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PMID |
Sentence |
1 |
1432977
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The bioneutralization activity of the antisera assessed by a specific bioassay in vitro, when the antibody titre was high, was 6.9 +/- 0.18 micrograms hFSH ml-1.
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2 |
9322065
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Three forms of OspA vaccine candidates were investigated by the induction of the cytokines interleukin (IL)-1 beta, IL-6, tumor necrosis factor (TNF)-alpha, IL-10 and interferon (IFN)-gamma as markers of monocyte activation and immune stimulation: lipidated OspA (L-OspA), non-lipidated OspA (NL-OspA), and a fusion protein of 81 amino acids of the nonstructural protein 1 of influenza virus with OspA (NS1-OspA).
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3 |
9322065
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All OspA preparations induced IL-1 beta, IL-6 and TNF-alpha in a concentration-dependent manner with peak levels at 12-24 h.
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4 |
9322065
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In peripheral blood mononuclear cells from 10 healthy donors, L-OspA at 10 micrograms ml-1 induced up to 4-fold more IL-1 beta, IL-6, and TNF-alpha than the other OspA preparations (P < or = 0.0068), followed by NS1-OspA, which was still superior to NL-OspA.
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5 |
9322065
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L-OspA also induced high levels of IL-10 within 24 h but no significant amounts of IFN-gamma.
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6 |
9751013
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The mean titres at 12 months were 107 +/- 12 IU ml-1 (Engerix B), 102 +/- 12 IU ml-1 (Gen Hevac B) and 117 +/- 12 IU ml-1 (Hepavax Gene).
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7 |
17048276
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This vaccine induced the production of antibodies that blocked IL-17A bioactivity in vitro but did not react with the other IL-17 isoforms, including IL-17F.
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8 |
17048276
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To test the ability of the vaccine to confer protection against an IL-17-dependent disorder, SJL mice were vaccinated with IL-17-OVA and encephalomyelitis (EAE) was induced by proteolipid protein (PLP) peptide 139-151.
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9 |
19038785
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Specifically, 12 immune biomolecules (including gamma interferon [IFN-gamma], interleukin-21 [IL-21], IL-27, IL-17f, CXCL9, CXCL10, and CXCL11) were differentially regulated, relative to the levels for naïve controls, in the lungs of vaccinated mice at this time point.
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10 |
19038785
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Although the vaccine-related immune responses evoked in mice immunized with the DNA vaccine were relatively limited at 10 days postinfection, upregulation of IFN-gamma RNA synthesis as well as increased expression levels of CXCL9, CXCL10, and CXCL11 chemokines were detected.
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11 |
20112107
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T helper type 17 (Th17) cells are a distinct lineage of T cells that produce the effector molecules IL-17, IL-17F, IL-21, and IL-22.
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12 |
20182729
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T helper type 17 (Th17) cells are a distinct lineage of T cells that produce the effector molecules IL-17, IL-17F, IL-21, and IL-22.
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13 |
20357059
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In this study, we assessed the immunizing activity of a recombinant modified vaccinia Ankara (MVA) construct (MVA/IL-15/5Mtb) which overexpresses five Mycobacterium tuberculosis antigens (antigen 85A, antigen 85B, ESAT6, HSP60, and Mtb39), as well as the molecular adjuvant interleukin-15 (IL-15).
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14 |
20357059
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At 16 months, when the Mycobacterium bovis BCG and MVA/IL-15/5Mtb vaccine-induced protection was essentially equivalent, the protective responses after a tuberculous challenge were associated with elevated levels of gamma interferon (IFN-gamma), IL-17F, Cxcl9, and Cxcl10.
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15 |
20357059
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Long-term memory after immunization with the E6-85-MVA/IL-15/5Mtb combination regimen was associated with the induction of monofunctional CD4 and CD8 IFN-gamma-producing T cells and multifunctional CD4 and CD8 T cells expressing IFN-gamma/tumor necrosis factor alpha (TNF-alpha), TNF-alpha/IL-2, and IFN-gamma/TNF-alpha/IL-2.
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16 |
20357059
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In contrast, BCG-induced protection was characterized by fewer CD4 and CD8 monofunctional T cells expressing IFN-gamma and only IFN-gamma/TNF-alpha and IFN-gamma/TNF-alpha/IL-2 expressing multifunctional T (MFT) cells.
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17 |
23886112
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These approaches have included: (1) the use of IL-17A and IL-17F-deficient mice, (2) specific antibodies directed against IL-17, (3) an IL-17 vaccine, (4) methods to block the IL-17 receptor and (5) small-molecule inhibitors of IL-17.
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18 |
23886112
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This paper will review the preclinical results using various pharmacological approaches [specific IL-17 antibodies, an IL-17 receptor fusion protein, IL-12/IL-23 p40 subunit and IL-17 vaccine approaches, as well as a small molecule inhibitor (Vidofludimus)] to inhibit IL-17 in animal models of IBD.
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19 |
23886112
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Finally, future pharmacological approaches of interest will be discussed, such as: (1) Retinoic acid receptor-related orphan nuclear receptor gamma t (Rorγt) antagonists, (2) Retinoic acid receptor alpha (RARα) antagonists, (3) Pim-1 kinase inhibitors and (4) Dual small-molecule inhibitors of NF-κB and STAT3, like synthetic triterpenoids.
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20 |
24045338
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TLR3, RIG-I and MDA5).
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21 |
24045338
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At the latest time points the up-regulation of IL-17A and IL-17F suggested that Th17 cells may participate in the earliest adaptive response to this vaccine.
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22 |
24333371
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These single nucleotide polymorphisms were distributed on five chicken chromosomes (GGA), involving GGA1, GGA3, GGA5, GGA8, and GGA9.
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23 |
24333371
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A genomic region containing a cluster of 13 beta-defensin (GAL1-13) and interleukin-17F genes on GGA3 probably plays an important role in the immune response against IBV.
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24 |
24412909
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IL-10 suppresses IL-17-mediated dermal inflammation and reduces the systemic burden of Vaccinia virus in a mouse model of eczema vaccinatum.
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25 |
24412909
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This was associated with enhanced production of IL-17A, IL-17F and CXCL2.
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26 |
24412909
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These findings suggest that IL-10 is important in limiting skin inflammation induced by VV and that abnormal IL-17-driven neutrophil recruitment at the primary infection site in the skin results in increased systemic viral dissemination.
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27 |
24600029
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Intrahepatic innate lymphoid cells secrete IL-17A and IL-17F that are crucial for T cell priming in viral infection.
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28 |
24600029
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Functional studies with mice deficient of IL-17R, IL-17A, and IL-17F further revealed that IL-17 signaling was critical for priming T cell responses in viral hepatitis.
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29 |
24600029
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IL-17A repressed IL-17F secretion in vitro and in vivo; IL-17F(+) intrahepatic cells expanded more vigorously in IL-17A knockout animals, permitting efficient Ag presentation and T cell function.
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30 |
24600029
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However, IL-17F neither inhibited IL-17A in vitro nor regulated its secretion in vivo.
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31 |
24600029
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Intrahepatic innate lymphoid cells secrete IL-17A and IL-17F that are crucial for T cell priming in viral infection.
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32 |
24600029
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Functional studies with mice deficient of IL-17R, IL-17A, and IL-17F further revealed that IL-17 signaling was critical for priming T cell responses in viral hepatitis.
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33 |
24600029
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IL-17A repressed IL-17F secretion in vitro and in vivo; IL-17F(+) intrahepatic cells expanded more vigorously in IL-17A knockout animals, permitting efficient Ag presentation and T cell function.
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34 |
24600029
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However, IL-17F neither inhibited IL-17A in vitro nor regulated its secretion in vivo.
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35 |
24600029
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Intrahepatic innate lymphoid cells secrete IL-17A and IL-17F that are crucial for T cell priming in viral infection.
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36 |
24600029
|
Functional studies with mice deficient of IL-17R, IL-17A, and IL-17F further revealed that IL-17 signaling was critical for priming T cell responses in viral hepatitis.
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37 |
24600029
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IL-17A repressed IL-17F secretion in vitro and in vivo; IL-17F(+) intrahepatic cells expanded more vigorously in IL-17A knockout animals, permitting efficient Ag presentation and T cell function.
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38 |
24600029
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However, IL-17F neither inhibited IL-17A in vitro nor regulated its secretion in vivo.
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39 |
24600029
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Intrahepatic innate lymphoid cells secrete IL-17A and IL-17F that are crucial for T cell priming in viral infection.
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40 |
24600029
|
Functional studies with mice deficient of IL-17R, IL-17A, and IL-17F further revealed that IL-17 signaling was critical for priming T cell responses in viral hepatitis.
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41 |
24600029
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IL-17A repressed IL-17F secretion in vitro and in vivo; IL-17F(+) intrahepatic cells expanded more vigorously in IL-17A knockout animals, permitting efficient Ag presentation and T cell function.
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42 |
24600029
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However, IL-17F neither inhibited IL-17A in vitro nor regulated its secretion in vivo.
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43 |
25141829
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Treatment with IL-17A/IL-17F or IL-22 expanded phosphoantigen 4-hydroxy-3-methyl-but-enyl pyrophosphate (HMBPP)-stimulated Vγ2Vδ2 T cells from BCG-vaccinated macaques but not from naïve animals, and IL-23 induced greater expansion than the other Th17-related cytokines.
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44 |
25141829
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Consistently, Mtb infection of macaques also enhanced the ability of IL-17/IL-22 or IL-23 to expand HMBPP-stimulated Vγ2Vδ2 T cells.
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45 |
25141829
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When evaluating IL-23 signaling as a prototype, we found that HMBPP/IL-23-expanded Vγ2Vδ2 T cells from macaques infected with Mtb or vaccinated with BCG or Listeria ΔactA prfA*-ESAT6/Ag85B produced IL-17, IL-22, IL-2, and IFN-γ.
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46 |
25141829
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Furthermore, HMBPP/IL-23-induced proliferation of Vγ2Vδ2 T cells appeared to require APC contact and involve the conventional and novel protein kinase C signaling pathways.
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47 |
25514671
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The five most significant cytokines in decreasing order of importance were IL-7, IL-4, TNF-α, IL-13, and IL-17F.
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