Vγ4+ T cells regulate host immune response to West Nile virus infection.
Vγ4+ T cells regulate host immune response to West Nile virus infection.
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DOI：
10.1111/j.1574-695x.2011.00840.x
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发表时间：
2011-11
影响因子：
--
通讯作者：
Wang T
中科院分区：
文献类型：
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作者：
Welte T;Aronson J;Gong B;Rachamallu A;Mendell N;Tesh R;Paessler S;Born WK;O'Brien RL;Wang T
Vγ4+ cells, a subpopulation of peripheral γδ T cells, are involved in West Nile virus (WNV) pathogenesis, but the underlying mechanism is unclear. In this study, we found that WNV-infected Vγ4+ cell-depleted mice had lower viremia and a reduced inflammatory response in the brain. Vγ4+ cells produced interleukin (IL)-17 during WNV infection, but blocking IL-17 signaling did not affect host susceptibility to WNV encephalitis. We also noted that there was an enhanced magnitude of protective splenic Vγ1+ cell expansion in Vγ4+ cell-depleted mice compared to that in controls during WNV infection. Additionally, Vγ4+ cells of WNV-infected mice had a higher potential for producing transforming growth factor (TGF)-β. γδ T cells of WNV-infected Vγ4+ cell-depleted mice had a higher proliferation rate than those of WNV-infected controls upon ex vivo stimulation with anti-CD3, and this difference was diminished in the presence of TGF-β inhibitor. Finally, Vγ4+ cells of infected mice contributed directly and indirectly to the higher level of IL-10, which is known to play a negative role in immunity against WNV infection. In summary, Vγ4+ cells suppress Vγ1+ cell expansion via TGF-β and increase IL-10 level during WNV infection, which together may lead to higher viremia and enhanced brain inflammation.
