期刊
JOURNAL OF IMMUNOLOGY
卷 184, 期 2, 页码 984-992出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.0902316
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资金
- Ministere de In Recherche et de l*Enseignement of Paris XI University
- Agence Nationale de Recherches sur le SIDA
- Fondation pour la Recherche Medicale
IL-17 is a potent effector cytokine involved in inflammatory response and antimicrobial defense. We report that SIV infection of rhesus macaques (RMs) results in the emergence of IL-17-expressing cells during the acute phase. This subpopulation appears at day 14 postinfection concomitantly with an increase in TGF-beta and IL-18 expression. This subset, which exhibits phenotypic markers of NK T cells (NKT), rather than Th17 CD4 cells, persists during the chronic phase and is higher in noncontrollers SIV-infected RMs compared with controllers SIV-infected RMs. In contrast, in the nonpathogenic model of SIVagm infection of African green monkeys, no change in the level of IL-17-expressing cells is observed in lymphoid organs. Consistent with the emergence of TGF-beta and IL-18 during the acute phase in SIV-infected RMs, but not in SIV-infected African green monkeys, we demonstrate that in vitro TGF-beta and IL-18 induce the differentiation and expansion of IL-17(+)NKT(+). Altogether, these results demonstrate that IL-17-producing NKT are associated with the pathogenesis of SIV in RMs and suggest that TGF-beta and IL-18 play a role in their development. The Journal of Immunology, 2010, 184: 984-992.
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