of a uniquely strong and prolonged signal 1. |
| 289 | 12111121 | Molecular requirements for CD8-mediated rejection of a MUC1-expressing pancreatic carcinoma: implications for tumor vaccines. |
| 290 | 12111121 | We confirmed that a CD8(+) effector cell was required to eliminate MUC1-expressing Panc02 tumors, and demonstrated that T cells expressing TCR-alpha/beta and co-stimulation through CD28 and CD40:CD40L interactions played critical roles during the initiation of the anti-Panc02.MUC1 immune response. |
| 291 | 12111121 | TCR-alpha/beta(+) cells were required to eliminate Panc02.MUC1 tumors, while TCR-gamma/delta(+) cells played a suppressive non-MUC1-specific role in anti-Panc02 tumor immunity. |
| 292 | 12111121 | Type 1 cytokine interferon-gamma (IFN-gamma), but not interleukin-12 (IL-12), was essential for eliminating MUC1-expressing tumors, while neither IL-4 nor IL-10 (type 2 cytokines) were required for tumor rejection. |
| 293 | 12111121 | In vitro studies demonstrated that IFN-gamma upregulated MHC class I, but not MHC class II, on Panc02.MUC1 tumor cells. |
| 294 | 12111121 | Surprisingly, both perforin and FasL played unique roles during the effector phase of immunity to Panc02.MUC1, while lymphotoxin-alpha, but not TNFR-1, was required for immunity against Panc02.MUC1 tumors. |
| 295 | 12133941 | These analyses revealed 1) optimal peptides capable of eliciting specific responses by themselves at doses as low as 2 pg/ml, with each log increase in dose eliciting ever-increasing frequencies of responding cells over a 4- to 5-log range; 2) significant augmentation of response frequencies at all submaximal peptide doses by CD28- and CD49d-mediated costimulation; 3) differential dose response and costimulatory characteristics for IFN-gamma and IL-2 responses; and 4) no association of activation requirements with the CD27-defined CD4(+) T cell memory differentiation pathway. |
| 296 | 12167647 | Chimeric co-stimulatory molecules that selectively act through CD28 or CTLA-4 on human T cells. |
| 297 | 12167647 | CD28 and CTLA-4 (CD152) play a pivotal role in the regulation of T cell activation. |
| 298 | 12167647 | Upon ligation by CD80 (B7-1) or CD86 (B7-2), CD28 induces T cell proliferation, cytokine production, and effector functions, whereas CTLA-4 signaling inhibits expansion of activated T cells and induces tolerance. |
| 299 | 12167647 | Therefore, we hypothesized that co-stimulatory molecules that preferentially bind CD28 or CTLA-4 would have dramatically altered biological properties. |
| 300 | 12167647 | In contrast to wild-type CD80, the evolved co-stimulatory molecules, termed CD28-binding protein (CD28BP) and CTLA-4-binding protein (CTLA-4BP), selectively bind to CD28 or CTLA-4, respectively. |
| 301 | 12167647 | Furthermore, CD28BP has improved capacity to induce human T cell proliferation and interferon-gamma production compared with wild-type CD80. |
| 302 | 12167647 | These molecules provide a new approach to characterization of CD28 and CTLA-4 signals and to manipulation of the T cell response. |
| 303 | 12167647 | Chimeric co-stimulatory molecules that selectively act through CD28 or CTLA-4 on human T cells. |
| 304 | 12167647 | CD28 and CTLA-4 (CD152) play a pivotal role in the regulation of T cell activation. |
| 305 | 12167647 | Upon ligation by CD80 (B7-1) or CD86 (B7-2), CD28 induces T cell proliferation, cytokine production, and effector functions, whereas CTLA-4 signaling inhibits expansion of activated T cells and induces tolerance. |
| 306 | 12167647 | Therefore, we hypothesized that co-stimulatory molecules that preferentially bind CD28 or CTLA-4 would have dramatically altered biological properties. |
| 307 | 12167647 | In contrast to wild-type CD80, the evolved co-stimulatory molecules, termed CD28-binding protein (CD28BP) and CTLA-4-binding protein (CTLA-4BP), selectively bind to CD28 or CTLA-4, respectively. |
| 308 | 12167647 | Furthermore, CD28BP has improved capacity to induce human T cell proliferation and interferon-gamma production compared with wild-type CD80. |
| 309 | 12167647 | These molecules provide a new approach to characterization of CD28 and CTLA-4 signals and to manipulation of the T cell response. |
| 310 | 12167647 | Chimeric co-stimulatory molecules that selectively act through CD28 or CTLA-4 on human T cells. |
| 311 | 12167647 | CD28 and CTLA-4 (CD152) play a pivotal role in the regulation of T cell activation. |
| 312 | 12167647 | Upon ligation by CD80 (B7-1) or CD86 (B7-2), CD28 induces T cell proliferation, cytokine production, and effector functions, whereas CTLA-4 signaling inhibits expansion of activated T cells and induces tolerance. |
| 313 | 12167647 | Therefore, we hypothesized that co-stimulatory molecules that preferentially bind CD28 or CTLA-4 would have dramatically altered biological properties. |
| 314 | 12167647 | In contrast to wild-type CD80, the evolved co-stimulatory molecules, termed CD28-binding protein (CD28BP) and CTLA-4-binding protein (CTLA-4BP), selectively bind to CD28 or CTLA-4, respectively. |
| 315 | 12167647 | Furthermore, CD28BP has improved capacity to induce human T cell proliferation and interferon-gamma production compared with wild-type CD80. |
| 316 | 12167647 | These molecules provide a new approach to characterization of CD28 and CTLA-4 signals and to manipulation of the T cell response. |
| 317 | 12167647 | Chimeric co-stimulatory molecules that selectively act through CD28 or CTLA-4 on human T cells. |
| 318 | 12167647 | CD28 and CTLA-4 (CD152) play a pivotal role in the regulation of T cell activation. |
| 319 | 12167647 | Upon ligation by CD80 (B7-1) or CD86 (B7-2), CD28 induces T cell proliferation, cytokine production, and effector functions, whereas CTLA-4 signaling inhibits expansion of activated T cells and induces tolerance. |
| 320 | 12167647 | Therefore, we hypothesized that co-stimulatory molecules that preferentially bind CD28 or CTLA-4 would have dramatically altered biological properties. |
| 321 | 12167647 | In contrast to wild-type CD80, the evolved co-stimulatory molecules, termed CD28-binding protein (CD28BP) and CTLA-4-binding protein (CTLA-4BP), selectively bind to CD28 or CTLA-4, respectively. |
| 322 | 12167647 | Furthermore, CD28BP has improved capacity to induce human T cell proliferation and interferon-gamma production compared with wild-type CD80. |
| 323 | 12167647 | These molecules provide a new approach to characterization of CD28 and CTLA-4 signals and to manipulation of the T cell response. |
| 324 | 12167647 | Chimeric co-stimulatory molecules that selectively act through CD28 or CTLA-4 on human T cells. |
| 325 | 12167647 | CD28 and CTLA-4 (CD152) play a pivotal role in the regulation of T cell activation. |
| 326 | 12167647 | Upon ligation by CD80 (B7-1) or CD86 (B7-2), CD28 induces T cell proliferation, cytokine production, and effector functions, whereas CTLA-4 signaling inhibits expansion of activated T cells and induces tolerance. |
| 327 | 12167647 | Therefore, we hypothesized that co-stimulatory molecules that preferentially bind CD28 or CTLA-4 would have dramatically altered biological properties. |
| 328 | 12167647 | In contrast to wild-type CD80, the evolved co-stimulatory molecules, termed CD28-binding protein (CD28BP) and CTLA-4-binding protein (CTLA-4BP), selectively bind to CD28 or CTLA-4, respectively. |
| 329 | 12167647 | Furthermore, CD28BP has improved capacity to induce human T cell proliferation and interferon-gamma production compared with wild-type CD80. |
| 330 | 12167647 | These molecules provide a new approach to characterization of CD28 and CTLA-4 signals and to manipulation of the T cell response. |
| 331 | 12167647 | Chimeric co-stimulatory molecules that selectively act through CD28 or CTLA-4 on human T cells. |
| 332 | 12167647 | CD28 and CTLA-4 (CD152) play a pivotal role in the regulation of T cell activation. |
| 333 | 12167647 | Upon ligation by CD80 (B7-1) or CD86 (B7-2), CD28 induces T cell proliferation, cytokine production, and effector functions, whereas CTLA-4 signaling inhibits expansion of activated T cells and induces tolerance. |
| 334 | 12167647 | Therefore, we hypothesized that co-stimulatory molecules that preferentially bind CD28 or CTLA-4 would have dramatically altered biological properties. |
| 335 | 12167647 | In contrast to wild-type CD80, the evolved co-stimulatory molecules, termed CD28-binding protein (CD28BP) and CTLA-4-binding protein (CTLA-4BP), selectively bind to CD28 or CTLA-4, respectively. |
| 336 | 12167647 | Furthermore, CD28BP has improved capacity to induce human T cell proliferation and interferon-gamma production compared with wild-type CD80. |
| 337 | 12167647 | These molecules provide a new approach to characterization of CD28 and CTLA-4 signals and to manipulation of the T cell response. |
| 338 | 12189248 | Using human leukocyte antigen (HLA) class I tetramers, we observed that HSV-specific CD8(+) T cells in the peripheral blood expressed high levels of cutaneous lymphocyte-associated antigen (CLA). |
| 339 | 12189248 | In contrast, CD8(+) T cells specific for non-skin-tropic herpesviruses lacked CLA expression. |
| 340 | 12189248 | CLA-positive HSV-2-specific CD8(+) T cells had the characteristics of central memory cells, expressing CCR7, CD62L, and CD28, and they proliferated briskly in response to antigen. |
| 341 | 12189248 | A higher proportion of HSV-specific CD8(+) T cells recovered from herpes lesions express CLA compared with blood, consistent with a role for CLA in skin homing. |
| 342 | 12391201 | CD28, TNF receptor, and IL-12 are critical for CD4-independent cross-priming of therapeutic antitumor CD8+ T cells. |
| 343 | 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. |
| 344 | 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. |
| 345 | 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. |
| 346 | 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. |
| 347 | 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. |
| 348 | 12391201 | Thus, cross-priming of therapeutic CD8(+) T cells by a tumor vaccine transduced with GM-CSF requires TNFR, IL-12, and CD28 signaling. |
| 349 | 12391201 | CD28, TNF receptor, and IL-12 are critical for CD4-independent cross-priming of therapeutic antitumor CD8+ T cells. |
| 350 | 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. |
| 351 | 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. |
| 352 | 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. |
| 353 | 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. |
| 354 | 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. |
| 355 | 12391201 | Thus, cross-priming of therapeutic CD8(+) T cells by a tumor vaccine transduced with GM-CSF requires TNFR, IL-12, and CD28 signaling. |
| 356 | 12433688 | This lack of proliferative ability of HIV-specific CD8(+) T cells is defined by surface expression of CD57 but not by absence of CD28 or CCR7. |
| 357 | 12433688 | This inability to proliferate in response to antigen cannot be overcome by exogenous interleukin-2 (IL-2) or IL-15. |
| 358 | 12433688 | Furthermore, CD57 expression on CD8(+) T cells, CD4(+) T cells, and NK cells is a general marker of proliferative inability, a history of more cell divisions, and short telomeres. |
| 359 | 12439609 | CD3+CD4+ and CD3+CD28+ cells as well as the proliferation rate of peripheral blood lymphocytes (PBL) increased significantly in the blood of patients during therapy. |
| 360 | 12444136 | B7/CD28-dependent CD4+CD25+ regulatory T cells are essential components of the memory-protective immunity to Candida albicans. |
| 361 | 12444136 | Here we show that CD4(+)CD25(+) T cells, negatively regulating antifungal Th1 reactivity, are generated in mice with candidiasis. |
| 362 | 12444136 | CD4(+)CD25(+) T cells were not generated in B7-2- or CD28-deficient mice or in condition of IL-10 signaling deficiency. |
| 363 | 12444136 | CD4(+)CD25(+) T cells poorly proliferated in vitro; were highly enriched for cells producing IL-4, IL-10, and TGF-beta; and required IL-10-producing, Candida hypha-activated dendritic cells for generation. |
| 364 | 12444136 | Adoptive transfer of CD4(+)CD25(+) T cells or IL-10-producing dendritic cells restored resistance to reinfection and decreased inflammation in B7-2-deficient mice. |
| 365 | 12444136 | B7/CD28-dependent CD4+CD25+ regulatory T cells are essential components of the memory-protective immunity to Candida albicans. |
| 366 | 12444136 | Here we show that CD4(+)CD25(+) T cells, negatively regulating antifungal Th1 reactivity, are generated in mice with candidiasis. |
| 367 | 12444136 | CD4(+)CD25(+) T cells were not generated in B7-2- or CD28-deficient mice or in condition of IL-10 signaling deficiency. |
| 368 | 12444136 | CD4(+)CD25(+) T cells poorly proliferated in vitro; were highly enriched for cells producing IL-4, IL-10, and TGF-beta; and required IL-10-producing, Candida hypha-activated dendritic cells for generation. |
| 369 | 12444136 | Adoptive transfer of CD4(+)CD25(+) T cells or IL-10-producing dendritic cells restored resistance to reinfection and decreased inflammation in B7-2-deficient mice. |
| 370 | 12445291 | In natural immune responses CD4+ T helper (Th) cells, reactive with peptide antigens presented by major histocompatibility complex (MHC) class II molecules on dendritic cells (DC), can drive the maturation of DC that is required for induction of CD8+ cytolytic T-lymphocyte (CTL) immunity. |
| 371 | 12445291 | Proper induction, expansion and maintenance of CTL responses are achieved through delicate interactions between CD4+ T cells, DC and CD8+ T cells involving several ligand-receptor pairs. |
| 372 | 12445291 | Th cells to a large extent operate through up-regulation of CD40L, which then interacts with CD40 on DC to cause DC maturation. |
| 373 | 12445291 | Subsequent CTL induction by activated DC requires CD80/CD86 on the DC to interact with the CD28 costimulatory receptor on CD8+ T cells. |
| 374 | 12445291 | Alternative molecular triggers of DC activation that can support induction of powerful CTL responses include agonistic anti-CD40 antibody or ligands of Toll-like receptors (TLR) such as LPS (TLR4 ligand) or oligodeoxynucleotides containing CpG-motifs (TLR9 ligand). |
| 375 | 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. |
| 376 | 12496166 | 4-1BB (CD137) is induced on activated CD4(+) and CD8(+) T cells and delivers a costimulatory signal upon binding the 4-1BB ligand (4-1BBL) expressed on antigen-presenting cells. |
| 377 | 12496166 | Induction of 4-1BB is dependent on activation via the T-cell receptor (TCR) and possibly CD28. |
| 378 | 12496166 | It was previously demonstrated that both an in vivo protein (pneumococcal surface protein A [PspA])- and polysaccharide (phosphorylcholine [PC] determinant of teichoic acid)-specific immunoglobulin (Ig) isotype response to Streptococcus pneumoniae was dependent on CD4(+) TCRalphabeta(+) T cells and B7-dependent costimulation through CD28. |
| 379 | 12496166 | However, injection of an agonistic anti-4-1BB monoclonal antibody (MAb), while having no significant effect on the anti-PC response, strongly inhibits the primary anti-PspA response, the generation of PspA-specific memory, and germinal center formation but does not induce a lasting state of tolerance. |
| 380 | 12496166 | This inhibition is independent of CD8(+) T cells and is associated with the expansion of CD4(+) T cells with an activated phenotype, which is partly dependent on B7-dependent costimulation. |
| 381 | 12496166 | 4-1BB (CD137) is induced on activated CD4(+) and CD8(+) T cells and delivers a costimulatory signal upon binding the 4-1BB ligand (4-1BBL) expressed on antigen-presenting cells. |
| 382 | 12496166 | Induction of 4-1BB is dependent on activation via the T-cell receptor (TCR) and possibly CD28. |
| 383 | 12496166 | It was previously demonstrated that both an in vivo protein (pneumococcal surface protein A [PspA])- and polysaccharide (phosphorylcholine [PC] determinant of teichoic acid)-specific immunoglobulin (Ig) isotype response to Streptococcus pneumoniae was dependent on CD4(+) TCRalphabeta(+) T cells and B7-dependent costimulation through CD28. |
| 384 | 12496166 | However, injection of an agonistic anti-4-1BB monoclonal antibody (MAb), while having no significant effect on the anti-PC response, strongly inhibits the primary anti-PspA response, the generation of PspA-specific memory, and germinal center formation but does not induce a lasting state of tolerance. |
| 385 | 12496166 | This inhibition is independent of CD8(+) T cells and is associated with the expansion of CD4(+) T cells with an activated phenotype, which is partly dependent on B7-dependent costimulation. |
| 386 | 12496450 | IL-4-producing CD8+ T cells with a CD62L++(bright) phenotype accumulate in a subgroup of older adults and are associated with the maintenance of intact humoral immunity in old age. |
| 387 | 12496450 | We now demonstrate an IL-4-producing subpopulation of CD8+ T cells in a subgroup of healthy older adults. |
| 388 | 12496450 | This T cell subset is substantial in size and has a characteristic phenotype expressing CD45RO, CD28, CD62L, and CD25. |
| 389 | 12496450 | IL-4-producing CD8+ T cells produce large amounts of IL-2 but not IFN-gamma or perforin, and these cells do not have a regulatory suppressive effect on other T cells. |
| 390 | 12496450 | In vivo IL-4-producing CD8+ T cells can be stably detected over a year. |
| 391 | 12496450 | In this age group, IL-4-producing CD8+ T cells are more frequent in persons who are still capable of raising a humoral immune response following immunization than in others who fail to produce protective Abs after vaccination. |
| 392 | 12517723 | A reduced capacity to produce this cytokine in the elderly, as demonstrated by our findings of significant decreases in IFN-gamma production in vitro on stimulation with bacterial products (LPS) or viral antigens (influenza vaccine), might therefore contribute to disease susceptibility. |
| 393 | 12517723 | Using tetramer technology and IFN-gamma ELISPOT assays, we found that the commonly-observed clonal expansions of CD8+ T-cells in the elderly were for the most part poorly-functional CMV- and EBV-specific cells, expressing little CD28. |
| 394 | 12594842 | CD28 is an important costimulatory molecule for T cells, and it has been shown that cell surface expression of its ligands, CD80 and CD86, can enhance cellular immune responses against tumor cells, however, these tumor cells do not normally express the ligands. |
| 395 | 12594842 | Many new vaccines will be based upon soluble recombinant antigens, and in vaccination with these antigens CD80 and CD86 would normally be expressed on activated antigen-presenting cells and additional stimulation through CD28 would not be predicted to enhance responses further. |
| 396 | 12594842 | The mode of action of CD28 antibodies appears to be linked to their ability to signal through CD28, but not to bind the negative feedback regulatory antigen, CTLA-4. |
| 397 | 12594842 | CD28 is an important costimulatory molecule for T cells, and it has been shown that cell surface expression of its ligands, CD80 and CD86, can enhance cellular immune responses against tumor cells, however, these tumor cells do not normally express the ligands. |
| 398 | 12594842 | Many new vaccines will be based upon soluble recombinant antigens, and in vaccination with these antigens CD80 and CD86 would normally be expressed on activated antigen-presenting cells and additional stimulation through CD28 would not be predicted to enhance responses further. |
| 399 | 12594842 | The mode of action of CD28 antibodies appears to be linked to their ability to signal through CD28, but not to bind the negative feedback regulatory antigen, CTLA-4. |
| 400 | 12594842 | CD28 is an important costimulatory molecule for T cells, and it has been shown that cell surface expression of its ligands, CD80 and CD86, can enhance cellular immune responses against tumor cells, however, these tumor cells do not normally express the ligands. |
| 401 | 12594842 | Many new vaccines will be based upon soluble recombinant antigens, and in vaccination with these antigens CD80 and CD86 would normally be expressed on activated antigen-presenting cells and additional stimulation through CD28 would not be predicted to enhance responses further. |
| 402 | 12594842 | The mode of action of CD28 antibodies appears to be linked to their ability to signal through CD28, but not to bind the negative feedback regulatory antigen, CTLA-4. |
| 403 | 12750275 | LAG-3 enables DNA vaccination to persistently prevent mammary carcinogenesis in HER-2/neu transgenic BALB/c mice. |
| 404 | 12750275 | A stronger and enduring r-p185(neu)-specific cytotoxicity, a sustained release of IFN-gamma and interleukin 4, and a marked expansion of both CD8(+)/CD11b(+)/CD28(+) effector and CD8(+)/CD11b(+)/CD28(-) memory effector T-cell populations were induced in immunized mice. |
| 405 | 12761091 | In this study, we investigated the role of this costimulatory pathway in resistance to Trypanosoma cruzi infection by using CD28-deficient mice and blocking antibodies against CD80 and CD86. |
| 406 | 12761091 | The blockade of both CD80 and CD86 by administering specific monoclonal antibodies also exacerbated T. cruzi infection in wild-type mice. |
| 407 | 12761091 | The induction of T. cruzi antigen-specific CD8(+) T cells was also impaired in T. cruzi-infected, CD28-deficient mice. |
| 408 | 12761091 | In addition to these defects in natural protection against T. cruzi infection, CD28-deficient mice were also defective in the induction of CD8(+)-T-cell-mediated protective immunity against T. cruzi infection by DNA vaccination. |
| 409 | 12761091 | In this study, we investigated the role of this costimulatory pathway in resistance to Trypanosoma cruzi infection by using CD28-deficient mice and blocking antibodies against CD80 and CD86. |
| 410 | 12761091 | The blockade of both CD80 and CD86 by administering specific monoclonal antibodies also exacerbated T. cruzi infection in wild-type mice. |
| 411 | 12761091 | The induction of T. cruzi antigen-specific CD8(+) T cells was also impaired in T. cruzi-infected, CD28-deficient mice. |
| 412 | 12761091 | In addition to these defects in natural protection against T. cruzi infection, CD28-deficient mice were also defective in the induction of CD8(+)-T-cell-mediated protective immunity against T. cruzi infection by DNA vaccination. |
| 413 | 12761091 | In this study, we investigated the role of this costimulatory pathway in resistance to Trypanosoma cruzi infection by using CD28-deficient mice and blocking antibodies against CD80 and CD86. |
| 414 | 12761091 | The blockade of both CD80 and CD86 by administering specific monoclonal antibodies also exacerbated T. cruzi infection in wild-type mice. |
| 415 | 12761091 | The induction of T. cruzi antigen-specific CD8(+) T cells was also impaired in T. cruzi-infected, CD28-deficient mice. |
| 416 | 12761091 | In addition to these defects in natural protection against T. cruzi infection, CD28-deficient mice were also defective in the induction of CD8(+)-T-cell-mediated protective immunity against T. cruzi infection by DNA vaccination. |
| 417 | 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. |
| 418 | 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. |
| 419 | 12922116 | The anti-influenza vaccine induced increase in TNFalpha and IL10 in the all non-responders, while cortisol increased only in the young. |
| 420 | 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. |
| 421 | 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. |
| 422 | 12922116 | The anti-influenza vaccine induced increase in TNFalpha and IL10 in the all non-responders, while cortisol increased only in the young. |
| 423 | 12960344 | Examination of phenotypic markers of the HA(306-318)-responsive T cells in the peripheral blood indicated that the majority were CD45RA(-), CD27(+), CD25(-), CD28(+), and CD62L(-), while T cell clones derived from this population were CD45RA(-), CD27(-), CD25(+), CD28(+), and CD62L(-). |
| 424 | 12965919 | Specifically the following parameters were assessed in baboons from 6 months to 26 years of age: relative numbers of B lymphocytes, CD4+ and CD8+ T lymphocytes, and T lymphocytes expressing CD28, CD25, and phytohemagglutinin-stimulated lymphoproliferative activity; and concentrations of total immunoglobulin, soluble interleukin-2 receptor alpha, and soluble CD30 in serum. |
| 425 | 12965919 | The increase in T-cell numbers involved both the CD4+ and CD8+ subsets. |
| 426 | 12965919 | In addition, there was a significant negative correlation of age with levels of soluble interleukin-2 receptor alpha in serum. |
| 427 | 14502004 | Nadir CD4+ T-cell count and numbers of CD28+ CD4+ T-cells predict functional responses to immunizations in chronic HIV-1 infection. |
| 428 | 14607891 | We show that, by controlling the MHC density on aAPCs, high- or low-avidity tumor-directed human CTL lines can be raised effectively in vitro if costimulation via CD28 and IL-12 is provided. |
| 429 | 14645154 | In IL-10(-/-) mice, inflammation of the vaccination site was increased with larger numbers of IL-12p40(+), MHC II(+) and CD86(+) cells in the dermal exudate, and was associated with elevated levels of skin-derived IL-12p40 and IL-1beta. |
| 430 | 14645154 | Moreover, such mice had increased numbers of CD4(+) sdLN cells that were CD25(+), CD28(+) or CD152(+) and accessory cells that were CD40(+) or MHC II(+). |
| 431 | 14645154 | Finally, the secretion of IFN-gamma (and IL-12p40) by in vitro cultured sdLN cells was substantially raised in IL-10(-/-) mice, but much reduced in IL-12p40(-/-) mice, resulting in the development of highly polarized T(h)1 and T(h)2 cytokine profiles in the two groups of mice respectively. |
| 432 | 14707048 | CD7 and CD28 are required for murine CD4+CD25+ regulatory T cell homeostasis and prevention of thyroiditis. |
| 433 | 14707048 | CD7 and CD28 are T cell Ig superfamily molecules that share common signaling mechanisms. |
| 434 | 14707048 | To determine roles CD7 and CD28 might play in peripheral lymphocyte development and function, we have generated CD7/CD28-double-deficient mice. |
| 435 | 14707048 | CD7- and CD28-single-deficient and CD7/CD28-double-deficient mice had normal levels of CD4 and CD8-single-positive T cells in thymus and spleen. |
| 436 | 14707048 | However, CD28-deficient mice had decreased CD4+CD25+ T cells in spleen compared with wild-type mice, and CD7/CD28-double-deficient mice had decreased numbers of CD4+CD25+ T cells in both thymus and spleen compared with both wild-type and CD28-deficient mice. |
| 437 | 14707048 | Functional studies demonstrated that CD4+CD25+ T cells from CD28-deficient and CD7/CD28-double-deficient mice could mediate suppression of CD3 mAb activation of CD4+CD25- wild-type T cells, but were less potent than wild-type CD4+CD25+ T regulatory cells. |
| 438 | 14707048 | Thyroiditis developed in aged CD7/CD28-double-deficient mice (>1 year) that was not seen in age-matched control mice or single CD7- or CD28-deficient mice, thus suggesting in vivo loss of T regulatory cells allowed for the development of spontaneous thyroiditis. |
| 439 | 14707048 | Taken together, these data demonstrated collaborative roles for both CD7 and CD28 in determination of number and function of CD4+CD25+ T regulatory cells in the thymus and peripheral immune sites and in the development of spontaneous thyroiditis. |
| 440 | 14707048 | CD7 and CD28 are required for murine CD4+CD25+ regulatory T cell homeostasis and prevention of thyroiditis. |
| 441 | 14707048 | CD7 and CD28 are T cell Ig superfamily molecules that share common signaling mechanisms. |
| 442 | 14707048 | To determine roles CD7 and CD28 might play in peripheral lymphocyte development and function, we have generated CD7/CD28-double-deficient mice. |
| 443 | 14707048 | CD7- and CD28-single-deficient and CD7/CD28-double-deficient mice had normal levels of CD4 and CD8-single-positive T cells in thymus and spleen. |
| 444 | 14707048 | However, CD28-deficient mice had decreased CD4+CD25+ T cells in spleen compared with wild-type mice, and CD7/CD28-double-deficient mice had decreased numbers of CD4+CD25+ T cells in both thymus and spleen compared with both wild-type and CD28-deficient mice. |
| 445 | 14707048 | Functional studies demonstrated that CD4+CD25+ T cells from CD28-deficient and CD7/CD28-double-deficient mice could mediate suppression of CD3 mAb activation of CD4+CD25- wild-type T cells, but were less potent than wild-type CD4+CD25+ T regulatory cells. |
| 446 | 14707048 | Thyroiditis developed in aged CD7/CD28-double-deficient mice (>1 year) that was not seen in age-matched control mice or single CD7- or CD28-deficient mice, thus suggesting in vivo loss of T regulatory cells allowed for the development of spontaneous thyroiditis. |
| 447 | 14707048 | Taken together, these data demonstrated collaborative roles for both CD7 and CD28 in determination of number and function of CD4+CD25+ T regulatory cells in the thymus and peripheral immune sites and in the development of spontaneous thyroiditis. |
| 448 | 14707048 | CD7 and CD28 are required for murine CD4+CD25+ regulatory T cell homeostasis and prevention of thyroiditis. |
| 449 | 14707048 | CD7 and CD28 are T cell Ig superfamily molecules that share common signaling mechanisms. |
| 450 | 14707048 | To determine roles CD7 and CD28 might play in peripheral lymphocyte development and function, we have generated CD7/CD28-double-deficient mice. |
| 451 | 14707048 | CD7- and CD28-single-deficient and CD7/CD28-double-deficient mice had normal levels of CD4 and CD8-single-positive T cells in thymus and spleen. |
| 452 | 14707048 | However, CD28-deficient mice had decreased CD4+CD25+ T cells in spleen compared with wild-type mice, and CD7/CD28-double-deficient mice had decreased numbers of CD4+CD25+ T cells in both thymus and spleen compared with both wild-type and CD28-deficient mice. |
| 453 | 14707048 | Functional studies demonstrated that CD4+CD25+ T cells from CD28-deficient and CD7/CD28-double-deficient mice could mediate suppression of CD3 mAb activation of CD4+CD25- wild-type T cells, but were less potent than wild-type CD4+CD25+ T regulatory cells. |
| 454 | 14707048 | Thyroiditis developed in aged CD7/CD28-double-deficient mice (>1 year) that was not seen in age-matched control mice or single CD7- or CD28-deficient mice, thus suggesting in vivo loss of T regulatory cells allowed for the development of spontaneous thyroiditis. |
| 455 | 14707048 | Taken together, these data demonstrated collaborative roles for both CD7 and CD28 in determination of number and function of CD4+CD25+ T regulatory cells in the thymus and peripheral immune sites and in the development of spontaneous thyroiditis. |
| 456 | 14707048 | CD7 and CD28 are required for murine CD4+CD25+ regulatory T cell homeostasis and prevention of thyroiditis. |
| 457 | 14707048 | CD7 and CD28 are T cell Ig superfamily molecules that share common signaling mechanisms. |
| 458 | 14707048 | To determine roles CD7 and CD28 might play in peripheral lymphocyte development and function, we have generated CD7/CD28-double-deficient mice. |
| 459 | 14707048 | CD7- and CD28-single-deficient and CD7/CD28-double-deficient mice had normal levels of CD4 and CD8-single-positive T cells in thymus and spleen. |
| 460 | 14707048 | However, CD28-deficient mice had decreased CD4+CD25+ T cells in spleen compared with wild-type mice, and CD7/CD28-double-deficient mice had decreased numbers of CD4+CD25+ T cells in both thymus and spleen compared with both wild-type and CD28-deficient mice. |
| 461 | 14707048 | Functional studies demonstrated that CD4+CD25+ T cells from CD28-deficient and CD7/CD28-double-deficient mice could mediate suppression of CD3 mAb activation of CD4+CD25- wild-type T cells, but were less potent than wild-type CD4+CD25+ T regulatory cells. |
| 462 | 14707048 | Thyroiditis developed in aged CD7/CD28-double-deficient mice (>1 year) that was not seen in age-matched control mice or single CD7- or CD28-deficient mice, thus suggesting in vivo loss of T regulatory cells allowed for the development of spontaneous thyroiditis. |
| 463 | 14707048 | Taken together, these data demonstrated collaborative roles for both CD7 and CD28 in determination of number and function of CD4+CD25+ T regulatory cells in the thymus and peripheral immune sites and in the development of spontaneous thyroiditis. |
| 464 | 14707048 | CD7 and CD28 are required for murine CD4+CD25+ regulatory T cell homeostasis and prevention of thyroiditis. |
| 465 | 14707048 | CD7 and CD28 are T cell Ig superfamily molecules that share common signaling mechanisms. |
| 466 | 14707048 | To determine roles CD7 and CD28 might play in peripheral lymphocyte development and function, we have generated CD7/CD28-double-deficient mice. |
| 467 | 14707048 | CD7- and CD28-single-deficient and CD7/CD28-double-deficient mice had normal levels of CD4 and CD8-single-positive T cells in thymus and spleen. |
| 468 | 14707048 | However, CD28-deficient mice had decreased CD4+CD25+ T cells in spleen compared with wild-type mice, and CD7/CD28-double-deficient mice had decreased numbers of CD4+CD25+ T cells in both thymus and spleen compared with both wild-type and CD28-deficient mice. |
| 469 | 14707048 | Functional studies demonstrated that CD4+CD25+ T cells from CD28-deficient and CD7/CD28-double-deficient mice could mediate suppression of CD3 mAb activation of CD4+CD25- wild-type T cells, but were less potent than wild-type CD4+CD25+ T regulatory cells. |
| 470 | 14707048 | Thyroiditis developed in aged CD7/CD28-double-deficient mice (>1 year) that was not seen in age-matched control mice or single CD7- or CD28-deficient mice, thus suggesting in vivo loss of T regulatory cells allowed for the development of spontaneous thyroiditis. |
| 471 | 14707048 | Taken together, these data demonstrated collaborative roles for both CD7 and CD28 in determination of number and function of CD4+CD25+ T regulatory cells in the thymus and peripheral immune sites and in the development of spontaneous thyroiditis. |
| 472 | 14707048 | CD7 and CD28 are required for murine CD4+CD25+ regulatory T cell homeostasis and prevention of thyroiditis. |
| 473 | 14707048 | CD7 and CD28 are T cell Ig superfamily molecules that share common signaling mechanisms. |
| 474 | 14707048 | To determine roles CD7 and CD28 might play in peripheral lymphocyte development and function, we have generated CD7/CD28-double-deficient mice. |
| 475 | 14707048 | CD7- and CD28-single-deficient and CD7/CD28-double-deficient mice had normal levels of CD4 and CD8-single-positive T cells in thymus and spleen. |
| 476 | 14707048 | However, CD28-deficient mice had decreased CD4+CD25+ T cells in spleen compared with wild-type mice, and CD7/CD28-double-deficient mice had decreased numbers of CD4+CD25+ T cells in both thymus and spleen compared with both wild-type and CD28-deficient mice. |
| 477 | 14707048 | Functional studies demonstrated that CD4+CD25+ T cells from CD28-deficient and CD7/CD28-double-deficient mice could mediate suppression of CD3 mAb activation of CD4+CD25- wild-type T cells, but were less potent than wild-type CD4+CD25+ T regulatory cells. |
| 478 | 14707048 | Thyroiditis developed in aged CD7/CD28-double-deficient mice (>1 year) that was not seen in age-matched control mice or single CD7- or CD28-deficient mice, thus suggesting in vivo loss of T regulatory cells allowed for the development of spontaneous thyroiditis. |
| 479 | 14707048 | Taken together, these data demonstrated collaborative roles for both CD7 and CD28 in determination of number and function of CD4+CD25+ T regulatory cells in the thymus and peripheral immune sites and in the development of spontaneous thyroiditis. |
| 480 | 14707048 | CD7 and CD28 are required for murine CD4+CD25+ regulatory T cell homeostasis and prevention of thyroiditis. |
| 481 | 14707048 | CD7 and CD28 are T cell Ig superfamily molecules that share common signaling mechanisms. |
| 482 | 14707048 | To determine roles CD7 and CD28 might play in peripheral lymphocyte development and function, we have generated CD7/CD28-double-deficient mice. |
| 483 | 14707048 | CD7- and CD28-single-deficient and CD7/CD28-double-deficient mice had normal levels of CD4 and CD8-single-positive T cells in thymus and spleen. |
| 484 | 14707048 | However, CD28-deficient mice had decreased CD4+CD25+ T cells in spleen compared with wild-type mice, and CD7/CD28-double-deficient mice had decreased numbers of CD4+CD25+ T cells in both thymus and spleen compared with both wild-type and CD28-deficient mice. |
| 485 | 14707048 | Functional studies demonstrated that CD4+CD25+ T cells from CD28-deficient and CD7/CD28-double-deficient mice could mediate suppression of CD3 mAb activation of CD4+CD25- wild-type T cells, but were less potent than wild-type CD4+CD25+ T regulatory cells. |
| 486 | 14707048 | Thyroiditis developed in aged CD7/CD28-double-deficient mice (>1 year) that was not seen in age-matched control mice or single CD7- or CD28-deficient mice, thus suggesting in vivo loss of T regulatory cells allowed for the development of spontaneous thyroiditis. |
| 487 | 14707048 | Taken together, these data demonstrated collaborative roles for both CD7 and CD28 in determination of number and function of CD4+CD25+ T regulatory cells in the thymus and peripheral immune sites and in the development of spontaneous thyroiditis. |
| 488 | 14707071 | A switch in costimulation from CD28 to 4-1BB during primary versus secondary CD8 T cell response to influenza in vivo. |
| 489 | 14707071 | In contrast, CD28(-/-) mice are defective in initial CD8 T cell expansion. |
| 490 | 14707071 | Using agonistic anti-4-1BB Ab to replace the CD28 or 4-1BB signal, we examined the timing of the required signals for CD28 vs 4-1BB costimulation. |
| 491 | 14707071 | A single dose of agonistic anti-4-1BB Ab added only during priming restores the secondary CD8 T cell response in CD28(-/-) mice. |
| 492 | 14707071 | Thus, there is a switch in costimulatory requirement from CD28 to 4-1BB during primary vs recall responses. |
| 493 | 14707071 | A switch in costimulation from CD28 to 4-1BB during primary versus secondary CD8 T cell response to influenza in vivo. |
| 494 | 14707071 | In contrast, CD28(-/-) mice are defective in initial CD8 T cell expansion. |
| 495 | 14707071 | Using agonistic anti-4-1BB Ab to replace the CD28 or 4-1BB signal, we examined the timing of the required signals for CD28 vs 4-1BB costimulation. |
| 496 | 14707071 | A single dose of agonistic anti-4-1BB Ab added only during priming restores the secondary CD8 T cell response in CD28(-/-) mice. |
| 497 | 14707071 | Thus, there is a switch in costimulatory requirement from CD28 to 4-1BB during primary vs recall responses. |
| 498 | 14707071 | A switch in costimulation from CD28 to 4-1BB during primary versus secondary CD8 T cell response to influenza in vivo. |
| 499 | 14707071 | In contrast, CD28(-/-) mice are defective in initial CD8 T cell expansion. |
| 500 | 14707071 | Using agonistic anti-4-1BB Ab to replace the CD28 or 4-1BB signal, we examined the timing of the required signals for CD28 vs 4-1BB costimulation. |
| 501 | 14707071 | A single dose of agonistic anti-4-1BB Ab added only during priming restores the secondary CD8 T cell response in CD28(-/-) mice. |
| 502 | 14707071 | Thus, there is a switch in costimulatory requirement from CD28 to 4-1BB during primary vs recall responses. |
| 503 | 14707071 | A switch in costimulation from CD28 to 4-1BB during primary versus secondary CD8 T cell response to influenza in vivo. |
| 504 | 14707071 | In contrast, CD28(-/-) mice are defective in initial CD8 T cell expansion. |
| 505 | 14707071 | Using agonistic anti-4-1BB Ab to replace the CD28 or 4-1BB signal, we examined the timing of the required signals for CD28 vs 4-1BB costimulation. |
| 506 | 14707071 | A single dose of agonistic anti-4-1BB Ab added only during priming restores the secondary CD8 T cell response in CD28(-/-) mice. |
| 507 | 14707071 | Thus, there is a switch in costimulatory requirement from CD28 to 4-1BB during primary vs recall responses. |
| 508 | 14707071 | A switch in costimulation from CD28 to 4-1BB during primary versus secondary CD8 T cell response to influenza in vivo. |
| 509 | 14707071 | In contrast, CD28(-/-) mice are defective in initial CD8 T cell expansion. |
| 510 | 14707071 | Using agonistic anti-4-1BB Ab to replace the CD28 or 4-1BB signal, we examined the timing of the required signals for CD28 vs 4-1BB costimulation. |
| 511 | 14707071 | A single dose of agonistic anti-4-1BB Ab added only during priming restores the secondary CD8 T cell response in CD28(-/-) mice. |
| 512 | 14707071 | Thus, there is a switch in costimulatory requirement from CD28 to 4-1BB during primary vs recall responses. |
| 513 | 14965468 | In the SIVmac251 model, TREC correlated with the percentage of CD4+ T cells (r(s) = 0.426; P = 0.048) and CD4+CD28+ T cells (r(s) = 0.624; P = 0.002), and inversely with CD8+ T cells (r(s) = -0.622; P = 0.002), CD8+CD28- T cells (r(s) = -0.516; P = 0.014), and serum viral loads (r(s) = -0.627; P = 0.039). |
| 514 | 14965468 | In the SIVmac251 model, the decline in TREC was related to increased immune activation and proliferation due to viral replication, as reflected by decreases in percentages of CD4+CD28+ T cells and increases in CD8+ and CD8+CD28- T cells. |
| 515 | 14965468 | In the SIVmac251 model, TREC correlated with the percentage of CD4+ T cells (r(s) = 0.426; P = 0.048) and CD4+CD28+ T cells (r(s) = 0.624; P = 0.002), and inversely with CD8+ T cells (r(s) = -0.622; P = 0.002), CD8+CD28- T cells (r(s) = -0.516; P = 0.014), and serum viral loads (r(s) = -0.627; P = 0.039). |
| 516 | 14965468 | In the SIVmac251 model, the decline in TREC was related to increased immune activation and proliferation due to viral replication, as reflected by decreases in percentages of CD4+CD28+ T cells and increases in CD8+ and CD8+CD28- T cells. |
| 517 | 15094217 | The development of folate/antibody conjugates specific for the T cell co-stimulatory molecule CD28 could yield activated T cells that recognize endogenous peptide-major histocompatibility complex (MHC) antigens on tumor cells. |
| 518 | 15109052 | Analysis of chicken TLR4, CD28, MIF, MD-2, and LITAF genes in a Salmonella enteritidis resource population. |
| 519 | 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). |
| 520 | 15109052 | The LITAF and MIF genes were homozygous for all sires. |
| 521 | 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. |
| 522 | 15109052 | Analysis of chicken TLR4, CD28, MIF, MD-2, and LITAF genes in a Salmonella enteritidis resource population. |
| 523 | 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). |
| 524 | 15109052 | The LITAF and MIF genes were homozygous for all sires. |
| 525 | 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. |
| 526 | 15109052 | Analysis of chicken TLR4, CD28, MIF, MD-2, and LITAF genes in a Salmonella enteritidis resource population. |
| 527 | 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). |
| 528 | 15109052 | The LITAF and MIF genes were homozygous for all sires. |
| 529 | 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. |
| 530 | 15149168 | Peptide-specific CD8 T cells in PBLs were analyzed ex vivo using fluorescent HLA-A2/Melan-A multimers and IFN-gamma ELISPOT assays. |
| 531 | 15149168 | In vivo expansion of Melan-A-specific CD8 T cells was observed in 13 patients (1/12 after vaccination with peptide in AS02B and 12/17 after vaccination with peptide in IFA). |
| 532 | 15149168 | The T cells produced IFN-gamma and downregulated CD45RA and CD28. |
| 533 | 15149168 | We conclude that repeated vaccination with Melan-A peptide in IFA frequently leads to sustained responses of specific CD8 T cells that are detectable ex vivo and correlate with inflammatory skin reactions. |
| 534 | 15255186 | Evidence for an interaction between leptin, T cell costimulatory antigens CD28, CTLA-4 and CD26 (dipeptidyl peptidase IV) in BCG-induced immune responses of leptin- and leptin receptor-deficient mice. |
| 535 | 15255186 | We assessed changes of the enzyme dipeptidyl peptidase IV (DPP IV, CD26) in the context of leptin or leptin receptor deficiency. |
| 536 | 15255186 | C57BL/6 mice, Leptin-deficient mice (ob/ob mice, B6.V-Lep<ob>) and Leptin-receptor-deficient mice (db/db mice, B6.Cg-m+/+Lepr) were infected with B. |
| 537 | 15255186 | The expression of DPP IV/CD26 on splenocytes was higher in ob/ob mice than in wild-type animals, and lower in db/db mice, and decreased upon stimulation with BCG in ob/ob mice only. |
| 538 | 15265915 | Emergence of a CD4+CD28- granzyme B+, cytomegalovirus-specific T cell subset after recovery of primary cytomegalovirus infection. |
| 539 | 15265915 | CD4(+)CD28(-) cells had an Ag-primed phenotype and expressed the cytolytic molecules granzyme B and perforin. |
| 540 | 15265915 | CD4(+)CD28(-) cells only produced IFN-gamma after stimulation with CMV-Ag, whereas CD4(+)CD28(+) cells also produced IFN-gamma in response to varicella-zoster virus and purified protein derivative. |
| 541 | 15265956 | We observed significantly decreased proliferation of the Ag-specific central memory CD4(+) T cell population (CD28(+)/CCR7(+)/CD45RA(-)) in the antiretroviral treated HIV-infected individuals compared with the seronegative controls. |
| 542 | 15353589 | CD26 up-regulates expression of CD86 on antigen-presenting cells by means of caveolin-1. |
| 543 | 15353589 | We now demonstrate that CD26 binds Caveolin-1 on antigen-presenting cells, and that residues 201-211 of CD26 along with the serine catalytic site at residue 630 contribute to binding to caveolin-1 scaffolding domain. |
| 544 | 15353589 | In addition, after CD26-caveolin-1 interaction on TT-loaded monocytes, caveolin-1 is phosphorylated, which links to activate NF-kappaB, followed by up-regulation of CD86. |
| 545 | 15353589 | Finally, reduced caveolin-1 expression on monocytes inhibits CD26-mediated CD86 up-regulation and abrogates CD26 effect on TT-induced T cell proliferation. |
| 546 | 15353589 | Taken together, these results strongly suggest that CD26-caveolin-1 interaction plays a role in the up-regulation of CD86 on TT-loaded monocytes and subsequent engagement with CD28 on T cells, leading to antigen-specific T cell activation. |
| 547 | 15585831 | Cutting edge: CD28-mediated transcriptional and posttranscriptional regulation of IL-2 expression are controlled through different signaling pathways. |
| 548 | 15585831 | PI3K was identified early as a candidate for CD28 signaling, but conflicting data during the past decade has left the role of PI3K unresolved. |
| 549 | 15585831 | We show that mutation of the PI3K interaction site in the cytosolic tail of CD28 site disrupts the ability of CD28 to recruit protein kinase C-theta; to the central supramolecular activation cluster (c-SMAC) region of the immunological synapse, promote NF-kappaB nuclear translocation, and enhance IL-2 gene transcription. |
| 550 | 15585831 | In contrast, mutation of the PI3K interaction site had no effect on the ability of CD28 to enhance IL-2 mRNA stability. |
| 551 | 15585831 | These results suggest that two distinct pathways mediate CD28-induced up-regulation of IL-2 expression, a PI3K-dependent pathway that may function through the immunological synapse to enhance IL-2 transcription and a PI3K-independent pathway that induces IL-2 mRNA stability. |
| 552 | 15585831 | Cutting edge: CD28-mediated transcriptional and posttranscriptional regulation of IL-2 expression are controlled through different signaling pathways. |
| 553 | 15585831 | PI3K was identified early as a candidate for CD28 signaling, but conflicting data during the past decade has left the role of PI3K unresolved. |
| 554 | 15585831 | We show that mutation of the PI3K interaction site in the cytosolic tail of CD28 site disrupts the ability of CD28 to recruit protein kinase C-theta; to the central supramolecular activation cluster (c-SMAC) region of the immunological synapse, promote NF-kappaB nuclear translocation, and enhance IL-2 gene transcription. |
| 555 | 15585831 | In contrast, mutation of the PI3K interaction site had no effect on the ability of CD28 to enhance IL-2 mRNA stability. |
| 556 | 15585831 | These results suggest that two distinct pathways mediate CD28-induced up-regulation of IL-2 expression, a PI3K-dependent pathway that may function through the immunological synapse to enhance IL-2 transcription and a PI3K-independent pathway that induces IL-2 mRNA stability. |
| 557 | 15585831 | Cutting edge: CD28-mediated transcriptional and posttranscriptional regulation of IL-2 expression are controlled through different signaling pathways. |
| 558 | 15585831 | PI3K was identified early as a candidate for CD28 signaling, but conflicting data during the past decade has left the role of PI3K unresolved. |
| 559 | 15585831 | We show that mutation of the PI3K interaction site in the cytosolic tail of CD28 site disrupts the ability of CD28 to recruit protein kinase C-theta; to the central supramolecular activation cluster (c-SMAC) region of the immunological synapse, promote NF-kappaB nuclear translocation, and enhance IL-2 gene transcription. |
| 560 | 15585831 | In contrast, mutation of the PI3K interaction site had no effect on the ability of CD28 to enhance IL-2 mRNA stability. |
| 561 | 15585831 | These results suggest that two distinct pathways mediate CD28-induced up-regulation of IL-2 expression, a PI3K-dependent pathway that may function through the immunological synapse to enhance IL-2 transcription and a PI3K-independent pathway that induces IL-2 mRNA stability. |
| 562 | 15585831 | Cutting edge: CD28-mediated transcriptional and posttranscriptional regulation of IL-2 expression are controlled through different signaling pathways. |
| 563 | 15585831 | PI3K was identified early as a candidate for CD28 signaling, but conflicting data during the past decade has left the role of PI3K unresolved. |
| 564 | 15585831 | We show that mutation of the PI3K interaction site in the cytosolic tail of CD28 site disrupts the ability of CD28 to recruit protein kinase C-theta; to the central supramolecular activation cluster (c-SMAC) region of the immunological synapse, promote NF-kappaB nuclear translocation, and enhance IL-2 gene transcription. |
| 565 | 15585831 | In contrast, mutation of the PI3K interaction site had no effect on the ability of CD28 to enhance IL-2 mRNA stability. |
| 566 | 15585831 | These results suggest that two distinct pathways mediate CD28-induced up-regulation of IL-2 expression, a PI3K-dependent pathway that may function through the immunological synapse to enhance IL-2 transcription and a PI3K-independent pathway that induces IL-2 mRNA stability. |
| 567 | 15585831 | Cutting edge: CD28-mediated transcriptional and posttranscriptional regulation of IL-2 expression are controlled through different signaling pathways. |
| 568 | 15585831 | PI3K was identified early as a candidate for CD28 signaling, but conflicting data during the past decade has left the role of PI3K unresolved. |
| 569 | 15585831 | We show that mutation of the PI3K interaction site in the cytosolic tail of CD28 site disrupts the ability of CD28 to recruit protein kinase C-theta; to the central supramolecular activation cluster (c-SMAC) region of the immunological synapse, promote NF-kappaB nuclear translocation, and enhance IL-2 gene transcription. |
| 570 | 15585831 | In contrast, mutation of the PI3K interaction site had no effect on the ability of CD28 to enhance IL-2 mRNA stability. |
| 571 | 15585831 | These results suggest that two distinct pathways mediate CD28-induced up-regulation of IL-2 expression, a PI3K-dependent pathway that may function through the immunological synapse to enhance IL-2 transcription and a PI3K-independent pathway that induces IL-2 mRNA stability. |
| 572 | 15622455 | Women from Nairobi had a significantly greater number of CD8+ T cells expressing the activation markers CD38 and HLA DR. |
| 573 | 15622455 | Kenyan women also had significantly higher levels of CTLA-4+ CD4 and CD8+ T cells, and reduced levels of CD28+ CD8+ cells. |
| 574 | 15622455 | Levels of CD95+ CD4+ T cells were higher in Kenyan women and, correspondingly, showed higher levels of spontaneous apoptosis. |
| 575 | 15688403 | We have comparatively evaluated the proliferative response of CTL induced in metastatic melanoma patients upon immunization against Melan-A/MART-1(27-35) tumor associated antigen (TAA) to IL-2, IL-7 or IL-15 cytokines, sharing a receptor common gamma-chain (c gamma-c cytokines). |
| 576 | 15688403 | All clones were able to kill tumor cell lines expressing HLA-A0201 and Melan-A/MART-1, and displayed phenotypic characteristics of effector/memory (CD45RA-/CCR7-) or CD45RA+/CCR7- effector cells in intermediate to late developmental stage (CD28-/CD276+/-) CTL. |
| 577 | 15688403 | Proliferative responses could be elicited or enhanced by IL-2 and IL-15, but not IL-7, in the absence or in the presence of T-cell receptor (TCR) triggering, respectively. |
| 578 | 15688403 | Accordingly, only IL-2 and IL-15 were able to promote the survival of the CTL clones under investigation. |
| 579 | 15688403 | CD8+ cells from one of the patients treated were obtained 6 months after the last vaccine boost and were cultured in the presence of Melan-A/MART-1(27-35) and each of the 3 cytokines under investigation. |
| 580 | 15688403 | Consistent with data from CTL clones, expansion of Melan-A/MART-1(27-35) tetramer positive cells was only observed in the presence of IL-2 or IL-15 but not IL-7. |
| 581 | 15688403 | Instead, when CD8+ cells from the same patient were sampled shortly (14 days) after an additional vaccination only IL-2 was able to promote the expansion of Melan-A/MART-1(27-35) tetramer positive cells. |
| 582 | 15699483 | LFA-1 co-stimulation inhibits T(h)2 differentiation by down-modulating IL-4 responsiveness. |
| 583 | 15699483 | Specifically, CD28 co-stimulation promotes T(h)2 differentiation, whereas leukocyte function-associated antigen-1 (LFA-1) co-stimulation promotes T(h)1 differentiation and inhibits T(h)2 differentiation. |
| 584 | 15699483 | We show that co-stimulation through LFA-1 does not decrease early IL-4 secretion, but rather induces a loss in IL-4 responsiveness. |
| 585 | 15699483 | T cells primed in the context of LFA-1 co-stimulation require a 5-fold increase in the concentration of IL-4 required to drive T(h)2 differentiation, which is not mediated by a loss in IL-4R expression. |
| 586 | 15699483 | To determine whether LFA-1 co-stimulation impacts on proximal signaling from the IL-4R, we first identified a kinetic window where we could separate IL-4-driven T(h)2 differentiation from initial T cell priming. |
| 587 | 15699483 | Proximal IL-4R signaling, as evidenced by tyrosine phosphorylation of signal transducer and activator of transcription-6 (STAT6), was not inhibited by initial co-stimulation through LFA-1, yet these T cells still required higher amounts of IL-4 and corresponding higher levels of STAT6 activation to up-regulate GATA-3 and induce T(h)2 differentiation. |
| 588 | 15699483 | Thus, LFA-1 co-stimulation appears to interfere with GATA-3 expression downstream of STAT6. |
| 589 | 15699483 | These results suggest that LFA-1 co-stimulation functions as a threshold modulator of T(h)2 differentiation, increasing the effective concentration of IL-4 required to drive T(h)2 responses. |
| 590 | 15746068 | Identification of CD19 and CD20 peptides for induction of antigen-specific CTLs against B-cell malignancies. |
| 591 | 15746068 | The purpose of these studies was to develop immunogenic peptides derived from the CD19 and CD20 self-antigens for the induction of antigen-specific CTLs against B-cell malignancies. |
| 592 | 15746068 | The CD19 or CD20 peptide-specific CTL cytotoxicity was confirmed using HLA-A2.1(+) T2 cells presenting the appropriate peptide. |
| 593 | 15746068 | In addition, the CTLs displayed a significant (P < 0.05) increase in cell proliferation and IFN-gamma secretion (>830 ng/mL) following restimulation with HLA-A2.1(+)/CD19(+)/CD20(+) tumor cells. |
| 594 | 15746068 | The CTLs also displayed a distinct phenotype consisting of a high percentage of CD69(+)/CD45RO(+) and a low percentage of CD45RA(+)/CCR7(+) CD4(+) or CD8(+) T cells characteristic of effector memory cell population. |
| 595 | 15746068 | Cyclic guanosine 3',5'-monophosphate culture conditions using serum-free AIM-V medium containing human AB serum, recombinant human interleukin 2 (Proleukin) and CD3/CD28 Dynabeads were developed resulting in a 35-fold expansion of CD20 peptide-specific CTLs. |
| 596 | 15752830 | We generated recombinant bispecific single-chain antibodies with one specificity directed against the CD3 or the CD28 antigen on human T cells and the other against the viral target molecule hemagglutinin-neuraminidase (HN) of Newcastle Disease Virus (NDV). |
| 597 | 15752830 | This was revealed by T cell proliferation, upregulation of CD69 and CD25 and by release of cytokines, interferons and chemokines. |
| 598 | 15858020 | Plasmids expressing the nucleocapsid protein (WHcAg) and e antigen (WHeAg) of woodchuck hepatitis virus (WHV) alone or in fusion to the extracellular domain of woodchuck CTLA-4 and CD28 were constructed. |
| 599 | 15858020 | In contrast, fusions of WHcAg to CTLA-4 and CD28 induced a specific antibody response with comparable levels of IgG1 and IgG2a. |
| 600 | 15858020 | Plasmids expressing the nucleocapsid protein (WHcAg) and e antigen (WHeAg) of woodchuck hepatitis virus (WHV) alone or in fusion to the extracellular domain of woodchuck CTLA-4 and CD28 were constructed. |
| 601 | 15858020 | In contrast, fusions of WHcAg to CTLA-4 and CD28 induced a specific antibody response with comparable levels of IgG1 and IgG2a. |
| 602 | 15879103 | Expression of killer cell lectin-like receptor G1 on antigen-specific human CD8+ T lymphocytes during active, latent, and resolved infection and its relation with CD57. |
| 603 | 15879103 | Killer cell lectin-like receptor G1 (KLRG1) is one of several inhibitory killer cell lectin-like receptors expressed by NK cells and T lymphocytes, mainly CD8(+) effector/memory cells that can secrete cytokines but have poor proliferative capacity. |
| 604 | 15879103 | Using multiparameter flow cytometry, we studied KLRG1 expression on CD8(+) T cells specific for epitopes of CMV, EBV, influenza, and HIV. |
| 605 | 15879103 | Over 92% of CD8(+) cells specific for CMV or EBV expressed KLRG1 during the latent stage of these chronic infections. |
| 606 | 15879103 | CD8(+) T cell cells specific for HIV epitopes were mostly (72-89%) KLRG1(+), even though not quite at the level of predominance noted with CMV or EBV. |
| 607 | 15879103 | Lower frequency of KLRG1 expression was observed among CD8(+) cells specific for influenza (40-73%), a resolved infection without a latent stage. |
| 608 | 15879103 | We further observed that CD8(+) cells expressing CD57, a marker of replicative senescence, also expressed KLRG1; however, a population of CD57(-)KLRG1(+) cells was also identified. |
| 609 | 15879103 | This population may represent a "memory" phenotype, because they also expressed CD27, CD28, CCR7, and CD127. |
| 610 | 15879103 | In contrast, CD57(+)KLRG1(+) cells did not express CD27, CD28, and CCR7, and expressed CD127 at a much lower frequency, indicating that they represent effector cells that are truly terminally differentiated. |
| 611 | 15879103 | The combination of KLRG1 and CD57 expression might thus aid in refining functional characterization of CD8(+) T cell subsets. |
| 612 | 15879103 | Expression of killer cell lectin-like receptor G1 on antigen-specific human CD8+ T lymphocytes during active, latent, and resolved infection and its relation with CD57. |
| 613 | 15879103 | Killer cell lectin-like receptor G1 (KLRG1) is one of several inhibitory killer cell lectin-like receptors expressed by NK cells and T lymphocytes, mainly CD8(+) effector/memory cells that can secrete cytokines but have poor proliferative capacity. |
| 614 | 15879103 | Using multiparameter flow cytometry, we studied KLRG1 expression on CD8(+) T cells specific for epitopes of CMV, EBV, influenza, and HIV. |
| 615 | 15879103 | Over 92% of CD8(+) cells specific for CMV or EBV expressed KLRG1 during the latent stage of these chronic infections. |
| 616 | 15879103 | CD8(+) T cell cells specific for HIV epitopes were mostly (72-89%) KLRG1(+), even though not quite at the level of predominance noted with CMV or EBV. |
| 617 | 15879103 | Lower frequency of KLRG1 expression was observed among CD8(+) cells specific for influenza (40-73%), a resolved infection without a latent stage. |
| 618 | 15879103 | We further observed that CD8(+) cells expressing CD57, a marker of replicative senescence, also expressed KLRG1; however, a population of CD57(-)KLRG1(+) cells was also identified. |
| 619 | 15879103 | This population may represent a "memory" phenotype, because they also expressed CD27, CD28, CCR7, and CD127. |
| 620 | 15879103 | In contrast, CD57(+)KLRG1(+) cells did not express CD27, CD28, and CCR7, and expressed CD127 at a much lower frequency, indicating that they represent effector cells that are truly terminally differentiated. |
| 621 | 15879103 | The combination of KLRG1 and CD57 expression might thus aid in refining functional characterization of CD8(+) T cell subsets. |
| 622 | 15882351 | Cultures of senescent CD8(+) T cells also show resistance to apoptosis, permanent loss of CD28 expression, altered cytokine profiles, reduced ability to respond to stress, and various functional changes. |
| 623 | 15882351 | CD8(+)CD28(-) T cells also accumulate in patients with certain types of cancer. |
| 624 | 15882351 | Cultures of senescent CD8(+) T cells also show resistance to apoptosis, permanent loss of CD28 expression, altered cytokine profiles, reduced ability to respond to stress, and various functional changes. |
| 625 | 15882351 | CD8(+)CD28(-) T cells also accumulate in patients with certain types of cancer. |
| 626 | 15919138 | However, it was not known if B7-1/Ig acted only by binding CD28 (amplifying a stimulatory signal) or by blocking CTLA-4 on T cells (removing inhibitory signals). |
| 627 | 15919138 | Here, we aimed to determine this using a plasmid encoding mutant B7-1/Ig (B7-1wa/Ig), which binds only to CTLA-4 but not to CD28. |
| 628 | 15919138 | We found that, in vitro, a significant fraction of CD3/CD28-activated T cells (in the absence of DCs) expressed CTLA-4 and B7-1. |
| 629 | 15919138 | Primed T cells of CTLA-4(+)B7-1(+/-) phenotype acted as regulatory T cells by inhibiting IFNgamma production by re-stimulated CTLA-4(-)B7-1(-) cells, and this was reversed by antibodies against IL-10 or TGF-beta1. |
| 630 | 15919138 | Both B7-1wa/Ig and CTLA-4/Ig, which bind to CTLA-4 and B7-1/B7-2 respectively, enhanced IFNgamma production, but not the proliferation or IL-4 release in mixed T-cell populations containing these two cell types. |
| 631 | 15919138 | In contrast, CTLA-4(-)B7-1(-) T cells produced IFNgamma which was not affected by B7-1wa/Ig or CTLA-4/Ig. |
| 632 | 15919138 | However, it was not known if B7-1/Ig acted only by binding CD28 (amplifying a stimulatory signal) or by blocking CTLA-4 on T cells (removing inhibitory signals). |
| 633 | 15919138 | Here, we aimed to determine this using a plasmid encoding mutant B7-1/Ig (B7-1wa/Ig), which binds only to CTLA-4 but not to CD28. |
| 634 | 15919138 | We found that, in vitro, a significant fraction of CD3/CD28-activated T cells (in the absence of DCs) expressed CTLA-4 and B7-1. |
| 635 | 15919138 | Primed T cells of CTLA-4(+)B7-1(+/-) phenotype acted as regulatory T cells by inhibiting IFNgamma production by re-stimulated CTLA-4(-)B7-1(-) cells, and this was reversed by antibodies against IL-10 or TGF-beta1. |
| 636 | 15919138 | Both B7-1wa/Ig and CTLA-4/Ig, which bind to CTLA-4 and B7-1/B7-2 respectively, enhanced IFNgamma production, but not the proliferation or IL-4 release in mixed T-cell populations containing these two cell types. |
| 637 | 15919138 | In contrast, CTLA-4(-)B7-1(-) T cells produced IFNgamma which was not affected by B7-1wa/Ig or CTLA-4/Ig. |
| 638 | 15919138 | However, it was not known if B7-1/Ig acted only by binding CD28 (amplifying a stimulatory signal) or by blocking CTLA-4 on T cells (removing inhibitory signals). |
| 639 | 15919138 | Here, we aimed to determine this using a plasmid encoding mutant B7-1/Ig (B7-1wa/Ig), which binds only to CTLA-4 but not to CD28. |
| 640 | 15919138 | We found that, in vitro, a significant fraction of CD3/CD28-activated T cells (in the absence of DCs) expressed CTLA-4 and B7-1. |
| 641 | 15919138 | Primed T cells of CTLA-4(+)B7-1(+/-) phenotype acted as regulatory T cells by inhibiting IFNgamma production by re-stimulated CTLA-4(-)B7-1(-) cells, and this was reversed by antibodies against IL-10 or TGF-beta1. |
| 642 | 15919138 | Both B7-1wa/Ig and CTLA-4/Ig, which bind to CTLA-4 and B7-1/B7-2 respectively, enhanced IFNgamma production, but not the proliferation or IL-4 release in mixed T-cell populations containing these two cell types. |
| 643 | 15919138 | In contrast, CTLA-4(-)B7-1(-) T cells produced IFNgamma which was not affected by B7-1wa/Ig or CTLA-4/Ig. |
| 644 | 15931636 | CD3 + , CD8 + , and CD4 + cells were severely depleted after ASCT. |
| 645 | 15931636 | Although total CD8 + T-cell numbers approached the normal range by 3 months, most of these cells were CD28 - . |
| 646 | 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. |
| 647 | 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. |
| 648 | 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. |
| 649 | 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. |
| 650 | 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. |
| 651 | 15981208 | The distinct patterns of cytokine induction by B7-1 and B7-2 obviously depend on the HLA Class I compatibility. |
| 652 | 16181751 | Full-length feline B7.1 and B7.2 produced from SPV vectors were natively processed and costimulated Jurkat cells to produce IL-2, in vitro. |
| 653 | 16181751 | Although feline sB7.1-his and sB7.2-his proteins bound to the human homolog receptors, CTLA-4 and CD28, both soluble ligands possessed greater affinity for CTLA-4, compared to CD28. |
| 654 | 16239544 | Cellular immunity mediated by T lymphocytes, in particular CD4+ and CD8+ type 1 cells, is the main defense against pathogenic fungi. |
| 655 | 16239544 | Disruption of CD28 costimulation reduced the number of type 1 CD4 and CD8 cells generated and impaired resistance to infection. |
| 656 | 16301632 | Peripheral tolerance is maintained in part by thymically derived CD25+CD4+ T cells (regulatory T cells (Tregs)). |
| 657 | 16301632 | Visualization of this time frame, using a sensitive single-cell assay for IL-2, revealed the early elaboration of target cell IL-2 producers in the first 6 h despite the presence of CD25+CD4+ Tregs. |
| 658 | 16301632 | Modulating target T cell activation signals with provision of CD28, IL-2, or high Ag dose all abrogated suppression of proliferation late in culture. |
| 659 | 16301632 | However, only CD28 signals enabled target T cells to resist the early Treg-induced down-regulation of IL-2. |
| 660 | 16301632 | Peripheral tolerance is maintained in part by thymically derived CD25+CD4+ T cells (regulatory T cells (Tregs)). |
| 661 | 16301632 | Visualization of this time frame, using a sensitive single-cell assay for IL-2, revealed the early elaboration of target cell IL-2 producers in the first 6 h despite the presence of CD25+CD4+ Tregs. |
| 662 | 16301632 | Modulating target T cell activation signals with provision of CD28, IL-2, or high Ag dose all abrogated suppression of proliferation late in culture. |
| 663 | 16301632 | However, only CD28 signals enabled target T cells to resist the early Treg-induced down-regulation of IL-2. |
| 664 | 16405934 | Following stimulation with phorbol 12-myristate 13-acetate and ionomycin, anti-CD3/CD28, antigen-specific peptide, or allogeneic cells, both CD4 and CD8 T cells expressed the transgene within 24h in a manner that was consistent with cellular activation markers. |
| 665 | 16530301 | The purpose of this article is to review recent advances in adjuvant development using approaches that directly exploit the immune system's own co-stimulatory pathways to exert their function; with a particular emphasis on CD40 and CD28 based therapies. |
| 666 | 16585571 | Engagement of CD28 outside of the immunological synapse results in up-regulation of IL-2 mRNA stability but not IL-2 transcription. |
| 667 | 16585571 | During T cell activation by APC, CD28 is colocalized with TCR in the central supramolecular activation cluster (cSMAC) region of the immunological synapse. |
| 668 | 16585571 | CD28 signaling through PI3K results in the recruitment of protein kinase C (PKC)theta to the cSMAC, activation of NF-kappaB, and induction of IL-2 transcription. |
| 669 | 16585571 | To test this model we have examined the mechanism of CD28-mediated induction of IL-2 secretion when CD28 is engaged outside of the immunological synapse. |
| 670 | 16585571 | CD4 T cells were stimulated with Ag presented by B7-negative APC and CD28 costimulation was provided in trans by anti-CD28-coated beads or by class II-negative, B7-positive cells. |
| 671 | 16585571 | We show that induction of IL-2 secretion under these conditions did not require expression of PKCtheta and did not induce NF-kappaB activation or IL-2 transcription. |
| 672 | 16585571 | In contrast, CD28 costimulation in trans did induce IL-2 mRNA stability, accounting for the up-regulation of IL-2 secretion. |
| 673 | 16585571 | These data indicate that the ability of CD28 to up-regulate IL-2 transcription requires colocalization of TCR and CD28 at the plasma membrane, possibly within the cSMAC of the immunological synapse. |
| 674 | 16585571 | In contrast, the ability of CD28 to promote IL-2 mRNA stability can be transduced from a distal site from the TCR, suggesting that signal integration occurs downstream from the plasma membrane. |
| 675 | 16585571 | Engagement of CD28 outside of the immunological synapse results in up-regulation of IL-2 mRNA stability but not IL-2 transcription. |
| 676 | 16585571 | During T cell activation by APC, CD28 is colocalized with TCR in the central supramolecular activation cluster (cSMAC) region of the immunological synapse. |
| 677 | 16585571 | CD28 signaling through PI3K results in the recruitment of protein kinase C (PKC)theta to the cSMAC, activation of NF-kappaB, and induction of IL-2 transcription. |
| 678 | 16585571 | To test this model we have examined the mechanism of CD28-mediated induction of IL-2 secretion when CD28 is engaged outside of the immunological synapse. |
| 679 | 16585571 | CD4 T cells were stimulated with Ag presented by B7-negative APC and CD28 costimulation was provided in trans by anti-CD28-coated beads or by class II-negative, B7-positive cells. |
| 680 | 16585571 | We show that induction of IL-2 secretion under these conditions did not require expression of PKCtheta and did not induce NF-kappaB activation or IL-2 transcription. |
| 681 | 16585571 | In contrast, CD28 costimulation in trans did induce IL-2 mRNA stability, accounting for the up-regulation of IL-2 secretion. |
| 682 | 16585571 | These data indicate that the ability of CD28 to up-regulate IL-2 transcription requires colocalization of TCR and CD28 at the plasma membrane, possibly within the cSMAC of the immunological synapse. |
| 683 | 16585571 | In contrast, the ability of CD28 to promote IL-2 mRNA stability can be transduced from a distal site from the TCR, suggesting that signal integration occurs downstream from the plasma membrane. |
| 684 | 16585571 | Engagement of CD28 outside of the immunological synapse results in up-regulation of IL-2 mRNA stability but not IL-2 transcription. |
| 685 | 16585571 | During T cell activation by APC, CD28 is colocalized with TCR in the central supramolecular activation cluster (cSMAC) region of the immunological synapse. |
| 686 | 16585571 | CD28 signaling through PI3K results in the recruitment of protein kinase C (PKC)theta to the cSMAC, activation of NF-kappaB, and induction of IL-2 transcription. |
| 687 | 16585571 | To test this model we have examined the mechanism of CD28-mediated induction of IL-2 secretion when CD28 is engaged outside of the immunological synapse. |
| 688 | 16585571 | CD4 T cells were stimulated with Ag presented by B7-negative APC and CD28 costimulation was provided in trans by anti-CD28-coated beads or by class II-negative, B7-positive cells. |
| 689 | 16585571 | We show that induction of IL-2 secretion under these conditions did not require expression of PKCtheta and did not induce NF-kappaB activation or IL-2 transcription. |
| 690 | 16585571 | In contrast, CD28 costimulation in trans did induce IL-2 mRNA stability, accounting for the up-regulation of IL-2 secretion. |
| 691 | 16585571 | These data indicate that the ability of CD28 to up-regulate IL-2 transcription requires colocalization of TCR and CD28 at the plasma membrane, possibly within the cSMAC of the immunological synapse. |
| 692 | 16585571 | In contrast, the ability of CD28 to promote IL-2 mRNA stability can be transduced from a distal site from the TCR, suggesting that signal integration occurs downstream from the plasma membrane. |
| 693 | 16585571 | Engagement of CD28 outside of the immunological synapse results in up-regulation of IL-2 mRNA stability but not IL-2 transcription. |
| 694 | 16585571 | During T cell activation by APC, CD28 is colocalized with TCR in the central supramolecular activation cluster (cSMAC) region of the immunological synapse. |
| 695 | 16585571 | CD28 signaling through PI3K results in the recruitment of protein kinase C (PKC)theta to the cSMAC, activation of NF-kappaB, and induction of IL-2 transcription. |
| 696 | 16585571 | To test this model we have examined the mechanism of CD28-mediated induction of IL-2 secretion when CD28 is engaged outside of the immunological synapse. |
| 697 | 16585571 | CD4 T cells were stimulated with Ag presented by B7-negative APC and CD28 costimulation was provided in trans by anti-CD28-coated beads or by class II-negative, B7-positive cells. |
| 698 | 16585571 | We show that induction of IL-2 secretion under these conditions did not require expression of PKCtheta and did not induce NF-kappaB activation or IL-2 transcription. |
| 699 | 16585571 | In contrast, CD28 costimulation in trans did induce IL-2 mRNA stability, accounting for the up-regulation of IL-2 secretion. |
| 700 | 16585571 | These data indicate that the ability of CD28 to up-regulate IL-2 transcription requires colocalization of TCR and CD28 at the plasma membrane, possibly within the cSMAC of the immunological synapse. |
| 701 | 16585571 | In contrast, the ability of CD28 to promote IL-2 mRNA stability can be transduced from a distal site from the TCR, suggesting that signal integration occurs downstream from the plasma membrane. |
| 702 | 16585571 | Engagement of CD28 outside of the immunological synapse results in up-regulation of IL-2 mRNA stability but not IL-2 transcription. |
| 703 | 16585571 | During T cell activation by APC, CD28 is colocalized with TCR in the central supramolecular activation cluster (cSMAC) region of the immunological synapse. |
| 704 | 16585571 | CD28 signaling through PI3K results in the recruitment of protein kinase C (PKC)theta to the cSMAC, activation of NF-kappaB, and induction of IL-2 transcription. |
| 705 | 16585571 | To test this model we have examined the mechanism of CD28-mediated induction of IL-2 secretion when CD28 is engaged outside of the immunological synapse. |
| 706 | 16585571 | CD4 T cells were stimulated with Ag presented by B7-negative APC and CD28 costimulation was provided in trans by anti-CD28-coated beads or by class II-negative, B7-positive cells. |
| 707 | 16585571 | We show that induction of IL-2 secretion under these conditions did not require expression of PKCtheta and did not induce NF-kappaB activation or IL-2 transcription. |
| 708 | 16585571 | In contrast, CD28 costimulation in trans did induce IL-2 mRNA stability, accounting for the up-regulation of IL-2 secretion. |
| 709 | 16585571 | These data indicate that the ability of CD28 to up-regulate IL-2 transcription requires colocalization of TCR and CD28 at the plasma membrane, possibly within the cSMAC of the immunological synapse. |
| 710 | 16585571 | In contrast, the ability of CD28 to promote IL-2 mRNA stability can be transduced from a distal site from the TCR, suggesting that signal integration occurs downstream from the plasma membrane. |
| 711 | 16585571 | Engagement of CD28 outside of the immunological synapse results in up-regulation of IL-2 mRNA stability but not IL-2 transcription. |
| 712 | 16585571 | During T cell activation by APC, CD28 is colocalized with TCR in the central supramolecular activation cluster (cSMAC) region of the immunological synapse. |
| 713 | 16585571 | CD28 signaling through PI3K results in the recruitment of protein kinase C (PKC)theta to the cSMAC, activation of NF-kappaB, and induction of IL-2 transcription. |
| 714 | 16585571 | To test this model we have examined the mechanism of CD28-mediated induction of IL-2 secretion when CD28 is engaged outside of the immunological synapse. |
| 715 | 16585571 | CD4 T cells were stimulated with Ag presented by B7-negative APC and CD28 costimulation was provided in trans by anti-CD28-coated beads or by class II-negative, B7-positive cells. |
| 716 | 16585571 | We show that induction of IL-2 secretion under these conditions did not require expression of PKCtheta and did not induce NF-kappaB activation or IL-2 transcription. |
| 717 | 16585571 | In contrast, CD28 costimulation in trans did induce IL-2 mRNA stability, accounting for the up-regulation of IL-2 secretion. |
| 718 | 16585571 | These data indicate that the ability of CD28 to up-regulate IL-2 transcription requires colocalization of TCR and CD28 at the plasma membrane, possibly within the cSMAC of the immunological synapse. |
| 719 | 16585571 | In contrast, the ability of CD28 to promote IL-2 mRNA stability can be transduced from a distal site from the TCR, suggesting that signal integration occurs downstream from the plasma membrane. |
| 720 | 16585571 | Engagement of CD28 outside of the immunological synapse results in up-regulation of IL-2 mRNA stability but not IL-2 transcription. |
| 721 | 16585571 | During T cell activation by APC, CD28 is colocalized with TCR in the central supramolecular activation cluster (cSMAC) region of the immunological synapse. |
| 722 | 16585571 | CD28 signaling through PI3K results in the recruitment of protein kinase C (PKC)theta to the cSMAC, activation of NF-kappaB, and induction of IL-2 transcription. |
| 723 | 16585571 | To test this model we have examined the mechanism of CD28-mediated induction of IL-2 secretion when CD28 is engaged outside of the immunological synapse. |
| 724 | 16585571 | CD4 T cells were stimulated with Ag presented by B7-negative APC and CD28 costimulation was provided in trans by anti-CD28-coated beads or by class II-negative, B7-positive cells. |
| 725 | 16585571 | We show that induction of IL-2 secretion under these conditions did not require expression of PKCtheta and did not induce NF-kappaB activation or IL-2 transcription. |
| 726 | 16585571 | In contrast, CD28 costimulation in trans did induce IL-2 mRNA stability, accounting for the up-regulation of IL-2 secretion. |
| 727 | 16585571 | These data indicate that the ability of CD28 to up-regulate IL-2 transcription requires colocalization of TCR and CD28 at the plasma membrane, possibly within the cSMAC of the immunological synapse. |
| 728 | 16585571 | In contrast, the ability of CD28 to promote IL-2 mRNA stability can be transduced from a distal site from the TCR, suggesting that signal integration occurs downstream from the plasma membrane. |
| 729 | 16585571 | Engagement of CD28 outside of the immunological synapse results in up-regulation of IL-2 mRNA stability but not IL-2 transcription. |
| 730 | 16585571 | During T cell activation by APC, CD28 is colocalized with TCR in the central supramolecular activation cluster (cSMAC) region of the immunological synapse. |
| 731 | 16585571 | CD28 signaling through PI3K results in the recruitment of protein kinase C (PKC)theta to the cSMAC, activation of NF-kappaB, and induction of IL-2 transcription. |
| 732 | 16585571 | To test this model we have examined the mechanism of CD28-mediated induction of IL-2 secretion when CD28 is engaged outside of the immunological synapse. |
| 733 | 16585571 | CD4 T cells were stimulated with Ag presented by B7-negative APC and CD28 costimulation was provided in trans by anti-CD28-coated beads or by class II-negative, B7-positive cells. |
| 734 | 16585571 | We show that induction of IL-2 secretion under these conditions did not require expression of PKCtheta and did not induce NF-kappaB activation or IL-2 transcription. |
| 735 | 16585571 | In contrast, CD28 costimulation in trans did induce IL-2 mRNA stability, accounting for the up-regulation of IL-2 secretion. |
| 736 | 16585571 | These data indicate that the ability of CD28 to up-regulate IL-2 transcription requires colocalization of TCR and CD28 at the plasma membrane, possibly within the cSMAC of the immunological synapse. |
| 737 | 16585571 | In contrast, the ability of CD28 to promote IL-2 mRNA stability can be transduced from a distal site from the TCR, suggesting that signal integration occurs downstream from the plasma membrane. |
| 738 | 16622001 | In the present study, we used polychromatic flow cytometry to assess the frequency and functional capacity of central memory (CD28(+)CD95(+)) and effector memory (CD28(-)CD95(+)) subpopulations of Gag-specific CD8(+) T cells in SIV/simian human immunodeficiency virus-infected rhesus monkeys. |
| 739 | 16622001 | We observed that vaccination was associated with the preservation of Gag-specific central memory CD8(+) T cells that were functionally capable of producing IFN-gamma, and effector memory CD8(+) T cells that were capable of producing granzyme B following viral Ag exposure. |
| 740 | 16730267 | The immunoglobulin superfamily occupies a central importance in this coordination of immune responses, and the CD28/cytotoxic T-lymphocyte antigen-4 (CTLA-4):B7.1/B7.2 receptor/ligand grouping represents the archetypal example of these immune regulators. |
| 741 | 16776575 | In vivo analysis of adenovirus-specific cytotoxic T lymphocyte response in mice deficient in CD28, fas ligand, and perforin. |
| 742 | 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. |
| 743 | 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. |
| 744 | 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. |
| 745 | 16776575 | In vivo analysis of adenovirus-specific cytotoxic T lymphocyte response in mice deficient in CD28, fas ligand, and perforin. |
| 746 | 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. |
| 747 | 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. |
| 748 | 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. |
| 749 | 16776575 | In vivo analysis of adenovirus-specific cytotoxic T lymphocyte response in mice deficient in CD28, fas ligand, and perforin. |
| 750 | 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. |
| 751 | 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. |
| 752 | 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. |
| 753 | 16790365 | However, in this study, we demonstrate protection against disease by covaccination with a mutant B7-1 molecule (B7-1wa) that binds the negative T cell regulator CTLA-4 (CD152), but not CD28. |
| 754 | 16790365 | In vitro, the T cells of covaccinated mice had negative responses to both insulin and GAD65, and this was restored by adding blocking antibodies to transforming growth factor beta1 (TGF-beta1), suggesting a role for this cytokine. |
| 755 | 16790365 | Furthermore, vaccinated mice had increased numbers of T cells with Tr-associated markers, such as CTLA-4, Foxp3, and membrane-bound TGF-beta1. |
| 756 | 16823910 | CD40 and CD28 based adjuvants are extremely potent and should avoid the inflammatory side effects induced by most adjuvants. |
| 757 | 16907911 | The methodology [currently presented for cytomegalovirus human leucocyte antigen (HLA)-A2 cognant peptide antigens] allows simultaneous ex vivo quantification of activated (cytokine-producing) and inactive tetramer-positive T cells following HLA class I/peptide/CD28 stimulation independent of endogenous antigen presentation. |
| 758 | 16982886 | Ligation of CD80 is critical for high-level CD25 expression on CD8+ T lymphocytes. |
| 759 | 16982886 | CD80 and CD86 have been shown to play a critical role in the optimal activation of T cells. |
| 760 | 16982886 | Although these two molecules bind the same ligand, CD28, the question of whether CD80 and CD86 provide unique signals or serve redundant roles remains controversial. |
| 761 | 16982886 | Previous studies have suggested that CD80 binding to CD28 may be superior to CD86 for the activation of naive CD8+ T cells. |
| 762 | 16982886 | Our study demonstrates a previously unappreciated role for CD80, its superiority over CD86 in promoting CD25 expression, increasing both the number of cells that express CD25 and the level expressed on a per cell basis. |
| 763 | 16982886 | These findings provide new insights into the role of CD80 vs CD86 and have important implications for the design of vaccines and immunotherapeutics aimed at the generation of a robust CD8+ T cell response in vivo. |
| 764 | 16982886 | Ligation of CD80 is critical for high-level CD25 expression on CD8+ T lymphocytes. |
| 765 | 16982886 | CD80 and CD86 have been shown to play a critical role in the optimal activation of T cells. |
| 766 | 16982886 | Although these two molecules bind the same ligand, CD28, the question of whether CD80 and CD86 provide unique signals or serve redundant roles remains controversial. |
| 767 | 16982886 | Previous studies have suggested that CD80 binding to CD28 may be superior to CD86 for the activation of naive CD8+ T cells. |
| 768 | 16982886 | Our study demonstrates a previously unappreciated role for CD80, its superiority over CD86 in promoting CD25 expression, increasing both the number of cells that express CD25 and the level expressed on a per cell basis. |
| 769 | 16982886 | These findings provide new insights into the role of CD80 vs CD86 and have important implications for the design of vaccines and immunotherapeutics aimed at the generation of a robust CD8+ T cell response in vivo. |
| 770 | 17003516 | A major focus of our laboratory is to investigate the role of costimulatory molecules of the TNFR and CD28 families in antiviral responses. |
| 771 | 17014937 | Several independent studies on immune correlates of poor vaccine responsiveness have identified a novel immune biomarker of reduced antibody response to vaccination, namely high proportions of memory CD8 T lymphocytes lacking expression of the CD28 costimulatory molecule. |
| 772 | 17014937 | Research on this population of CD8(+)CD28(-) T lymphocytes has documented characteristics suggestive of replicative senescence, including inability to proliferate, reduced telomere length, and altered cytokine profiles. |
| 773 | 17014937 | CD8(+)CD28(-) T lymphocytes have also been associated with suppressor functions and with early mortality in the elderly. |
| 774 | 17014937 | Several independent studies on immune correlates of poor vaccine responsiveness have identified a novel immune biomarker of reduced antibody response to vaccination, namely high proportions of memory CD8 T lymphocytes lacking expression of the CD28 costimulatory molecule. |
| 775 | 17014937 | Research on this population of CD8(+)CD28(-) T lymphocytes has documented characteristics suggestive of replicative senescence, including inability to proliferate, reduced telomere length, and altered cytokine profiles. |
| 776 | 17014937 | CD8(+)CD28(-) T lymphocytes have also been associated with suppressor functions and with early mortality in the elderly. |
| 777 | 17014937 | Several independent studies on immune correlates of poor vaccine responsiveness have identified a novel immune biomarker of reduced antibody response to vaccination, namely high proportions of memory CD8 T lymphocytes lacking expression of the CD28 costimulatory molecule. |
| 778 | 17014937 | Research on this population of CD8(+)CD28(-) T lymphocytes has documented characteristics suggestive of replicative senescence, including inability to proliferate, reduced telomere length, and altered cytokine profiles. |
| 779 | 17014937 | CD8(+)CD28(-) T lymphocytes have also been associated with suppressor functions and with early mortality in the elderly. |
| 780 | 17052145 | In this study, we retrovirally transduce human primary T cells with a cDNA encoding the extracellular domain of FcRI linked to the hinge and transmembrane domains of FcRI and the cytoplasmic domains of CD28 and T cell receptor zeta chain (FcRI-CD28-zeta). |
| 781 | 17079436 | CD27 and CD57 expression reveals atypical differentiation of human immunodeficiency virus type 1-specific memory CD8+ T cells. |
| 782 | 17079436 | We characterized and compared the expressions of CD27, CD28, CD57, and CD62L by Epstein-Barr virus (EBV)-, cytomegalovirus (CMV)-, and HIV-1-specific CD8+ T cells by six-color, eight-parameter flow cytometry. |
| 783 | 17079436 | In contrast to the maturation of EBV- and CMV-specific memory CD8+ T cells, we found that HIV-1-specific CD8+ T cells did not display coordinated down-regulation of CD27 and up-regulation of CD57 and accumulated in an atypical CD27(high) CD57(low) subset. |
| 784 | 17079436 | Moreover, the accumulation of CD27(high) CD57(low) HIV-1-specific CD8+ T cells was positively correlated with HIV-1 plasma viremia. |
| 785 | 17081609 | Immunization of cattle with a Leptospira borgpetersenii serovar hardjo-bovis vaccine results in the development of a recall response by WC1(+) gammadelta T cells and CD4(+) alphabeta T cells characterized by proliferation and interferon-gamma production. |
| 786 | 17081609 | Both T cell populations had similar transcript profiles for effector molecules, including IFN-gamma, FasL and granzyme B. |
| 787 | 17081609 | In contrast, transcripts for costimulatory receptors and ligands were notably different following activation, as WC1(+) T cells expressed no or lower levels of transcripts for CD28 and CD40L, while CD4(+) T cells expressed substantial levels of both. |
| 788 | 17081609 | These results strengthen the hypothesis that these particular activated WC1(+) and CD4(+) T cells have overlapping effector functions and therefore may differ principally with regard to how they are recruited into immune responses. |
| 789 | 17182206 | Cultures of senescent CD8 T cells show altered cytokine patterns, resistance to apoptosis, and absence of expression of the CD28 costimulatory receptor. |
| 790 | 17182206 | CD8(+)CD28(-) T cells have also been shown to exert suppressive activity on other immune cells. |
| 791 | 17182206 | Gene therapy of HIV-specific CD8 T cells with the telomerase catalytic component (hTERT) results in enhanced proliferative capacity, increased anti-viral functions, and a delay in the loss of CD28 expression, with no changes in karyotype or growth kinetics. |
| 792 | 17182206 | Cultures of senescent CD8 T cells show altered cytokine patterns, resistance to apoptosis, and absence of expression of the CD28 costimulatory receptor. |
| 793 | 17182206 | CD8(+)CD28(-) T cells have also been shown to exert suppressive activity on other immune cells. |
| 794 | 17182206 | Gene therapy of HIV-specific CD8 T cells with the telomerase catalytic component (hTERT) results in enhanced proliferative capacity, increased anti-viral functions, and a delay in the loss of CD28 expression, with no changes in karyotype or growth kinetics. |
| 795 | 17182206 | Cultures of senescent CD8 T cells show altered cytokine patterns, resistance to apoptosis, and absence of expression of the CD28 costimulatory receptor. |
| 796 | 17182206 | CD8(+)CD28(-) T cells have also been shown to exert suppressive activity on other immune cells. |
| 797 | 17182206 | Gene therapy of HIV-specific CD8 T cells with the telomerase catalytic component (hTERT) results in enhanced proliferative capacity, increased anti-viral functions, and a delay in the loss of CD28 expression, with no changes in karyotype or growth kinetics. |
| 798 | 17191384 | CD28 and CD27 costimulation of CD8+ T cells: a story of survival. |
| 799 | 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. |
| 800 | 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? |
| 801 | 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? |
| 802 | 17191384 | CD28 and CD27 costimulation of CD8+ T cells: a story of survival. |
| 803 | 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. |
| 804 | 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? |
| 805 | 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? |
| 806 | 17191384 | CD28 and CD27 costimulation of CD8+ T cells: a story of survival. |
| 807 | 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. |
| 808 | 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? |
| 809 | 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? |
| 810 | 17191384 | CD28 and CD27 costimulation of CD8+ T cells: a story of survival. |
| 811 | 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. |
| 812 | 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? |
| 813 | 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? |
| 814 | 17237418 | The strongest correlates of preserved CD4(+) T cell counts were a low percentage of circulating effector T cells (CD28(-)CD95(+) and/or IL-7R/CD127(-)) and a high percentage of CD4(+)CD25(+) T cells. |
| 815 | 17237418 | The absence of AIDS in these "CD4(low)" naturally SIV-infected SMs defines a protective role of the reduced immune activation even in the context of a significant CD4(+) T cell depletion. |
| 816 | 17293384 | Targeting HER-2/neu in early breast cancer development using dendritic cells with staged interleukin-12 burst secretion. |
| 817 | 17293384 | Before surgical resection, HER-2/neu(pos) DCIS patients (n = 13) received 4 weekly vaccinations of dendritic cells pulsed with HER-2/neu HLA class I and II peptides. |
| 818 | 17293384 | Before vaccination, many subjects possessed HER-2/neu-HLA-A2 tetramer-staining CD8(pos) T cells that expressed low levels of CD28 and high levels of the inhibitory B7 ligand CTLA-4, but this ratio inverted after vaccination. |
| 819 | 17293384 | The vaccinated subjects also showed high rates of peptide-specific sensitization for both IFN-gamma-secreting CD4(pos) (85%) and CD8(pos) (80%) T cells, with recognition of antigenically relevant breast cancer lines, accumulation of T and B lymphocytes in the breast, and induction of complement-dependent, tumor-lytic antibodies. |
| 820 | 17427008 | M1(58-66)-specific CD8+ T cells were either CD45RA(low)CD45RO(low) or CD45RA-CD45RO+, expressed CD28 and CD62L and did not produce perforin. |
| 821 | 17427008 | They also acquired a CD45RO+CD28+ CD62L(+/-) phenotype and produced perforin. |
| 822 | 17427008 | M1(58-66)-specific CD8+ T cells were either CD45RA(low)CD45RO(low) or CD45RA-CD45RO+, expressed CD28 and CD62L and did not produce perforin. |
| 823 | 17427008 | They also acquired a CD45RO+CD28+ CD62L(+/-) phenotype and produced perforin. |
| 824 | 17444958 | MTB-reactive CD4(+) T cells reside predominantly in the CD45RA(+) CD28(+) and CD45(-) CD28(+) T-cell subset and recognize naturally processed and presented MTB epitopes. |
| 825 | 17444958 | HLA-DR4-restricted, Ag85B or ESAT-6-specific CD4(+) T cells show similar dynamics over time in peripheral blood mononuclear cells (PBMC) when compared with CD8(+) T cells directed against the corresponding HLA-A2-presented MTB epitopes in patients with pulmonary MTB infection and subsequent successful therapy. |
| 826 | 17545626 | Furthermore, the tumors displayed significant morphologic changes and increased apoptosis, as shown by up-regulation of gene expression of the proapoptotic markers Fas, caspase-8, and caspase-3. |
| 827 | 17545626 | The residual tumor masses seen in the HC-Vacc/ACT-treated mice were infiltrated with CD4+ and CD8+ lymphocytes and showed elevated IFNgamma expression. |
| 828 | 17545626 | Moreover, splenic enlargement observed in HC-Vacc/ACT-treated mice reflected the increased functionality of T cells, as also indicated by increased expression of markers for CTL activation, differentiation, and proliferation (Cd28, Icosl, Tnfrsf13, and Tnfsf14). |
| 829 | 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. |
| 830 | 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. |
| 831 | 17563737 | Production of Th2 cytokines IL-5 and IL-13 was superior to production of Th1 cytokines IFN-gamma and TNF-alpha. |
| 832 | 17570460 | Virus-specific CD8 effector T cells with the phenotype, GrB+ CD62L(high) CD8 T(CM), were found to be the source of the early CTL response to influenza virus. |
| 833 | 17570460 | Comparing the CD8 T cell response in 5-day PBMC cultures of 161 adult subjects, the response of GrB+ CD62L(high) CD8 T(CM) lymphocytes in older individuals was significantly lower than in younger adults after viral stimulation (p<0.001). |
| 834 | 17570460 | The increase in the proportion of CD28(null) CD8 T cells in fresh PBMC negatively correlated with the proportion GrB+ CD62L(high) CD8 T(CM) lymphocytes in virus-stimulated PBMC. |
| 835 | 17570460 | Thus, the increase in CD28(null) CD8 T cells with age may contribute to the limited CTL response to influenza vaccination and diminished protection in older adults. |
| 836 | 17570460 | Virus-specific CD8 effector T cells with the phenotype, GrB+ CD62L(high) CD8 T(CM), were found to be the source of the early CTL response to influenza virus. |
| 837 | 17570460 | Comparing the CD8 T cell response in 5-day PBMC cultures of 161 adult subjects, the response of GrB+ CD62L(high) CD8 T(CM) lymphocytes in older individuals was significantly lower than in younger adults after viral stimulation (p<0.001). |
| 838 | 17570460 | The increase in the proportion of CD28(null) CD8 T cells in fresh PBMC negatively correlated with the proportion GrB+ CD62L(high) CD8 T(CM) lymphocytes in virus-stimulated PBMC. |
| 839 | 17570460 | Thus, the increase in CD28(null) CD8 T cells with age may contribute to the limited CTL response to influenza vaccination and diminished protection in older adults. |
| 840 | 17629370 | In contrast, the absence of endogenous IL-12/IL-23 or IL-4 had little impact on the magnitude of the antibody response but instead caused a dramatic change in the pattern of IgG isotypes. |
| 841 | 17629370 | IFN-gamma was produced by NK, dendritic cells, CD4+ and CD8+ T cells stimulated in vitro with CpG ODN. |
| 842 | 17629370 | Adoptive transfer experiments confirmed that CD4+ or CD8+ T cells were in fact relevant sources of IFN-gamma in vivo. |
| 843 | 17629370 | Following CpG ODN injection, splenic dendritic cells from IFN-gamma deficient mice did not up-regulate CD86 or CD40 expression, suggesting a role for these molecules. |
| 844 | 17629370 | The importance of CD28 (CD86 ligand) was confirmed using CD28 deficient mice which presented severely impaired immune responses following CpG ODN-assisted immunization. |
| 845 | 17982038 | Memory CD8+ T cells require CD28 costimulation. |
| 846 | 17982038 | A current paradigm in immunology is that naive CD8(+) T cells require CD28 costimulation, whereas memory CD8(+) T cells do not. |
| 847 | 17982038 | In the absence of CD28 costimulation, secondary CD8(+) T cell responses are greatly reduced and this impairs viral clearance. |
| 848 | 17982038 | The failure of CD8(+) T cells to expand in the absence of CD28 costimulation is CD4(+) T cell help independent and is accompanied by a failure to down-regulate Bcl-2 and by cell cycle arrest. |
| 849 | 17982038 | Thus, contrary to current dogma, memory CD8(+) T cells require CD28 costimulation to generate maximal secondary responses against pathogens. |
| 850 | 17982038 | Memory CD8+ T cells require CD28 costimulation. |
| 851 | 17982038 | A current paradigm in immunology is that naive CD8(+) T cells require CD28 costimulation, whereas memory CD8(+) T cells do not. |
| 852 | 17982038 | In the absence of CD28 costimulation, secondary CD8(+) T cell responses are greatly reduced and this impairs viral clearance. |
| 853 | 17982038 | The failure of CD8(+) T cells to expand in the absence of CD28 costimulation is CD4(+) T cell help independent and is accompanied by a failure to down-regulate Bcl-2 and by cell cycle arrest. |
| 854 | 17982038 | Thus, contrary to current dogma, memory CD8(+) T cells require CD28 costimulation to generate maximal secondary responses against pathogens. |
| 855 | 17982038 | Memory CD8+ T cells require CD28 costimulation. |
| 856 | 17982038 | A current paradigm in immunology is that naive CD8(+) T cells require CD28 costimulation, whereas memory CD8(+) T cells do not. |
| 857 | 17982038 | In the absence of CD28 costimulation, secondary CD8(+) T cell responses are greatly reduced and this impairs viral clearance. |
| 858 | 17982038 | The failure of CD8(+) T cells to expand in the absence of CD28 costimulation is CD4(+) T cell help independent and is accompanied by a failure to down-regulate Bcl-2 and by cell cycle arrest. |
| 859 | 17982038 | Thus, contrary to current dogma, memory CD8(+) T cells require CD28 costimulation to generate maximal secondary responses against pathogens. |
| 860 | 17982038 | Memory CD8+ T cells require CD28 costimulation. |
| 861 | 17982038 | A current paradigm in immunology is that naive CD8(+) T cells require CD28 costimulation, whereas memory CD8(+) T cells do not. |
| 862 | 17982038 | In the absence of CD28 costimulation, secondary CD8(+) T cell responses are greatly reduced and this impairs viral clearance. |
| 863 | 17982038 | The failure of CD8(+) T cells to expand in the absence of CD28 costimulation is CD4(+) T cell help independent and is accompanied by a failure to down-regulate Bcl-2 and by cell cycle arrest. |
| 864 | 17982038 | Thus, contrary to current dogma, memory CD8(+) T cells require CD28 costimulation to generate maximal secondary responses against pathogens. |
| 865 | 17982038 | Memory CD8+ T cells require CD28 costimulation. |
| 866 | 17982038 | A current paradigm in immunology is that naive CD8(+) T cells require CD28 costimulation, whereas memory CD8(+) T cells do not. |
| 867 | 17982038 | In the absence of CD28 costimulation, secondary CD8(+) T cell responses are greatly reduced and this impairs viral clearance. |
| 868 | 17982038 | The failure of CD8(+) T cells to expand in the absence of CD28 costimulation is CD4(+) T cell help independent and is accompanied by a failure to down-regulate Bcl-2 and by cell cycle arrest. |
| 869 | 17982038 | Thus, contrary to current dogma, memory CD8(+) T cells require CD28 costimulation to generate maximal secondary responses against pathogens. |
| 870 | 18071585 | Using STAT4(-/-) mice, we found that modulated IFN gamma secretion in wt TDLN cells after anti-CD3/CD28/4-1BB activation in vitro was lost in similarly stimulated STAT4(-/-) TDLN cells. |
| 871 | 18071585 | Additionally, anti-4-1BB administration failed to augment the therapeutic efficacy of T cell therapy in STAT4(-/-) mice. |
| 872 | 18071585 | Together, these results indicate that administered anti-4-1BB mAb can serve as an effective adjuvant to augment the antitumor reactivity of adoptively transferred T cells by recruiting the host NK cells; increasing the persistence of infused effector T cells, and modulating the STAT4 molecular signaling pathway. |
| 873 | 18243433 | Results showed increased frequency of monocytes and NK cell subpopulations besides unexpected up-regulation of granulocytes activation status (CD28+/CD23+ and CD28+/HLA-DR+, respectively). |
| 874 | 18360705 | Here, we demonstrated the strong potentiation of the T cell stimulatory activity of such a vaccine upon attachment of bispecific or trispecific fusion proteins which bind with one arm to viral HN molecules of the vaccine, and with the other arm either to CD3 (signal 1), to CD28 (costimulatory signal 2a), or to interleukin-2 receptor (costimulatory signal 2b) on T cells. |
| 875 | 18566382 | Coligation of the hepatitis C virus receptor CD81 with CD28 primes naive T lymphocytes to acquire type 2 effector function. |
| 876 | 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. |
| 877 | 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. |
| 878 | 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. |
| 879 | 18566382 | The hepatitis C virus envelope protein E2 is the only ligand known for CD81. |
| 880 | 18566382 | Coligation of the hepatitis C virus receptor CD81 with CD28 primes naive T lymphocytes to acquire type 2 effector function. |
| 881 | 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. |
| 882 | 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. |
| 883 | 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. |
| 884 | 18566382 | The hepatitis C virus envelope protein E2 is the only ligand known for CD81. |
| 885 | 18600180 | Costimulatory molecules B7.1 (CD80) and B7.2 (CD86) have improved the efficacy of gene-based and cell-based vaccines in animal models and are under investigation in clinical trials. |
| 886 | 18600180 | However, their efficacy as vaccine adjuvants is likely limited by the fact that they mediate both stimulatory and inhibitory signals to T cells via CD28 and CTLA-4, respectively. |
| 887 | 18600180 | To overcome these limitations, we have generated a B7.1-like, chimeric costimulatory molecule with preferential binding to CD28, named CD28-binding protein (CD28BP), which we combined with a modified, nonself tumor antigen variant of epithelial cell adhesion molecule (EpCAM), named TAg25. |
| 888 | 18600180 | In contrast, TAg25 combined with CD28BP induced both CD4 and CD8 T cells specific for EpCAM. |
| 889 | 18600180 | Costimulatory molecules B7.1 (CD80) and B7.2 (CD86) have improved the efficacy of gene-based and cell-based vaccines in animal models and are under investigation in clinical trials. |
| 890 | 18600180 | However, their efficacy as vaccine adjuvants is likely limited by the fact that they mediate both stimulatory and inhibitory signals to T cells via CD28 and CTLA-4, respectively. |
| 891 | 18600180 | To overcome these limitations, we have generated a B7.1-like, chimeric costimulatory molecule with preferential binding to CD28, named CD28-binding protein (CD28BP), which we combined with a modified, nonself tumor antigen variant of epithelial cell adhesion molecule (EpCAM), named TAg25. |
| 892 | 18600180 | In contrast, TAg25 combined with CD28BP induced both CD4 and CD8 T cells specific for EpCAM. |
| 893 | 19017952 | During T cell interaction with APC, CD28 is recruited to the central region (cSMAC) of the immunological synapse. |
| 894 | 19017952 | CD28-mediated signaling through PI3K results in the recruitment of protein kinase C-theta (PKCtheta) to the cSMAC, activation of NF-kappaB, and up-regulation of IL-2 transcription. |
| 895 | 19017952 | In this report, we show that CD28 recruitment and persistence at the immunological synapse requires TCR signals and CD80 engagement. |
| 896 | 19017952 | Addition of mAb to either MHC class II or CD80 results in the rapid displacement of CD28 from the immunological synapse. |
| 897 | 19017952 | Ligand binding is not sufficient for CD28 localization to the immunological synapse, as truncation of the cytosolic tail of CD28 disrupts synapse localization without effecting the ability of CD28 to bind CD80. |
| 898 | 19017952 | Mutation of tyrosine 188 also results in diminished activation of NF-kappaB, suggesting that CD28-mediated localization of PKCtheta to the cSMAC is important for efficient signal transduction. |
| 899 | 19017952 | During T cell interaction with APC, CD28 is recruited to the central region (cSMAC) of the immunological synapse. |
| 900 | 19017952 | CD28-mediated signaling through PI3K results in the recruitment of protein kinase C-theta (PKCtheta) to the cSMAC, activation of NF-kappaB, and up-regulation of IL-2 transcription. |
| 901 | 19017952 | In this report, we show that CD28 recruitment and persistence at the immunological synapse requires TCR signals and CD80 engagement. |
| 902 | 19017952 | Addition of mAb to either MHC class II or CD80 results in the rapid displacement of CD28 from the immunological synapse. |
| 903 | 19017952 | Ligand binding is not sufficient for CD28 localization to the immunological synapse, as truncation of the cytosolic tail of CD28 disrupts synapse localization without effecting the ability of CD28 to bind CD80. |
| 904 | 19017952 | Mutation of tyrosine 188 also results in diminished activation of NF-kappaB, suggesting that CD28-mediated localization of PKCtheta to the cSMAC is important for efficient signal transduction. |
| 905 | 19017952 | During T cell interaction with APC, CD28 is recruited to the central region (cSMAC) of the immunological synapse. |
| 906 | 19017952 | CD28-mediated signaling through PI3K results in the recruitment of protein kinase C-theta (PKCtheta) to the cSMAC, activation of NF-kappaB, and up-regulation of IL-2 transcription. |
| 907 | 19017952 | In this report, we show that CD28 recruitment and persistence at the immunological synapse requires TCR signals and CD80 engagement. |
| 908 | 19017952 | Addition of mAb to either MHC class II or CD80 results in the rapid displacement of CD28 from the immunological synapse. |
| 909 | 19017952 | Ligand binding is not sufficient for CD28 localization to the immunological synapse, as truncation of the cytosolic tail of CD28 disrupts synapse localization without effecting the ability of CD28 to bind CD80. |
| 910 | 19017952 | Mutation of tyrosine 188 also results in diminished activation of NF-kappaB, suggesting that CD28-mediated localization of PKCtheta to the cSMAC is important for efficient signal transduction. |
| 911 | 19017952 | During T cell interaction with APC, CD28 is recruited to the central region (cSMAC) of the immunological synapse. |
| 912 | 19017952 | CD28-mediated signaling through PI3K results in the recruitment of protein kinase C-theta (PKCtheta) to the cSMAC, activation of NF-kappaB, and up-regulation of IL-2 transcription. |
| 913 | 19017952 | In this report, we show that CD28 recruitment and persistence at the immunological synapse requires TCR signals and CD80 engagement. |
| 914 | 19017952 | Addition of mAb to either MHC class II or CD80 results in the rapid displacement of CD28 from the immunological synapse. |
| 915 | 19017952 | Ligand binding is not sufficient for CD28 localization to the immunological synapse, as truncation of the cytosolic tail of CD28 disrupts synapse localization without effecting the ability of CD28 to bind CD80. |
| 916 | 19017952 | Mutation of tyrosine 188 also results in diminished activation of NF-kappaB, suggesting that CD28-mediated localization of PKCtheta to the cSMAC is important for efficient signal transduction. |
| 917 | 19017952 | During T cell interaction with APC, CD28 is recruited to the central region (cSMAC) of the immunological synapse. |
| 918 | 19017952 | CD28-mediated signaling through PI3K results in the recruitment of protein kinase C-theta (PKCtheta) to the cSMAC, activation of NF-kappaB, and up-regulation of IL-2 transcription. |
| 919 | 19017952 | In this report, we show that CD28 recruitment and persistence at the immunological synapse requires TCR signals and CD80 engagement. |
| 920 | 19017952 | Addition of mAb to either MHC class II or CD80 results in the rapid displacement of CD28 from the immunological synapse. |
| 921 | 19017952 | Ligand binding is not sufficient for CD28 localization to the immunological synapse, as truncation of the cytosolic tail of CD28 disrupts synapse localization without effecting the ability of CD28 to bind CD80. |
| 922 | 19017952 | Mutation of tyrosine 188 also results in diminished activation of NF-kappaB, suggesting that CD28-mediated localization of PKCtheta to the cSMAC is important for efficient signal transduction. |
| 923 | 19017952 | During T cell interaction with APC, CD28 is recruited to the central region (cSMAC) of the immunological synapse. |
| 924 | 19017952 | CD28-mediated signaling through PI3K results in the recruitment of protein kinase C-theta (PKCtheta) to the cSMAC, activation of NF-kappaB, and up-regulation of IL-2 transcription. |
| 925 | 19017952 | In this report, we show that CD28 recruitment and persistence at the immunological synapse requires TCR signals and CD80 engagement. |
| 926 | 19017952 | Addition of mAb to either MHC class II or CD80 results in the rapid displacement of CD28 from the immunological synapse. |
| 927 | 19017952 | Ligand binding is not sufficient for CD28 localization to the immunological synapse, as truncation of the cytosolic tail of CD28 disrupts synapse localization without effecting the ability of CD28 to bind CD80. |
| 928 | 19017952 | Mutation of tyrosine 188 also results in diminished activation of NF-kappaB, suggesting that CD28-mediated localization of PKCtheta to the cSMAC is important for efficient signal transduction. |
| 929 | 19050242 | A novel ICOS-independent, but CD28- and SAP-dependent, pathway of T cell-dependent, polysaccharide-specific humoral immunity in response to intact Streptococcus pneumoniae versus pneumococcal conjugate vaccine. |
| 930 | 19050242 | Polysaccharide (PS)- and protein-specific murine IgG responses to intact Streptococcus pneumoniae (Pn) are both dependent on CD4(+) T cell help, B7-dependent costimulation, and CD40/CD40 ligand interactions. |
| 931 | 19050242 | We now demonstrate that ICOS(-/-), relative to wild-type, mice elicit a normal PS-specific IgG isotype response to Pn, despite marked inhibition of both the primary and secondary IgG anti-protein (i.e., PspA, PspC, and PsaA) response. |
| 932 | 19050242 | Finally, although mice that lack the adaptor molecule SAP (SLAM-associated protein) resemble ICOS(-/-) mice (and can exhibit decreased ICOS expression), we observe that the PS-specific, as well as protein-specific, IgG responses to both Pn and conjugate are markedly defective in SAP(-/-) mice. |
| 933 | 19050242 | These data define a novel T cell-, SAP-, and B7-dependent, but ICOS-independent, extrafollicular pathway of Ig induction. |
| 934 | 19107191 | The 60 kDa heat shock protein (HSP60) has been reported to influence T-cell responses in two ways: as a ligand of toll-like receptor 2 signalling and as an antigen. |
| 935 | 19107191 | Presentation of HSP60 by activated T cells was found to be MHC-restricted and dependent on accessory molecules - CD28, CD80 and CD86. |
| 936 | 19107191 | Anti-ergotypic T cells responded to T-cell HSP60 by proliferation and secreted IFNgamma and TGFbeta1. |
| 937 | 19107191 | In vivo, adoptive transfer of an anti-ergotypic HSP60-specific T-cell line led to decreased secretion of IFNgamma by arthritogenic T cells and ameliorated adjuvant arthritis (AA). |
| 938 | 19124723 | The recently described cytokines IL-19, IL-20, and IL-24 share structural homology with IL-10 and are therefore classified as members of the IL-10 family of cytokines. |
| 939 | 19124723 | Although it has long been speculated that signaling by their heterodimeric receptor complexes (IL-20R1/IL-20R2 and IL-22R/IL-20R2) influences immunological processes, the target cells for this group of cytokines are still unclear. |
| 940 | 19124723 | By generating a knockout mouse strain deficient for the common IL-20R beta-chain (IL-20R2), we show that IFN-gamma and IL-2 secretion is significantly elevated after stimulation of IL-20R2-/--deficient CD8 and CD4 T cells with Con A or anti-CD3/CD28 in vitro. |
| 941 | 19124723 | IL-10 secretion by activated IL-20R2-/- CD4 cells was diminished. |
| 942 | 19124723 | Consistent with our in vitro results, significantly more Ag-specific CD8 IFN-gamma+ and CD4 IFN-gamma+ T cells developed to locally applied DNA vaccines in IL-20R2-deficient mice. |
| 943 | 19124723 | Thus, IL-20R2 signaling directly regulates CD8 and CD4 T cell answers in vitro and in vivo. |
| 944 | 19124723 | For the first time, we provide evidence that IL-19, IL-20, and IL-24 are part of a signaling network that normally down-modulates T cell responses in mice. |
| 945 | 19268606 | The activation and expansion of naïve T cells require costimulatory signals provided by CD28 and TNF family members. |
| 946 | 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. |
| 947 | 19268606 | The activation and expansion of naïve T cells require costimulatory signals provided by CD28 and TNF family members. |
| 948 | 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. |
| 949 | 19483649 | Using this model, we found that induction of lymphopenia before adoptive transfer of ex vivo anti-CD3/CD28 activated and interleukin-2 expanded D5-G6 tumor draining lymph node cells enhanced the antitumor efficacy of the infused cells in both pulmonary metastases and subcutaneous D5 bearing mice. |
| 950 | 19483649 | This enhanced antitumor activity was associated with a selective increase in proliferation, accumulation, and function of CD4+ rather than CD8+ infused cells. |
| 951 | 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(-)). |
| 952 | 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. |
| 953 | 19556898 | T-cell activation requires both antigen presentation to the T-cell receptor and a second signal mediated by CD80 and CD86 on antigen-presenting cells and CD28 on the T cell. |
| 954 | 19556898 | Ligand binding to CD28 on the T-cell surface leads to T-cell proliferation and expression of activating cytokines such as interleukin-2. |
| 955 | 19556898 | Cytotoxic T-lymphocyte antigen-4 (CTLA-4), an inhibitory protein expressed on T cells, competes for the same ligands as CD28 and modulates T-cell activation. |
| 956 | 19556898 | Because CTLA-4 has a significantly higher binding efficiency than CD28, CTLA-4 is critical in maintaining immune tolerance to self-antigens and may also limit responses to tumor antigens and vaccine therapy. |
| 957 | 19556898 | T-cell activation requires both antigen presentation to the T-cell receptor and a second signal mediated by CD80 and CD86 on antigen-presenting cells and CD28 on the T cell. |
| 958 | 19556898 | Ligand binding to CD28 on the T-cell surface leads to T-cell proliferation and expression of activating cytokines such as interleukin-2. |
| 959 | 19556898 | Cytotoxic T-lymphocyte antigen-4 (CTLA-4), an inhibitory protein expressed on T cells, competes for the same ligands as CD28 and modulates T-cell activation. |
| 960 | 19556898 | Because CTLA-4 has a significantly higher binding efficiency than CD28, CTLA-4 is critical in maintaining immune tolerance to self-antigens and may also limit responses to tumor antigens and vaccine therapy. |
| 961 | 19556898 | T-cell activation requires both antigen presentation to the T-cell receptor and a second signal mediated by CD80 and CD86 on antigen-presenting cells and CD28 on the T cell. |
| 962 | 19556898 | Ligand binding to CD28 on the T-cell surface leads to T-cell proliferation and expression of activating cytokines such as interleukin-2. |
| 963 | 19556898 | Cytotoxic T-lymphocyte antigen-4 (CTLA-4), an inhibitory protein expressed on T cells, competes for the same ligands as CD28 and modulates T-cell activation. |
| 964 | 19556898 | Because CTLA-4 has a significantly higher binding efficiency than CD28, CTLA-4 is critical in maintaining immune tolerance to self-antigens and may also limit responses to tumor antigens and vaccine therapy. |
| 965 | 19556898 | T-cell activation requires both antigen presentation to the T-cell receptor and a second signal mediated by CD80 and CD86 on antigen-presenting cells and CD28 on the T cell. |
| 966 | 19556898 | Ligand binding to CD28 on the T-cell surface leads to T-cell proliferation and expression of activating cytokines such as interleukin-2. |
| 967 | 19556898 | Cytotoxic T-lymphocyte antigen-4 (CTLA-4), an inhibitory protein expressed on T cells, competes for the same ligands as CD28 and modulates T-cell activation. |
| 968 | 19556898 | Because CTLA-4 has a significantly higher binding efficiency than CD28, CTLA-4 is critical in maintaining immune tolerance to self-antigens and may also limit responses to tumor antigens and vaccine therapy. |
| 969 | 19561536 | As T cells themselves may serve as effective antigen-presenting cells (T antigen-presenting cells; TAPC) and may be useful in vivo as cellular vaccines, we examined whether CD8(+) T cells genetically modified to produce IL-21 could induce immune responses to tumor associated antigen peptides in healthy human leukocyte antigen-A2(+) donors. |
| 970 | 19561536 | We found that IL-21 modified TAPC enhanced both the proliferation and survival of MART-1 specific CD8(+) T cells, which were enriched by >8-fold over cultures with control nontransgenic TAPC. |
| 971 | 19561536 | MART-1-specific CTL produced interferon-gamma in response to cognate peptide antigen and killed primary tumor cells expressing MART-1 in a major histocompatibility complex restricted manner. |
| 972 | 19561536 | IL-21 modified TAPC similarly enhanced generation of functional CTL against melanoma antigen gp100 and the B-cell chronic lymphocytic leukemia associated RHAMM antigen. |
| 973 | 19561536 | Antigen-specific CTL generated using IL-21 gene-modified TAPC had a central memory phenotype characterized by CD45RA(-), CD44(high), CD27(high), CD28(high), CD62L(high), and IL-7 receptor-alpha(high), contrasting with the terminal effector phenotype of CTL generated in the absence of IL-21. |
| 974 | 19656991 | Age-dependent association between low frequency of CD27/CD28 expression on pp65 CD8+ T cells and cytomegalovirus replication after transplantation. |
| 975 | 19656991 | In this cross-sectional study of 42 solid organ transplant recipients, the association of human cytomegalovirus (HCMV) replication and age with the phenotype of the HCMV-specific CD8(+) T cells was analyzed by using the CMV pp65 HLA-A*0201 pentamer. |
| 976 | 19656991 | A correlation between the proportion of CD28(-) HCMV-specific CD8(+) T cells and age was observed in patients without HCMV replication (r = 0.50; P = 0.02) but not in patients with HCMV replication (r = -0.05; P = 0.83), a finding which differs from that observed for total CD8(+) T cells. |
| 977 | 19656991 | Within the group of patients younger than 50 years of age, patients with HCVM replication after transplantation had higher percentages of CD28(-) HCMV-specific CD8(+) T cells (85.6 compared with 58.7% for patients without HCMV replication; P = 0.004) and CD27(-) HCMV-specific CD8(+) T cells (90.7 compared with 68.8% for patients without HCMV replication; P = 0.03). |
| 978 | 19656991 | However, in patients older than age 50 years, a high frequency of these two subpopulations was observed in patients both with and without previous HCMV replication (for CD28(-) HCMV-specific CD8(+) T cells, 84.4 and 80.9%, respectively [P = 0.39]; for CD27(-) HCMV-specific CD8(+) T cells 86.6 and 81.5%, respectively [P = 0.16]). |
| 979 | 19656991 | In conclusion, the present study shows that in the group of recipients younger than age 50 years, HCMV replication after transplantation is associated with a high percentage of CD27(-) and CD28(-) HCMV-specific CD8(+) T cells. |
| 980 | 19656991 | These results suggest that the increased percentage of CD27(-) or CD28(-) HCMV-specific subsets can be considered a biomarker of HCMV replication in solid organ transplant recipients younger than age 50 years but not in older patients. |
| 981 | 19656991 | Age-dependent association between low frequency of CD27/CD28 expression on pp65 CD8+ T cells and cytomegalovirus replication after transplantation. |
| 982 | 19656991 | In this cross-sectional study of 42 solid organ transplant recipients, the association of human cytomegalovirus (HCMV) replication and age with the phenotype of the HCMV-specific CD8(+) T cells was analyzed by using the CMV pp65 HLA-A*0201 pentamer. |
| 983 | 19656991 | A correlation between the proportion of CD28(-) HCMV-specific CD8(+) T cells and age was observed in patients without HCMV replication (r = 0.50; P = 0.02) but not in patients with HCMV replication (r = -0.05; P = 0.83), a finding which differs from that observed for total CD8(+) T cells. |
| 984 | 19656991 | Within the group of patients younger than 50 years of age, patients with HCVM replication after transplantation had higher percentages of CD28(-) HCMV-specific CD8(+) T cells (85.6 compared with 58.7% for patients without HCMV replication; P = 0.004) and CD27(-) HCMV-specific CD8(+) T cells (90.7 compared with 68.8% for patients without HCMV replication; P = 0.03). |
| 985 | 19656991 | However, in patients older than age 50 years, a high frequency of these two subpopulations was observed in patients both with and without previous HCMV replication (for CD28(-) HCMV-specific CD8(+) T cells, 84.4 and 80.9%, respectively [P = 0.39]; for CD27(-) HCMV-specific CD8(+) T cells 86.6 and 81.5%, respectively [P = 0.16]). |
| 986 | 19656991 | In conclusion, the present study shows that in the group of recipients younger than age 50 years, HCMV replication after transplantation is associated with a high percentage of CD27(-) and CD28(-) HCMV-specific CD8(+) T cells. |
| 987 | 19656991 | These results suggest that the increased percentage of CD27(-) or CD28(-) HCMV-specific subsets can be considered a biomarker of HCMV replication in solid organ transplant recipients younger than age 50 years but not in older patients. |
| 988 | 19656991 | Age-dependent association between low frequency of CD27/CD28 expression on pp65 CD8+ T cells and cytomegalovirus replication after transplantation. |
| 989 | 19656991 | In this cross-sectional study of 42 solid organ transplant recipients, the association of human cytomegalovirus (HCMV) replication and age with the phenotype of the HCMV-specific CD8(+) T cells was analyzed by using the CMV pp65 HLA-A*0201 pentamer. |
| 990 | 19656991 | A correlation between the proportion of CD28(-) HCMV-specific CD8(+) T cells and age was observed in patients without HCMV replication (r = 0.50; P = 0.02) but not in patients with HCMV replication (r = -0.05; P = 0.83), a finding which differs from that observed for total CD8(+) T cells. |
| 991 | 19656991 | Within the group of patients younger than 50 years of age, patients with HCVM replication after transplantation had higher percentages of CD28(-) HCMV-specific CD8(+) T cells (85.6 compared with 58.7% for patients without HCMV replication; P = 0.004) and CD27(-) HCMV-specific CD8(+) T cells (90.7 compared with 68.8% for patients without HCMV replication; P = 0.03). |
| 992 | 19656991 | However, in patients older than age 50 years, a high frequency of these two subpopulations was observed in patients both with and without previous HCMV replication (for CD28(-) HCMV-specific CD8(+) T cells, 84.4 and 80.9%, respectively [P = 0.39]; for CD27(-) HCMV-specific CD8(+) T cells 86.6 and 81.5%, respectively [P = 0.16]). |
| 993 | 19656991 | In conclusion, the present study shows that in the group of recipients younger than age 50 years, HCMV replication after transplantation is associated with a high percentage of CD27(-) and CD28(-) HCMV-specific CD8(+) T cells. |
| 994 | 19656991 | These results suggest that the increased percentage of CD27(-) or CD28(-) HCMV-specific subsets can be considered a biomarker of HCMV replication in solid organ transplant recipients younger than age 50 years but not in older patients. |
| 995 | 19656991 | Age-dependent association between low frequency of CD27/CD28 expression on pp65 CD8+ T cells and cytomegalovirus replication after transplantation. |
| 996 | 19656991 | In this cross-sectional study of 42 solid organ transplant recipients, the association of human cytomegalovirus (HCMV) replication and age with the phenotype of the HCMV-specific CD8(+) T cells was analyzed by using the CMV pp65 HLA-A*0201 pentamer. |
| 997 | 19656991 | A correlation between the proportion of CD28(-) HCMV-specific CD8(+) T cells and age was observed in patients without HCMV replication (r = 0.50; P = 0.02) but not in patients with HCMV replication (r = -0.05; P = 0.83), a finding which differs from that observed for total CD8(+) T cells. |
| 998 | 19656991 | Within the group of patients younger than 50 years of age, patients with HCVM replication after transplantation had higher percentages of CD28(-) HCMV-specific CD8(+) T cells (85.6 compared with 58.7% for patients without HCMV replication; P = 0.004) and CD27(-) HCMV-specific CD8(+) T cells (90.7 compared with 68.8% for patients without HCMV replication; P = 0.03). |
| 999 | 19656991 | However, in patients older than age 50 years, a high frequency of these two subpopulations was observed in patients both with and without previous HCMV replication (for CD28(-) HCMV-specific CD8(+) T cells, 84.4 and 80.9%, respectively [P = 0.39]; for CD27(-) HCMV-specific CD8(+) T cells 86.6 and 81.5%, respectively [P = 0.16]). |
| 1000 | 19656991 | In conclusion, the present study shows that in the group of recipients younger than age 50 years, HCMV replication after transplantation is associated with a high percentage of CD27(-) and CD28(-) HCMV-specific CD8(+) T cells. |
| 1001 | 19656991 | These results suggest that the increased percentage of CD27(-) or CD28(-) HCMV-specific subsets can be considered a biomarker of HCMV replication in solid organ transplant recipients younger than age 50 years but not in older patients. |
| 1002 | 19656991 | Age-dependent association between low frequency of CD27/CD28 expression on pp65 CD8+ T cells and cytomegalovirus replication after transplantation. |
| 1003 | 19656991 | In this cross-sectional study of 42 solid organ transplant recipients, the association of human cytomegalovirus (HCMV) replication and age with the phenotype of the HCMV-specific CD8(+) T cells was analyzed by using the CMV pp65 HLA-A*0201 pentamer. |
| 1004 | 19656991 | A correlation between the proportion of CD28(-) HCMV-specific CD8(+) T cells and age was observed in patients without HCMV replication (r = 0.50; P = 0.02) but not in patients with HCMV replication (r = -0.05; P = 0.83), a finding which differs from that observed for total CD8(+) T cells. |
| 1005 | 19656991 | Within the group of patients younger than 50 years of age, patients with HCVM replication after transplantation had higher percentages of CD28(-) HCMV-specific CD8(+) T cells (85.6 compared with 58.7% for patients without HCMV replication; P = 0.004) and CD27(-) HCMV-specific CD8(+) T cells (90.7 compared with 68.8% for patients without HCMV replication; P = 0.03). |
| 1006 | 19656991 | However, in patients older than age 50 years, a high frequency of these two subpopulations was observed in patients both with and without previous HCMV replication (for CD28(-) HCMV-specific CD8(+) T cells, 84.4 and 80.9%, respectively [P = 0.39]; for CD27(-) HCMV-specific CD8(+) T cells 86.6 and 81.5%, respectively [P = 0.16]). |
| 1007 | 19656991 | In conclusion, the present study shows that in the group of recipients younger than age 50 years, HCMV replication after transplantation is associated with a high percentage of CD27(-) and CD28(-) HCMV-specific CD8(+) T cells. |
| 1008 | 19656991 | These results suggest that the increased percentage of CD27(-) or CD28(-) HCMV-specific subsets can be considered a biomarker of HCMV replication in solid organ transplant recipients younger than age 50 years but not in older patients. |
| 1009 | 19656991 | Age-dependent association between low frequency of CD27/CD28 expression on pp65 CD8+ T cells and cytomegalovirus replication after transplantation. |
| 1010 | 19656991 | In this cross-sectional study of 42 solid organ transplant recipients, the association of human cytomegalovirus (HCMV) replication and age with the phenotype of the HCMV-specific CD8(+) T cells was analyzed by using the CMV pp65 HLA-A*0201 pentamer. |
| 1011 | 19656991 | A correlation between the proportion of CD28(-) HCMV-specific CD8(+) T cells and age was observed in patients without HCMV replication (r = 0.50; P = 0.02) but not in patients with HCMV replication (r = -0.05; P = 0.83), a finding which differs from that observed for total CD8(+) T cells. |
| 1012 | 19656991 | Within the group of patients younger than 50 years of age, patients with HCVM replication after transplantation had higher percentages of CD28(-) HCMV-specific CD8(+) T cells (85.6 compared with 58.7% for patients without HCMV replication; P = 0.004) and CD27(-) HCMV-specific CD8(+) T cells (90.7 compared with 68.8% for patients without HCMV replication; P = 0.03). |
| 1013 | 19656991 | However, in patients older than age 50 years, a high frequency of these two subpopulations was observed in patients both with and without previous HCMV replication (for CD28(-) HCMV-specific CD8(+) T cells, 84.4 and 80.9%, respectively [P = 0.39]; for CD27(-) HCMV-specific CD8(+) T cells 86.6 and 81.5%, respectively [P = 0.16]). |
| 1014 | 19656991 | In conclusion, the present study shows that in the group of recipients younger than age 50 years, HCMV replication after transplantation is associated with a high percentage of CD27(-) and CD28(-) HCMV-specific CD8(+) T cells. |
| 1015 | 19656991 | These results suggest that the increased percentage of CD27(-) or CD28(-) HCMV-specific subsets can be considered a biomarker of HCMV replication in solid organ transplant recipients younger than age 50 years but not in older patients. |
| 1016 | 19706700 | Vaccination conferred strong protection against a massive intrarectal challenge with SIVmac251, as evidenced both by the reduction of viremia at the peak of acute infection (a mean of over 2 log(10) fold reduction) and by the full preservation of the CD28(+) CD95(+) memory CD4(+) T cells during the acute phase, a strong correlate of protection against pathogenesis. |
| 1017 | 19836479 | Agonistic Abs to select costimulatory members of CD28 and TNFR family have shown efficacy in various preclinical cancer immunotherapeutic settings. |
| 1018 | 20029165 | CD45RO+/KLRG1+/CD57+/CD28-), enhanced IL-2 production and T-lymphocyte expression of the IL-2 receptor, longer chromosome telomere lengths in blood leukocytes and in vivo immune responses to vaccines and recall antigens. |
| 1019 | 20100932 | Transient CD86 expression on hepatitis C virus-specific CD8+ T cells in acute infection is linked to sufficient IL-2 signaling. |
| 1020 | 20100932 | Costimulatory signals via B7/CD28 family molecules (signal 2) are critical for effective adaptive CD8(+) T cell immune responses. |
| 1021 | 20100932 | In acute hepatitis C virus (HCV) infection, programmed death receptor 1, an inhibitory receptor in the CD28 family, is highly expressed on virus-specific CD8(+) T cells, yet vigorous immune responses often develop. |
| 1022 | 20100932 | In this study, we found that CD86 was highly expressed on HCV-specific CD8(+) T cells early in acute HCV infection and was lost on transition to chronic HCV infection; the expression of CD86 was different from other activation markers, because expression was delayed after in vitro TCR stimulation and required sufficient IL-2 signaling; and HCV-specific CD8(+) T cells in the liver of patients with chronic HCV infection were highly activated (CD69, CD38, and HLA-DR expression), but only a minority expressed CD86 or showed evidence of recent IL-2 signaling (low basal phosphorylated STAT5), despite persistent viremia. |
| 1023 | 20100932 | Our study identified B7 ligand expression on HCV-specific CD8(+) T cells as a distinct marker of effective T cell stimulation with IL-2 signaling in acute HCV infection. |
| 1024 | 20100932 | Transient CD86 expression on hepatitis C virus-specific CD8+ T cells in acute infection is linked to sufficient IL-2 signaling. |
| 1025 | 20100932 | Costimulatory signals via B7/CD28 family molecules (signal 2) are critical for effective adaptive CD8(+) T cell immune responses. |
| 1026 | 20100932 | In acute hepatitis C virus (HCV) infection, programmed death receptor 1, an inhibitory receptor in the CD28 family, is highly expressed on virus-specific CD8(+) T cells, yet vigorous immune responses often develop. |
| 1027 | 20100932 | In this study, we found that CD86 was highly expressed on HCV-specific CD8(+) T cells early in acute HCV infection and was lost on transition to chronic HCV infection; the expression of CD86 was different from other activation markers, because expression was delayed after in vitro TCR stimulation and required sufficient IL-2 signaling; and HCV-specific CD8(+) T cells in the liver of patients with chronic HCV infection were highly activated (CD69, CD38, and HLA-DR expression), but only a minority expressed CD86 or showed evidence of recent IL-2 signaling (low basal phosphorylated STAT5), despite persistent viremia. |
| 1028 | 20100932 | Our study identified B7 ligand expression on HCV-specific CD8(+) T cells as a distinct marker of effective T cell stimulation with IL-2 signaling in acute HCV infection. |
| 1029 | 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. |
| 1030 | 20121696 | Programmed death-1 (PD-1), another member of the CD28 family, may contribute to functional defects of helpless memory CD8+ T cells. |
| 1031 | 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. |
| 1032 | 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. |
| 1033 | 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. |
| 1034 | 20121696 | Programmed death-1 (PD-1), another member of the CD28 family, may contribute to functional defects of helpless memory CD8+ T cells. |
| 1035 | 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. |
| 1036 | 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. |
| 1037 | 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. |
| 1038 | 20121696 | Programmed death-1 (PD-1), another member of the CD28 family, may contribute to functional defects of helpless memory CD8+ T cells. |
| 1039 | 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. |
| 1040 | 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. |
| 1041 | 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. |
| 1042 | 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. |
| 1043 | 20411566 | In contrast to HIV-1, HIV-2-specific T cells are at an early stage of differentiation (CD27(+)CD28(+)), a finding that relates directly to CD4(+) T-cell levels and inversely to immune activation. |
| 1044 | 20483749 | We found that the loss of naive CD4 and CD8 T cells, and the appearance of persisting T cell clonal expansions predicted poor CD8 responses in individual monkeys. |
| 1045 | 20483749 | There was strong correlation between early CD8 responses in the transitory CD28+ CD62L- CD8+ T cell compartment and the peak Ab titers upon boost in individual animals, as well as a correlation of both parameters of immune response to the frequency of naive CD8+ T cells in old but not in adult monkeys. |
| 1046 | 20630696 | Their peripheral blood lymphocytes showed a shift in the percentage of CD8 effector cells as judged by expression of cell surface markers CD8+ CD28+. |
| 1047 | 20630696 | Furthermore, the increase in the percentage of peripheral blood monomorphonucleated cells (PBMNCs) with effector phenotype, i.e., CD8+ CD28+ in vaccinated patients might explain their prolonged survival time. |
| 1048 | 20630696 | Their peripheral blood lymphocytes showed a shift in the percentage of CD8 effector cells as judged by expression of cell surface markers CD8+ CD28+. |
| 1049 | 20630696 | Furthermore, the increase in the percentage of peripheral blood monomorphonucleated cells (PBMNCs) with effector phenotype, i.e., CD8+ CD28+ in vaccinated patients might explain their prolonged survival time. |
| 1050 | 20695769 | Potent antirheumatic activity of a new DNA vaccine targeted to B7-2/CD28 costimulatory signaling pathway in autoimmune arthritis. |
| 1051 | 20695769 | Rheumatoid arthritis is a proinflammatory autoimmune disease attributed to failure of both CD4(+)CD25(+) regulatory T (Tr) and CD8(+)CD28(-) suppressor T (Ts) cells to control autoreactive CD4(+)CD28(+) Th1 (Th1) and autoantibody-producing B cells. |
| 1052 | 20695769 | Here we show a single intramuscular injection of our novel targeted DNA vaccine encoding Pseudomonas exotoxin A and costimulatory molecule B7-2 without autoantigens in a collagen-induced arthritis model simultaneously increased Tr and Ts cells and selectively decreased autoreactive Th1 cells. |
| 1053 | 20695769 | The vaccine induced a shift from Th1 to Th2 and Th3 cellular and cytokine profiles and a decrease in CD4(+)/CD8(+) cell ratios. |
| 1054 | 20695769 | Potent antirheumatic activity of a new DNA vaccine targeted to B7-2/CD28 costimulatory signaling pathway in autoimmune arthritis. |
| 1055 | 20695769 | Rheumatoid arthritis is a proinflammatory autoimmune disease attributed to failure of both CD4(+)CD25(+) regulatory T (Tr) and CD8(+)CD28(-) suppressor T (Ts) cells to control autoreactive CD4(+)CD28(+) Th1 (Th1) and autoantibody-producing B cells. |
| 1056 | 20695769 | Here we show a single intramuscular injection of our novel targeted DNA vaccine encoding Pseudomonas exotoxin A and costimulatory molecule B7-2 without autoantigens in a collagen-induced arthritis model simultaneously increased Tr and Ts cells and selectively decreased autoreactive Th1 cells. |
| 1057 | 20695769 | The vaccine induced a shift from Th1 to Th2 and Th3 cellular and cytokine profiles and a decrease in CD4(+)/CD8(+) cell ratios. |
| 1058 | 20702730 | Emergence of simian immunodeficiency virus-specific cytotoxic CD4+ T cells and increased humoral responses correlate with control of rebounding viremia in CD8-depleted macaques infected with Rev-independent live-attenuated simian immunodeficiency virus. |
| 1059 | 20702730 | Monitoring immune responses at the time of viral control demonstrated a burst of circulating SIV-specific CD4(+) T cells characterized as CD45RA(-)CD28(+)CD95(+)CCR7(-) and also granzyme B(+), suggesting cytotoxic ability. |
| 1060 | 20702730 | These data demonstrate that a combination of cellular responses mediated by CD4(+) T cells and humoral responses was associated with the rapid control of the rebounding viremia in macaques infected by the Rev-independent live-attenuated SIV, even in the absence of measurable SIV-specific CD8(+) T cells in the blood, emphasizing the importance of different components of the immune response for full control of SIV infection. |
| 1061 | 20721608 | Sustained CD28 expression delays multiple features of replicative senescence in human CD8 T lymphocytes. |
| 1062 | 20721608 | During aging and chronic infection with HIV-1, there are increased proportions of CD8 T lymphocytes that lack CD28 expression and show additional features of replicative senescence. |
| 1063 | 20721608 | Nevertheless, the transduced cultures eventually do reach senescence, which is associated with increased CTLA-4 gene expression and a loss of CD28 cell surface expression. |
| 1064 | 20721608 | Sustained CD28 expression delays multiple features of replicative senescence in human CD8 T lymphocytes. |
| 1065 | 20721608 | During aging and chronic infection with HIV-1, there are increased proportions of CD8 T lymphocytes that lack CD28 expression and show additional features of replicative senescence. |
| 1066 | 20721608 | Nevertheless, the transduced cultures eventually do reach senescence, which is associated with increased CTLA-4 gene expression and a loss of CD28 cell surface expression. |
| 1067 | 20721608 | Sustained CD28 expression delays multiple features of replicative senescence in human CD8 T lymphocytes. |
| 1068 | 20721608 | During aging and chronic infection with HIV-1, there are increased proportions of CD8 T lymphocytes that lack CD28 expression and show additional features of replicative senescence. |
| 1069 | 20721608 | Nevertheless, the transduced cultures eventually do reach senescence, which is associated with increased CTLA-4 gene expression and a loss of CD28 cell surface expression. |
| 1070 | 20878068 | They bind with one arm to the viral hemagglutinin-neuraminidase (HN) or fusion (F) protein of NDV expressed at the surface of the vaccine cells while the second arm is directed either against CD3 or CD28 of T cells. |
| 1071 | 21042712 | Herein we describe T cell costimulation via CD25, the interleukin (IL)-2 receptor, during priming of naive T cells with a tumor vaccine. |
| 1072 | 21042712 | To this end, we produced, purified and characterized the fusion protein bsHN-IL2 which contains the IL-2 cytokine and an antibody scFv fragment directed towards the Hemagglutinin-Neuraminidase (HN) protein of Newcastle Disease Virus (NDV). |
| 1073 | 21042712 | In the presence of CD3-mediated signal 1, the vaccine/bsHN-IL2 provided via CD25 a strong bystander antitumor effect in vitro leading to tumor growth inhibition, even stronger than the vaccine/bsHN-CD28 which provides costimulation via CD28. |
| 1074 | 21042712 | Transcriptome analysis of naive T cells which were stimulated with the vaccine/bsHN-IL2 showed, similarly to the vaccine/bsHN-CD28, upregulation of 71 genes belonging to different signalling pathways, including PLC-γ1, Grb-2, Vav-1 and PDE-4A. |
| 1075 | 21061197 | Programmed cell death-1 (PD-1) is a member of the CD28 superfamily that delivers negative signals upon interaction with its two ligands, PD-L1 or PD-L2. |
| 1076 | 21061197 | PD-1 and its ligands are broadly expressed and exert a wider range of immunoregulatory roles in T cells activation and tolerance compared with other CD28 members. |
| 1077 | 21061197 | Programmed cell death-1 (PD-1) is a member of the CD28 superfamily that delivers negative signals upon interaction with its two ligands, PD-L1 or PD-L2. |
| 1078 | 21061197 | PD-1 and its ligands are broadly expressed and exert a wider range of immunoregulatory roles in T cells activation and tolerance compared with other CD28 members. |
| 1079 | 21209773 | CD4+ and CD8+ T cells with an effector memory phenotype infiltrate human tumor microenvironments, but most are hyporesponsive to stimulation via the T cell receptor (TCR) and CD28 under conditions that activate memory T cells derived from the peripheral blood of the cancer patients or normal donors. |
| 1080 | 21210234 | NKG2D expression in CD4+ T lymphocytes as a marker of senescence in the aged immune system. |
| 1081 | 21210234 | These changes are more frequently found in CD8+ T cells, and there are not well-defined markers of differentiation in the CD4+ subset. |
| 1082 | 21210234 | Typical features of cell immunosenescence are characteristics of pathologies in which the aberrant expression of NKG2D in CD4+ T cells has been described. |
| 1083 | 21210234 | To evaluate a possible age-related expression of NKG2D in CD4+ T cells, we compared their percentage in peripheral blood from 100 elderly and 50 young adults. |
| 1084 | 21210234 | The median percentage of CD4+ NKG2D+ in elders was 5.3% (interquartile range (IR): 8.74%) versus 1.4% (IR: 1.7%) in young subjects (p < 0.3 × 10(-10)). |
| 1085 | 21210234 | CD28 expression distinguished two subsets of CD4+ NKG2D+ cells with distinct functional properties and differentiation status. |
| 1086 | 21210234 | CD28+ cells showed an immature phenotype associated with high frequencies of CD45RA and CD31. |
| 1087 | 21210234 | However, most of the NKG2D+ cells belonged to the CD28(null) compartment and shared their phenotypical properties. |
| 1088 | 21210234 | Moreover, the frequency of the CD4+ NKG2D+ subset was clearly related to the status of the T cells. |
| 1089 | 21210234 | Higher frequencies of the NKG2D+ subset were accompanied with a gradual decrease of NAIVE and central memory cells, but also with a higher level of more differentiated subsets of CD4+ T cells. |
| 1090 | 21210234 | In conclusion, CD4+ NKG2D+ represent a subset of highly differentiated T cells which characterizes the senescence of the immune system. |
| 1091 | 21210234 | NKG2D expression in CD4+ T lymphocytes as a marker of senescence in the aged immune system. |
| 1092 | 21210234 | These changes are more frequently found in CD8+ T cells, and there are not well-defined markers of differentiation in the CD4+ subset. |
| 1093 | 21210234 | Typical features of cell immunosenescence are characteristics of pathologies in which the aberrant expression of NKG2D in CD4+ T cells has been described. |
| 1094 | 21210234 | To evaluate a possible age-related expression of NKG2D in CD4+ T cells, we compared their percentage in peripheral blood from 100 elderly and 50 young adults. |
| 1095 | 21210234 | The median percentage of CD4+ NKG2D+ in elders was 5.3% (interquartile range (IR): 8.74%) versus 1.4% (IR: 1.7%) in young subjects (p < 0.3 × 10(-10)). |
| 1096 | 21210234 | CD28 expression distinguished two subsets of CD4+ NKG2D+ cells with distinct functional properties and differentiation status. |
| 1097 | 21210234 | CD28+ cells showed an immature phenotype associated with high frequencies of CD45RA and CD31. |
| 1098 | 21210234 | However, most of the NKG2D+ cells belonged to the CD28(null) compartment and shared their phenotypical properties. |
| 1099 | 21210234 | Moreover, the frequency of the CD4+ NKG2D+ subset was clearly related to the status of the T cells. |
| 1100 | 21210234 | Higher frequencies of the NKG2D+ subset were accompanied with a gradual decrease of NAIVE and central memory cells, but also with a higher level of more differentiated subsets of CD4+ T cells. |
| 1101 | 21210234 | In conclusion, CD4+ NKG2D+ represent a subset of highly differentiated T cells which characterizes the senescence of the immune system. |
| 1102 | 21210234 | NKG2D expression in CD4+ T lymphocytes as a marker of senescence in the aged immune system. |
| 1103 | 21210234 | These changes are more frequently found in CD8+ T cells, and there are not well-defined markers of differentiation in the CD4+ subset. |
| 1104 | 21210234 | Typical features of cell immunosenescence are characteristics of pathologies in which the aberrant expression of NKG2D in CD4+ T cells has been described. |
| 1105 | 21210234 | To evaluate a possible age-related expression of NKG2D in CD4+ T cells, we compared their percentage in peripheral blood from 100 elderly and 50 young adults. |
| 1106 | 21210234 | The median percentage of CD4+ NKG2D+ in elders was 5.3% (interquartile range (IR): 8.74%) versus 1.4% (IR: 1.7%) in young subjects (p < 0.3 × 10(-10)). |
| 1107 | 21210234 | CD28 expression distinguished two subsets of CD4+ NKG2D+ cells with distinct functional properties and differentiation status. |
| 1108 | 21210234 | CD28+ cells showed an immature phenotype associated with high frequencies of CD45RA and CD31. |
| 1109 | 21210234 | However, most of the NKG2D+ cells belonged to the CD28(null) compartment and shared their phenotypical properties. |
| 1110 | 21210234 | Moreover, the frequency of the CD4+ NKG2D+ subset was clearly related to the status of the T cells. |
| 1111 | 21210234 | Higher frequencies of the NKG2D+ subset were accompanied with a gradual decrease of NAIVE and central memory cells, but also with a higher level of more differentiated subsets of CD4+ T cells. |
| 1112 | 21210234 | In conclusion, CD4+ NKG2D+ represent a subset of highly differentiated T cells which characterizes the senescence of the immune system. |
| 1113 | 21240487 | Various studies have shown that positive costimulatory pathways such as the CD28 and CD40 pathways can influence the expansion and cytokine production by iNKT cells. |
| 1114 | 21240487 | To study whether PD-L1 deficiency on NKT cells would enhance antigen-specific T-cell responses, we utilized CD8(+) OT-1 OVA transgenic T cells. α-GalCer enhanced the expansion and cytokine production of OT-1 CD8(+) cells after adoptive transfer into wild-type recipients. |
| 1115 | 21240487 | However, this expansion was significantly enhanced when OT-1 CD8(+) T cells were adoptively transferred into PD-L1(-/-) recipients. |
| 1116 | 21240487 | PD-L1(-/-) mice given dendritic cells loaded with antigen and α-GalCer had a significant reduction in tumor growth and this was associated with increased trafficking of antigen-presenting cells and CD8(+) T cells to the tumors. |
| 1117 | 21240487 | These data demonstrate that abrogating PDL1:PD-1 interactions during the activation of iNKT cells amplifies an anti-tumor response when coupled with DC vaccination. |
| 1118 | 21376795 | Impaired hepatitis B vaccine responses during chronic hepatitis C infection: involvement of the PD-1 pathway in regulating CD4(+) T cell responses. |
| 1119 | 21376795 | In this report, we further investigated the role of the PD-1 pathway in regulation of CD4(+) T cell responses to HBV vaccination in HCV-infected individuals. |
| 1120 | 21376795 | CD4(+) T cell responses to ex vivo stimulations of anti-CD3/CD28 antibodies or hepatitis B surface antigen (HBsAg) were found to be lower in HBV vaccine non-responders compared to those responders in HCV-infected individuals who had received a series of HBV immunizations. |
| 1121 | 21376795 | PD-1 expression on CD4(+) T cells was detected at relatively higher levels in these HBV vaccine non-responders than those who responded, and this was inversely associated with the cell activation status. |
| 1122 | 21376795 | Importantly, blocking the PD-1 pathway improved T cell activation and proliferation in response to ex vivo HBsAg or anti-CD3/CD28 stimulation in HBV vaccine non-responders. |
| 1123 | 21376795 | These results suggest that PD-1 signaling may be involved in impairing CD4(+) T cell responses to HBV vaccination in subjects with HCV infection, and raise the possibility that blocking this negative signaling pathway might improve success rates of immunization in the setting of chronic viral infection. |
| 1124 | 21376795 | Impaired hepatitis B vaccine responses during chronic hepatitis C infection: involvement of the PD-1 pathway in regulating CD4(+) T cell responses. |
| 1125 | 21376795 | In this report, we further investigated the role of the PD-1 pathway in regulation of CD4(+) T cell responses to HBV vaccination in HCV-infected individuals. |
| 1126 | 21376795 | CD4(+) T cell responses to ex vivo stimulations of anti-CD3/CD28 antibodies or hepatitis B surface antigen (HBsAg) were found to be lower in HBV vaccine non-responders compared to those responders in HCV-infected individuals who had received a series of HBV immunizations. |
| 1127 | 21376795 | PD-1 expression on CD4(+) T cells was detected at relatively higher levels in these HBV vaccine non-responders than those who responded, and this was inversely associated with the cell activation status. |
| 1128 | 21376795 | Importantly, blocking the PD-1 pathway improved T cell activation and proliferation in response to ex vivo HBsAg or anti-CD3/CD28 stimulation in HBV vaccine non-responders. |
| 1129 | 21376795 | These results suggest that PD-1 signaling may be involved in impairing CD4(+) T cell responses to HBV vaccination in subjects with HCV infection, and raise the possibility that blocking this negative signaling pathway might improve success rates of immunization in the setting of chronic viral infection. |
| 1130 | 21383769 | Reinforcement of cancer immunotherapy by adoptive transfer of cblb-deficient CD8+ T cells combined with a DC vaccine. |
| 1131 | 21383769 | The E3 ubiquitin ligase Cbl-b is a key regulator of T cell activation and is established to regulate TGF-β sensitivity. cblb-deficient animals reject tumors via CD8(+) T cells, which make Cbl-b an ideal target for improvement of adoptive T-cell transfer (ATC) therapy. |
| 1132 | 21383769 | In this study, we show that cblb-deficient CD8(+) T cells are hyper-responsive to T-cell receptor (TCR)/CD28-stimulation and are in part protected against the negative cues induced by TGF-β in vitro. |
| 1133 | 21383769 | Thus, cblb-deficient ATC requires proper in vivo re-activation by a dendritic cell (DC) vaccine. |
| 1134 | 21422474 | To determine whether patients receiving HAART possess CD8+ T cells with Tcm qualities that are amenable to augmentation, HIV-specific CD8+ T-cell clones were derived from HIV-reactive CD28+CD8+ T-cell lines isolated from 7 HIV+ HAART-treated patients, expanded ex vivo, and reinfused into their autologous host. |
| 1135 | 21422474 | Tracking of the cells in vivo revealed that clones could persist for ≥ 84 days, maintain expression and/or re-express CD28, up-regulate CD62L, secrete IL-2, proliferate on cognate Ag encounter and localize to the rectal mucosa. |
| 1136 | 21422474 | To determine whether patients receiving HAART possess CD8+ T cells with Tcm qualities that are amenable to augmentation, HIV-specific CD8+ T-cell clones were derived from HIV-reactive CD28+CD8+ T-cell lines isolated from 7 HIV+ HAART-treated patients, expanded ex vivo, and reinfused into their autologous host. |
| 1137 | 21422474 | Tracking of the cells in vivo revealed that clones could persist for ≥ 84 days, maintain expression and/or re-express CD28, up-regulate CD62L, secrete IL-2, proliferate on cognate Ag encounter and localize to the rectal mucosa. |
| 1138 | 21493800 | Priming CD8+ T cells with dendritic cells matured using TLR4 and TLR7/8 ligands together enhances generation of CD8+ T cells retaining CD28. |
| 1139 | 21493800 | Maturation of DCs with lipopolysaccharide (LPS; TLR4) concurrently with R848 (TLR7/8) induced a heterogeneous population of DCs that produced high levels of IL12 p70. |
| 1140 | 21493800 | Compared with DCs matured with LPS or R848 alone, the DC population matured with both adjuvants primed CD8+ T-cell responses containing an increased proportion of antigen-specific T cells retaining CD28 expression. |
| 1141 | 21493800 | Priming with a homogenous subpopulation of LPS/R848-matured DCs that were CD83(Hi)/CD80+/CD86+ reduced this CD28+ subpopulation and induced T cells with an effector cytokine signature, whereas priming with the less mature subpopulations of DCs resulted in minimal T-cell expansion. |
| 1142 | 21493800 | Priming CD8+ T cells with dendritic cells matured using TLR4 and TLR7/8 ligands together enhances generation of CD8+ T cells retaining CD28. |
| 1143 | 21493800 | Maturation of DCs with lipopolysaccharide (LPS; TLR4) concurrently with R848 (TLR7/8) induced a heterogeneous population of DCs that produced high levels of IL12 p70. |
| 1144 | 21493800 | Compared with DCs matured with LPS or R848 alone, the DC population matured with both adjuvants primed CD8+ T-cell responses containing an increased proportion of antigen-specific T cells retaining CD28 expression. |
| 1145 | 21493800 | Priming with a homogenous subpopulation of LPS/R848-matured DCs that were CD83(Hi)/CD80+/CD86+ reduced this CD28+ subpopulation and induced T cells with an effector cytokine signature, whereas priming with the less mature subpopulations of DCs resulted in minimal T-cell expansion. |
| 1146 | 21493800 | Priming CD8+ T cells with dendritic cells matured using TLR4 and TLR7/8 ligands together enhances generation of CD8+ T cells retaining CD28. |
| 1147 | 21493800 | Maturation of DCs with lipopolysaccharide (LPS; TLR4) concurrently with R848 (TLR7/8) induced a heterogeneous population of DCs that produced high levels of IL12 p70. |
| 1148 | 21493800 | Compared with DCs matured with LPS or R848 alone, the DC population matured with both adjuvants primed CD8+ T-cell responses containing an increased proportion of antigen-specific T cells retaining CD28 expression. |
| 1149 | 21493800 | Priming with a homogenous subpopulation of LPS/R848-matured DCs that were CD83(Hi)/CD80+/CD86+ reduced this CD28+ subpopulation and induced T cells with an effector cytokine signature, whereas priming with the less mature subpopulations of DCs resulted in minimal T-cell expansion. |
| 1150 | 21502499 | Adenovirus type-35 vectors block human CD4+ T-cell activation via CD46 ligation. |
| 1151 | 21502499 | Whereas rAd5 binds coxsackie-adenovirus receptor (CAR), rAd35 binds the complement regulatory protein CD46. |
| 1152 | 21502499 | Although rAd35 infected and phenotypically matured human blood dendritic cells (DCs) more efficiently than rAd5, we show here that rAd35 markedly suppressed DC-induced activation of naive CD4(+) T cells. rAd35 specifically blocked both DCs and anti-CD3/CD28 mAb-induced naive T-cell proliferation and IL-2 production. |
| 1153 | 21502499 | Our findings provide insights into the basic biology of adenoviruses and indicate that CD46 binding may have an impact on the generation of primary CD4(+) T-cell responses by Ad35. |
| 1154 | 21505013 | Active and inactive SLE individuals had more CD38 molecules/CD8+ T cells and more CD4+ T, CD8+ T and B cells in apoptosis (as assessed by caspase-3 expression) than the control group. |
| 1155 | 21505013 | Patients with active SLE had a diminished CD28 expression on both CD4+ T and on CD8+ T cells and a higher CD86 expression on B cells than the control group. |
| 1156 | 21528289 | This is an effective alternative to somatic gene therapy strategies using genes coding for ligands of CD28 such as CD80 (B7-1) or CD86 (B7-2). |
| 1157 | 21528289 | The bsAb HN x CD28 attaches with its anti-HN binding site to the NDV derived hemagglutinin-neuraminidase (HN) molecule which serves as a common foreign anchoring molecule in the vaccine. |
| 1158 | 21528289 | This is an effective alternative to somatic gene therapy strategies using genes coding for ligands of CD28 such as CD80 (B7-1) or CD86 (B7-2). |
| 1159 | 21528289 | The bsAb HN x CD28 attaches with its anti-HN binding site to the NDV derived hemagglutinin-neuraminidase (HN) molecule which serves as a common foreign anchoring molecule in the vaccine. |
| 1160 | 21695776 | Altered T cell differentiation associated with loss of CD27 and CD28 in HIV infected Indian individuals. |
| 1161 | 21821307 | The development of the anti-CTLA-4 antibody (ipilimumab; marketed as Yervoy) immune regulatory therapy was based on the premise that "Abrogation of the function of CTLA-4 would permit CD28 to function unopposed and might swing the balance in favor of immune stimulation, tolerance breakdown and tumor eradication…" (Weber, 2009). |
| 1162 | 22021080 | ECOG 1696 was a Phase II multi-center trial testing vaccination with melanoma peptides, gp100, MART-1 and tyrosinase delivered alone, with GM-CSF, IFN-α2b or both cytokines to HLA-A2(+) patients with metastatic melanoma. |
| 1163 | 22021080 | Multiparameter flow cytometry was used to measure the frequency of CD8(+) T cells specific for gp100, MART-1, tyrosinase and influenza (FLU) peptides. |
| 1164 | 22021080 | Expression of CD45RA/CCR7 on CD8(+) tet(+) T cells and CD25, CD27, CD28 on all circulating T cells was determined. |
| 1165 | 22021080 | Only gp100- and MART-1-specific T cells differentiated to CD45RA(+) CCR7(-) effector/memory T cells. |
| 1166 | 22021080 | Delivery of GM-CSF and/or IFN-α2b had no effects on the frequency or differentiation of CD8(+) tet(+) , CD8+ or CD4+ T cells. |
| 1167 | 22025707 | CD4(+)CD25(+)Forkhead box P3 (Foxp3)(+) regulatory T cells (Tregs) control immune responses to self and foreign antigens in secondary lymphoid organs and at tissue sites of inflammation. |
| 1168 | 22025707 | CD28 signaling is known to abrogate Treg suppression of IL-2 secretion and proliferation, but our studies show that Treg suppression of IFN-γ during Th1 priming proceeds despite enhanced CD28 signaling. |
| 1169 | 22025707 | In vivo, Tregs potently controlled CD4 IFN-γ and CD4 effector cell expansion in the lymph node (four- to fivefold reduction) but not Th1 programming, independent of IL-10. |
| 1170 | 22025707 | Tregs additionally reduced CD4 IFN-γ in the inflamed dermis (twofold reduction) dependent on their production of IL-10. |
| 1171 | 22237888 | Furthermore, we tested the use of different ratios and different types of Dynabeads® CD3/CD28 and CD3/CD28/CD137 T-cell expander, for optimized expansion of tumor-specific T cells. |
| 1172 | 22365383 | Neuropeptide Y (NPY) suppressed clinical experimental autoimmune encephalomyelitis (EAE) and reduced numbers of CD28+, CD11b+ and CD80+ cells among spinal cord infiltrating cells at the peak of disease in Dark Agouti rat strain. |
| 1173 | 22365383 | Suppression of EAE was accompanied by the reduced expression of costimulatory CD80 and CD86 molecules on ED1+ macrophages and OX62+ dendritic cells in draining lymph nodes during the inductive phase of EAE. |
| 1174 | 22365383 | An inhibitor of dipeptidyl peptidase 4, an enzyme which terminates the action of NPY on Y1 receptor subtype, did not sustain the suppressive effect of NPY on the EAE development, suggesting involvement of Y2 and Y5 receptors. |
| 1175 | 22733396 | We demonstrate that exposure to lenalidomide in the context of T-cell expansion with direct ligation of CD3/CD28 complex results in polarization toward a Th1 phenotype characterized by increased IFN-γ, but not IL-10 expression. |
| 1176 | 22814402 | Isolating, immunophenotyping and ex vivo stimulation of CD4+ and CD8+ gastric lymphocytes during murine Helicobacter pylori infection. |
| 1177 | 22814402 | Following isolation we compared lymphocyte stimulation by CD3/CD28, phorbol 12-myristate 13-acetate (PMA) and ionomycin or H. pylori lysate and determined that CD3/CD28 effectively induces stimulation of IFNγ and IL 17A, but impairs Foxp3 expression. |
| 1178 | 22908331 | The interaction of CD28, which is constitutively expressed on T cells, with B7.1/B7.2 expressed on APCs is critical for T cell activation. |
| 1179 | 22908331 | Plasma cells also express the ligand for CD28, B7.1, and B7.2. |
| 1180 | 22908331 | Surprisingly, deficiency of B7.1 and B7.2 in B cells also led to higher Ab levels, analogous to Cd28(-/-) plasma cells. |
| 1181 | 22908331 | The interaction of CD28, which is constitutively expressed on T cells, with B7.1/B7.2 expressed on APCs is critical for T cell activation. |
| 1182 | 22908331 | Plasma cells also express the ligand for CD28, B7.1, and B7.2. |
| 1183 | 22908331 | Surprisingly, deficiency of B7.1 and B7.2 in B cells also led to higher Ab levels, analogous to Cd28(-/-) plasma cells. |
| 1184 | 22908331 | The interaction of CD28, which is constitutively expressed on T cells, with B7.1/B7.2 expressed on APCs is critical for T cell activation. |
| 1185 | 22908331 | Plasma cells also express the ligand for CD28, B7.1, and B7.2. |
| 1186 | 22908331 | Surprisingly, deficiency of B7.1 and B7.2 in B cells also led to higher Ab levels, analogous to Cd28(-/-) plasma cells. |
| 1187 | 23144170 | TLR4- and TRIF-dependent stimulation of B lymphocytes by peptide liposomes enables T cell-independent isotype switch in mice. |
| 1188 | 23144170 | Independency was confirmed in mice lacking T cells and in mice deficient for MHC class II, CD40L, and CD28. |
| 1189 | 23196209 | Here, we correlate the distribution of different circulating CD4+ and CD8+ T-cell phenotypes with the humoral response to vaccination with Intanza, an intradermal seasonal vaccine, in 54 individuals of different ages. |
| 1190 | 23196209 | Unlike reported data, late-differentiated (CD45RA+CCR7-CD27-CD28-) CD4+, but not CD8+ T-cells associated with a poorer vaccine response. |
| 1191 | 23196209 | Thus, latent CMV infection has a deleterious effect on influenza antibody responses in the elderly, which might be mediated through CD4 T-cells lacking CCR7, CD27 and CD28 and re-expressing CD45RA. |
| 1192 | 23243590 | We found that Pam3Cys increases the proliferation of both CD4(+) effector T cells (Teffs) and Tregs co-cultured in vitro, but did not induce the proliferation of Tregs alone upon CD3 and CD28 stimulation. |
| 1193 | 23243590 | Teff from Pam3Cys-treated mice produced increased levels of Th1 and Th2-type cytokines and an interleukin (IL)-6-dependent secretion of IL-17 was observed in Teff:Treg co-cultures, suggesting that TLR2 stimulation had skewed the immune response toward a Th17 profile. |
| 1194 | 23271970 | In the aged cohort, the CD8+ T cell compartment displayed a marked reduction in the frequency of naïve CD8+ T cells and increased frequencies of CD8+ T cells that expressed CD57 and lacked CD28, as previously described. |
| 1195 | 23271970 | However, we did not observe an influence of age on either the frequency of virus-specific CD8+ T cells within the circulating pool nor their functionality (based on the production of IFNγ, TNFα, IL2, Granzyme B, Perforin and mobilization of CD107a). |
| 1196 | 23377669 | A major challenge associated with allogeneic hematopoietic stem cell transplantation is effective prevention and/or attenuation of symptoms associated with acute graft-versus-host disease (aGVHD) that can result from a failure of either host and/or donor CD4(+)CD25(+) regulatory T (Tr) and CD8(+)CD28 suppressor T (Ts) cells to dampen immunopathogenic responses mediated by alloreactive donor CD4(+)CD28(+) Th1 (Th1) and CD8(+)CD28(-) Tc1 (Tc1) cell-mediated inflammatory processes. |
| 1197 | 23377669 | In addition, immunized mice presented with significantly diminished Th1-cytokines interferon-γ and interleukin-2 response and a moderately upregulated Th2-cytokine interleukin-10 and Th3-cytokine transforming growth factor-β response. |
| 1198 | 23390376 | Cytotoxic T lymphocyte antigen-4 (CTLA-4) is a key negative regulator of T cell activation. |
| 1199 | 23390376 | A complex integration of positive and negative co-stimulatory signals in the well-defined B7:CD28/CTLA-4 pathway modulates the generation and maintenance of immune responses. |
| 1200 | 23456839 | While the CD28 receptor and its ligands B7.1/B7.2 are also expressed on plasma cells, little is known of the role of the CD28/B7 pathway in plasma cell function. |
| 1201 | 23716685 | HHLA2 is a member of the B7 family and inhibits human CD4 and CD8 T-cell function. |
| 1202 | 23716685 | Here we describe HERV-H LTR-associating protein 2 (HHLA2) as a member of the B7 family that shares 10-18% amino acid identity and 23-33% similarity to other human B7 proteins and phylogenetically forms a subfamily with B7x and B7-H3 within the family. |
| 1203 | 23716685 | HHLA2 is expressed in humans but not in mice, which is unique within the B7 and CD28 families. |
| 1204 | 23716685 | HHLA2 does not interact with other known members of the CD28 family or the B7 family, but does bind a putative receptor that is constitutively expressed not only on resting and activated CD4 and CD8 T cells but also on antigen-presenting cells. |
| 1205 | 23716685 | HHLA2 inhibits proliferation of both CD4 and CD8 T cells in the presence of T-cell receptor signaling. |
| 1206 | 23716685 | In addition, HHLA2 significantly reduces cytokine production by T cells including IFN-γ, TNF-α, IL-5, IL-10, IL-13, IL-17A, and IL-22. |
| 1207 | 23716685 | Thus, we have identified a unique B7 pathway that is able to inhibit human CD4 and CD8 T-cell proliferation and cytokine production. |
| 1208 | 23716685 | HHLA2 is a member of the B7 family and inhibits human CD4 and CD8 T-cell function. |
| 1209 | 23716685 | Here we describe HERV-H LTR-associating protein 2 (HHLA2) as a member of the B7 family that shares 10-18% amino acid identity and 23-33% similarity to other human B7 proteins and phylogenetically forms a subfamily with B7x and B7-H3 within the family. |
| 1210 | 23716685 | HHLA2 is expressed in humans but not in mice, which is unique within the B7 and CD28 families. |
| 1211 | 23716685 | HHLA2 does not interact with other known members of the CD28 family or the B7 family, but does bind a putative receptor that is constitutively expressed not only on resting and activated CD4 and CD8 T cells but also on antigen-presenting cells. |
| 1212 | 23716685 | HHLA2 inhibits proliferation of both CD4 and CD8 T cells in the presence of T-cell receptor signaling. |
| 1213 | 23716685 | In addition, HHLA2 significantly reduces cytokine production by T cells including IFN-γ, TNF-α, IL-5, IL-10, IL-13, IL-17A, and IL-22. |
| 1214 | 23716685 | Thus, we have identified a unique B7 pathway that is able to inhibit human CD4 and CD8 T-cell proliferation and cytokine production. |
| 1215 | 24041689 | Co-stimulatory signaling pathway triggered by the binding of B7.1/B7.2 (CD80/86) of antigen-presenting cells (APCs) to CD28 of T cells is required for optimal T-cell activation. |
| 1216 | 24041689 | Cytotoxic T lymphocyte-associated antigen-4 (CTLA-4) is a negative regulator of T cell activation, which competes with CD28 for B7.1/B7.2 binding with a greater affinity. |
| 1217 | 24041689 | To develop a novel therapeutics specifically targeting CTLA-4, we constructed a DNA vaccine by cloning the sequence of CTLA-4 fused with a transmembrane domain sequence of placental alkaline phosphatase (PLAP) into a mammalian expression plasmid, pVAC-1. |
| 1218 | 24041689 | Co-stimulatory signaling pathway triggered by the binding of B7.1/B7.2 (CD80/86) of antigen-presenting cells (APCs) to CD28 of T cells is required for optimal T-cell activation. |
| 1219 | 24041689 | Cytotoxic T lymphocyte-associated antigen-4 (CTLA-4) is a negative regulator of T cell activation, which competes with CD28 for B7.1/B7.2 binding with a greater affinity. |
| 1220 | 24041689 | To develop a novel therapeutics specifically targeting CTLA-4, we constructed a DNA vaccine by cloning the sequence of CTLA-4 fused with a transmembrane domain sequence of placental alkaline phosphatase (PLAP) into a mammalian expression plasmid, pVAC-1. |
| 1221 | 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. |
| 1222 | 24291199 | By analyzing the differentiation state of IFN-γ-secreting CD8(+) T cells, we found a CCR7(-)CD45RA(-)CD28(+int)/CD28(-) profile (>85%) belonging to a subset of intermediate-differentiated effector T cells for HIV, FLU, and EBV. |
| 1223 | 24291199 | The percentage of single IFN-γ T cell producers in response to HIV was 62% of the total of secreting T cells compared with 35% for FLU and EBV, dual and triple (IFN-γ/IL-2/CD107a) T cell producers could also be detected but at lower levels (8% compared with 37%). |
| 1224 | 24550729 | CD103+ and CD11b+ populations of CD11c+MHCIIhi murine dendritic cells (DCs) have been shown to carry antigens from the lung through the afferent lymphatics to mediastinal lymph nodes (MLN). |
| 1225 | 24550729 | Blocking CD28-mediated costimulatory signals during adult infection demonstrated that signals from this costimulatory pathway influence the hierarchy of the CD8+ T cell response to RSV, suggesting that limited costimulation provided by neonatal CD103+ DCs is one mechanism whereby neonates generate a distinct CD8+ T cell response from that of adults. |
| 1226 | 24586641 | Using a micropipet adhesion frequency assay, we show that TCR signaling enhances the direct binding between CD28 and its ligand, CD80. |
| 1227 | 24595607 | We compared the influence of F. tularensis antigens (tularinum) in vitro on production of IL-1, IL-5, IL-6, IL-17, IFN-γ, and TNF-α by splenocytes obtained from intact mice and mice immunized with mutant F. tularensis 15∆23A and/or F. tularensis 15 NIIEG strains. |
| 1228 | 24595607 | We also compared expression of CD28, CD154, TLR-2, and CD69 markers on CD4 and CD8 T-cells after activation with tularinum in vitro. |
| 1229 | 24595607 | We found that tularinum-induced CD4(+) T-cells increased TNF-α and IFN-γ synthesis and expression of CD69 only in group mice with high degree of post immunization protection against F. tularensis Schu challenge. |
| 1230 | 24595607 | Estimation of CD69 expression on CD3(+)CD4(+) cells and IFN-γ, TNF-α synthesis by CD4(+) T-lymphocytes could be useful for determination protect ability of antitularemia immunity. |
| 1231 | 24619679 | The effective induction of TAA-specific T cell immune responses requires activation of T cells by CD3/CD28 antibodies and the presence of proinflammatory cytokines such as interleukin-7 (IL-7) and interleukin-12 (IL-12). |
| 1232 | 24642562 | We analyzed the expression of Tim-3 and PD-1, two recently identified T cell negative immune checkpoint receptors, over the course of WNV infection. |
| 1233 | 24642562 | Symptomatic WNV+ donors exhibited higher frequencies of Tim-3+ cells than asymptomatic subjects within naïve/early differentiated CD28+/-CD57-CD4+ and differentiated CD28-CD57-CD8+ T cells. |
| 1234 | 24713579 | Artificial antigen-presenting cells expressing CD80, CD70, and 4-1BB ligand efficiently expand functional T cells specific to tumor-associated antigens. |
| 1235 | 24713579 | Here, in order to develop a novel aAPC system, we established K562 erythroleukemia cells expressing different combinations of co-stimulatory molecule ligands, CD80, CD70, and/or 4-1BB ligand (4-1BBL). |
| 1236 | 24713579 | When nucleofected with in vitro-generated mRNA encoding a tumor-associated antigen, MART-1, the K562 cells expressing all of CD80, CD70, and 4-1BBL were the most efficient for expansion of functional T cells specific to an HLA-A2-restricted immunodominant epitope, MART-126-35. |
| 1237 | 24713579 | In addition, only the K562 cells expressing all three of these co-stimulatory molecule ligands could clearly expand T cells specific to other less immunogenic antigen epitopes, gp100154-162 and Cyp1B1239-247, through transfection with in vitro generated gp100 and Cyp1B1 mRNA, respectively. |
| 1238 | 24713579 | These results indicated that non-redundant and synergistic effects of co-stimulation via CD28/CD80, CD27/CD70, and 4-1BB/4-1BBL might be critical for eliciting efficient expansion of T cells; co-stimulation via the 4-1BB/4-1BBL interaction might expand antigen-specific T cells by preventing apoptotic cell death triggered by specific antigens in the presence of the CD28/CD80 and CD27/CD70 signaling. |
| 1239 | 24713579 | Taken together, our findings suggested that this K562-based aAPC system expressing CD80, CD70, and 4-1BBL would be useful for efficiently stimulating functional antigen-specific T cells ex vivo, in particular when detailed information on the epitope specificities is unavailable. |
| 1240 | 24845157 | CD80 and CD86 IgC domains are important for quaternary structure, receptor binding and co-signaling function. |
| 1241 | 24845157 | CD86 and CD80, the ligands for the co-stimulatory molecules CD28 and CTLA-4, are members of the Ig superfamily. |
| 1242 | 24845157 | Herein, we have used deletion and chimeric human CD80 and CD86 molecules in co-stimulation assays to study the impact of the multimeric state of IgV and IgC domains on receptor binding properties and on co-stimulatory function in a peptide-specific T cell activation model. |
| 1243 | 24845157 | We report for the first time the presence of CD80 dimers and CD86 monomers in living cells. |
| 1244 | 24845157 | Moreover, we show that the IgC domain of both molecules inhibits multimer formation and greatly affects binding to the co-receptors CD28 and CTLA-4. |
| 1245 | 24845157 | These findings reveal the distinct but complementary roles of CD80 and CD86 IgV and IgC domains in T cell activation. |
| 1246 | 24845157 | CD80 and CD86 IgC domains are important for quaternary structure, receptor binding and co-signaling function. |
| 1247 | 24845157 | CD86 and CD80, the ligands for the co-stimulatory molecules CD28 and CTLA-4, are members of the Ig superfamily. |
| 1248 | 24845157 | Herein, we have used deletion and chimeric human CD80 and CD86 molecules in co-stimulation assays to study the impact of the multimeric state of IgV and IgC domains on receptor binding properties and on co-stimulatory function in a peptide-specific T cell activation model. |
| 1249 | 24845157 | We report for the first time the presence of CD80 dimers and CD86 monomers in living cells. |
| 1250 | 24845157 | Moreover, we show that the IgC domain of both molecules inhibits multimer formation and greatly affects binding to the co-receptors CD28 and CTLA-4. |
| 1251 | 24845157 | These findings reveal the distinct but complementary roles of CD80 and CD86 IgV and IgC domains in T cell activation. |
| 1252 | 24951814 | Priming of CD8 T cells by adenoviral vectors is critically dependent on B7 and dendritic cells but only partially dependent on CD28 ligation on CD8 T cells. |
| 1253 | 24951814 | Moreover, we found that CD80/86, but not CD28, was essential for efficient generation of both primary effectors and memory CD8 T cells. |
| 1254 | 24951814 | Interestingly, the lack of CD28 expression resulted in a delayed primary response, whereas memory CD8 T cells generated in CD28-deficient mice appeared almost normal in terms of both phenotype and effector cytokine profile, but they exhibited a significantly reduced proliferative capacity upon secondary challenge while retaining immediate in vivo effector capabilities: in vivo cytotoxicity and short-term in vivo protective capacity. |
| 1255 | 24951814 | Overall, our data point to an absolute requirement for professional APCs and the expression of the costimulatory molecules CD80/86 for efficient CD8 T cell priming by adenoviral vectors. |
| 1256 | 24951814 | Additionally, our results suggest the existence of an alternative receptor for CD80/86, which may substitute, in part, for CD28. |
| 1257 | 24951814 | Priming of CD8 T cells by adenoviral vectors is critically dependent on B7 and dendritic cells but only partially dependent on CD28 ligation on CD8 T cells. |
| 1258 | 24951814 | Moreover, we found that CD80/86, but not CD28, was essential for efficient generation of both primary effectors and memory CD8 T cells. |
| 1259 | 24951814 | Interestingly, the lack of CD28 expression resulted in a delayed primary response, whereas memory CD8 T cells generated in CD28-deficient mice appeared almost normal in terms of both phenotype and effector cytokine profile, but they exhibited a significantly reduced proliferative capacity upon secondary challenge while retaining immediate in vivo effector capabilities: in vivo cytotoxicity and short-term in vivo protective capacity. |
| 1260 | 24951814 | Overall, our data point to an absolute requirement for professional APCs and the expression of the costimulatory molecules CD80/86 for efficient CD8 T cell priming by adenoviral vectors. |
| 1261 | 24951814 | Additionally, our results suggest the existence of an alternative receptor for CD80/86, which may substitute, in part, for CD28. |
| 1262 | 24951814 | Priming of CD8 T cells by adenoviral vectors is critically dependent on B7 and dendritic cells but only partially dependent on CD28 ligation on CD8 T cells. |
| 1263 | 24951814 | Moreover, we found that CD80/86, but not CD28, was essential for efficient generation of both primary effectors and memory CD8 T cells. |
| 1264 | 24951814 | Interestingly, the lack of CD28 expression resulted in a delayed primary response, whereas memory CD8 T cells generated in CD28-deficient mice appeared almost normal in terms of both phenotype and effector cytokine profile, but they exhibited a significantly reduced proliferative capacity upon secondary challenge while retaining immediate in vivo effector capabilities: in vivo cytotoxicity and short-term in vivo protective capacity. |
| 1265 | 24951814 | Overall, our data point to an absolute requirement for professional APCs and the expression of the costimulatory molecules CD80/86 for efficient CD8 T cell priming by adenoviral vectors. |
| 1266 | 24951814 | Additionally, our results suggest the existence of an alternative receptor for CD80/86, which may substitute, in part, for CD28. |
| 1267 | 24951814 | Priming of CD8 T cells by adenoviral vectors is critically dependent on B7 and dendritic cells but only partially dependent on CD28 ligation on CD8 T cells. |
| 1268 | 24951814 | Moreover, we found that CD80/86, but not CD28, was essential for efficient generation of both primary effectors and memory CD8 T cells. |
| 1269 | 24951814 | Interestingly, the lack of CD28 expression resulted in a delayed primary response, whereas memory CD8 T cells generated in CD28-deficient mice appeared almost normal in terms of both phenotype and effector cytokine profile, but they exhibited a significantly reduced proliferative capacity upon secondary challenge while retaining immediate in vivo effector capabilities: in vivo cytotoxicity and short-term in vivo protective capacity. |
| 1270 | 24951814 | Overall, our data point to an absolute requirement for professional APCs and the expression of the costimulatory molecules CD80/86 for efficient CD8 T cell priming by adenoviral vectors. |
| 1271 | 24951814 | Additionally, our results suggest the existence of an alternative receptor for CD80/86, which may substitute, in part, for CD28. |
| 1272 | 25049283 | We compared CAR.GD2 constructs that encoded the CD3ζ chain alone, with CD28, 4-1BB, or CD28 and 4-1BB costimulatory endodomains. |
| 1273 | 25049283 | We observed a striking T helper 1-like polarization of NKT cells by 4-1BB-containing CARs. |
| 1274 | 25049283 | Importantly, expression of both CD28 and 4-1BB endodomains in the CAR.GD2 enhanced in vivo persistence of NKT cells. |
| 1275 | 25049283 | We compared CAR.GD2 constructs that encoded the CD3ζ chain alone, with CD28, 4-1BB, or CD28 and 4-1BB costimulatory endodomains. |
| 1276 | 25049283 | We observed a striking T helper 1-like polarization of NKT cells by 4-1BB-containing CARs. |
| 1277 | 25049283 | Importantly, expression of both CD28 and 4-1BB endodomains in the CAR.GD2 enhanced in vivo persistence of NKT cells. |
| 1278 | 25187662 | The percentage of donors with CD8 responses to influenza A virus was lower than those with CD4; this was not influenced by whether the subjects were CMV seropositive or seronegative. |
| 1279 | 25187662 | CMV-seropositive responders had significantly higher frequencies of late-differentiated CD4 T-cells (CD45RA(+/-)CCR7(-)CD27(-)CD28(-)) compared with CMV-infected nonresponders. |
| 1280 | 25573986 | Unlike CD19(+) PC, CD19(-) PC were restricted to BM, expressed predominantly IgG, and they carried a prosurvival, distinctly mature phenotype, that is, HLA-DR(low)Ki-67(-)CD95(low)CD28(+)CD56(+/-), with increased BCL2 and they resisted their mobilization from the BM after systemic vaccination. |
| 1281 | 25617474 | HLA-A02:01-restricted epitopes identified from the herpes simplex virus tegument protein VP11/12 preferentially recall polyfunctional effector memory CD8+ T cells from seropositive asymptomatic individuals and protect humanized HLA-A*02:01 transgenic mice against ocular herpes. |
| 1282 | 25617474 | In this study, we used multiple prediction computer-assisted algorithms to identify 10 potential HLA-A*02:01-restricted CD8(+) T cell epitopes from the 718-aa sequence of VP11/12. |
| 1283 | 25617474 | In 10 sequentially studied HLA-A*02:01-positive and HSV-1-seropositive ASYMP individuals, the most frequent, robust, and polyfunctional effector CD8(+) T cell responses, as assessed by a combination of tetramer frequency, granzyme B, granzyme K, perforin, CD107(a/b) cytotoxic degranulation, IFN-γ, and multiplex cytokines assays, were predominantly directed against three epitopes: VP11/1266-74, VP11/12220-228, and VP11/12702-710. |
| 1284 | 25617474 | Interestingly, ASYMP individuals had a significantly higher proportion of CD45RA(low)CCR7(low)CD44(high)CD62L(low)CD27(low)CD28(low)CD8(+) effector memory CD8(+) T cells (TEMs) specific to the three epitopes, compared with symptomatic individuals (with a history of numerous episodes of recurrent ocular herpetic disease). |
| 1285 | 25617474 | Moreover, immunization of HLA-A*02:01 transgenic mice with the three ASYMP CD8(+) TEM cell epitopes induced robust and polyfunctional epitope-specific CD8(+) TEM cells that were associated with a strong protective immunity against ocular herpes infection and disease. |
| 1286 | 25792524 | The vaccines were aimed at activating type I CD4(+)T cells and consisted of tumor cells transfected with genes encoding syngeneic MHC class II and CD80 costimulatory molecules, and lacking the MHC II-associated invariant chain. |
| 1287 | 25792524 | During the course of the vaccine studies, we observed that CD80 not only costimulated naïve T cells, but also bound to PD-L1 and prevented tumor cell-expressed PD-L1 from binding to its receptor PD-1 on activated T cells. |
| 1288 | 25792524 | A soluble form of CD80 (CD80-Fc) had the same effect and sustained IFNγ production by both human and murine PD-1(+) activated T cells in the presence of PD-L1(+) human or mouse tumor cells, respectively. |
| 1289 | 25792524 | In vitro studies with human tumor cells indicated that CD80-Fc was more effective than antibodies to either PD-1 or PD-L1 in sustaining T cell production of IFNγ. |
| 1290 | 25792524 | Studies with human T cells blocked for CD28 and with T cells from CD28 knockout mice demonstrated that CD80-Fc simultaneously inhibited PD-L1/PD-1-mediated immune suppression and delivered costimulatory signals to activated T cells, thereby amplifying T cell activation. |
| 1291 | 26228786 | Molecular characterization of HCMV-specific immune responses: Parallels between CD8(+) T cells, CD4(+) T cells, and NK cells. |
| 1292 | 26228786 | The HCMV-specific CD8(+) T-cell response is characterized by the accumulation of terminally differentiated effector cells that have downregulated the costimulatory molecules CD27 and CD28. |
| 1293 | 26228786 | These HCMV-specific CD8(+) T cells maintain high levels of cytotoxic molecules such as granzyme B and rapidly produce the inflammatory cytokine IFN-γ upon activation. |
| 1294 | 26228786 | HCMV also induces the differentiation of effector CD4(+) T cells and NK cells, which share characteristics with HCMV-specific CD8(+) T cells. |
| 1295 | 26228786 | We propose that the overlap in differentiation of NK cells, CD4(+) and CD8(+) T cells after HCMV infection may be regulated by a shared transcriptional machinery. |
| 1296 | 21926977 | These cells, specific to multiple viral and self-tumor antigens, were found within a CD45RO(-), CCR7(+), CD45RA(+), CD62L(+), CD27(+), CD28(+) and IL-7Rα(+) T cell compartment characteristic of naive T cells. |
| 1297 | 21926977 | However, they expressed large amounts of CD95, IL-2Rβ, CXCR3, and LFA-1, and showed numerous functional attributes distinctive of memory cells. |