IL-10 inhibits neuraminidase-activated TGF-β and facilitates Th1 phenotype during early phase of infection

Avijit Dutta, Ching-Tai Huang (), Tse-Ching Chen, Chun-Yen Lin, Cheng-Hsun Chiu, Yung-Chang Lin, Chia-Shiang Chang and Yueh-Chia He
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Avijit Dutta: Chang Gung Memorial Hospital, Chang Gung University
Ching-Tai Huang: Chang Gung Memorial Hospital, Chang Gung University
Tse-Ching Chen: Chang Gung Memorial Hospital, Chang Gung University
Chun-Yen Lin: Chang Gung Memorial Hospital, Chang Gung University
Cheng-Hsun Chiu: Chang Gung Memorial Hospital, Chang Gung University
Yung-Chang Lin: Chang Gung Memorial Hospital, Chang Gung University
Chia-Shiang Chang: Chang Gung Memorial Hospital, Chang Gung University
Yueh-Chia He: Chang Gung Memorial Hospital, Chang Gung University

Nature Communications, 2015, vol. 6, issue 1, 1-11

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 haemagglutinin-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 haemagglutinin-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 upregulated 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.

Date: 2015
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DOI: 10.1038/ncomms7374

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