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- W4313356772 abstract "Abstract Th1 cells control their activity by producing regulatory IL-10. Here we report that Th1 cell-derived IL-10 facilitates their expansion and in addition, augments Th1 cell production of IFN-γ, TNF-α, and IL-2 during the early phase of influenza. In our antigen-specific mouse experimental system, influenza hemagglutinin-specific CD4+ T cells respond to infection with the induction of T-bet, and produce both IFN-γ and IL-10. In the early phase of infection, an abundance of viral neuraminidase causes TGF-β activation of hemagglutinin-specific CD4+ T cells. CD4+ T cell-derived IL-10 inhibits neuraminidase-driven TGF-β activation and counteracts the virus-mediated immune suppression. As the host eradicates the virus, neuraminidase activity wanes and IL-10 receptors are up-regulated on CD4+ T cells in the late phase of infection. IL-10 then suppresses immune activation and aids in recovery from infection and inflammation. These results reveal a previously unrecognized function of Th1 cell-derived IL-10 in vivo." @default.
- W4313356772 created "2023-01-06" @default.
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- W4313356772 date "2015-05-01" @default.
- W4313356772 modified "2023-10-16" @default.
- W4313356772 title "IL-10 inhibits neuraminidase activated-TGF-β and facilitates Th1 phenotype during early phase of infection (VIR1P.1129)" @default.
- W4313356772 doi "https://doi.org/10.4049/jimmunol.194.supp.74.6" @default.
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