| First Author | Dutta A | Year | 2015 |
| Journal | Nat Commun | Volume | 6 |
| Pages | 6374 | PubMed ID | 25728041 |
| Mgi Jnum | J:221784 | Mgi Id | MGI:5641562 |
| Doi | 10.1038/ncomms7374 | Citation | Dutta A, et al. (2015) IL-10 inhibits neuraminidase-activated TGF-beta and facilitates Th1 phenotype during early phase of infection. Nat Commun 6:6374 |
| abstractText | 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-gamma, TNF-alpha 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-gamma and IL-10. In the early phase of infection, an abundance of viral neuraminidase causes TGF-beta activation of haemagglutinin-specific CD4(+) T cells. CD4(+) T-cell-derived IL-10 inhibits neuraminidase-driven TGF-beta 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. |
