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- W4313350052 abstract "Abstract Vγ4+ cells, a subpopulation of peripheral γδ T cells are involved in West Nile virus (WNV) pathogenesis but the underlying mechanism is unclear. Here, we further investigated the role of Vγ4+ cells in WNV encephalitis and found that Vγ4+ cell-depleted mice had a lower viremia and reduced inflammation in the brain following WNV infection. Although Vγ4+ cells contributed to interleukin (IL-17) production during infection, blocking IL-17 signaling did not affect host susceptibility to WNV encephalitis. Furthermore, there was an enhanced magnitude of protective Vγ1+ cell expansion in the spleen and more Vγ1+ cell infiltration into the brains of Vγ4+ cell-depleted mice than controls during WNV infection. Vγ4+ cells of WNV-infected mice had a higher potential for producing transforming growth factor (TGF)-β. We noted that the difference in anti-CD3-stimulated γδ T cell proliferation between those of controls and Vγ4+ cell-depleted mice was diminished in the presence of TGF-β inhibitor. Moreover, Vγ4+ cells contributed to the production of IL-10, which is known to play a negative role in immunity against WNV infection, either directly or by increasing IL-10-producing αβ T cells. These results suggest that Vγ4+ cells may suppress Vγ1+ cell expansion via TGF-β and promote IL-10 production, which leads to higher viremia and enhanced brain inflammation during WNV infection." @default.
- W4313350052 created "2023-01-06" @default.
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- W4313350052 date "2011-04-01" @default.
- W4313350052 modified "2023-10-16" @default.
- W4313350052 title "Vγ4+ T cells regulate host immune response to West Nile virus infection (154.33)" @default.
- W4313350052 doi "https://doi.org/10.4049/jimmunol.186.supp.154.33" @default.
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