tetano
Editor, Senior Moderator
Nat Commun. 2015 Mar 2;6:6374. doi: 10.1038/ncomms7374.
[h=1]IL-10 inhibits neuraminidase-activated TGF-β and facilitates Th1 phenotype during early phase of infection.[/h] Dutta A[SUP]1[/SUP], Huang CT[SUP]1[/SUP], Chen TC[SUP]2[/SUP], Lin CY[SUP]3[/SUP], Chiu CH[SUP]4[/SUP], Lin YC[SUP]5[/SUP], Chang CS[SUP]1[/SUP], He YC[SUP]1[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] 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.
PMID: 25728041 [PubMed - in process]
[h=1]IL-10 inhibits neuraminidase-activated TGF-β and facilitates Th1 phenotype during early phase of infection.[/h] Dutta A[SUP]1[/SUP], Huang CT[SUP]1[/SUP], Chen TC[SUP]2[/SUP], Lin CY[SUP]3[/SUP], Chiu CH[SUP]4[/SUP], Lin YC[SUP]5[/SUP], Chang CS[SUP]1[/SUP], He YC[SUP]1[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] 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.
PMID: 25728041 [PubMed - in process]