tetano
Editor, Senior Moderator
J Immunol. 2016 Sep 19. pii: 1600033. [Epub ahead of print]
[h=1]Direct IL-6 Signals Maximize Protective Secondary CD4 T Cell Responses against Influenza.[/h] Strutt TM[SUP]1[/SUP], McKinstry KK[SUP]1[/SUP], Kuang Y[SUP]2[/SUP], Finn CM[SUP]3[/SUP], Hwang JH[SUP]3[/SUP], Dhume K[SUP]3[/SUP], Sell S[SUP]4[/SUP], Swain SL[SUP]2[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Memory T cells can often respond against pathogens that have evaded neutralizing Abs and are thus key to vaccine-induced protection, yet the signals needed to optimize their responses are unclear. In this study, we identify a dramatic and selective requirement for IL-6 to achieve optimal memory CD4 T cell recall following heterosubtypic influenza A virus (IAV) challenge of mice primed previously with wild-type or attenuated IAV strains. Through analysis of endogenous T cell responses and adoptive transfer of IAV-specific memory T cell populations, we find that without IL-6, CD4[SUP]+[/SUP], but not CD8[SUP]+[/SUP], secondary effector populations expand less and have blunted function and antiviral impact. Early and direct IL-6 signals to memory CD4 T cells are required to program maximal secondary effector responses at the site of infection during heterosubtypic challenge, indicating a novel role for a costimulatory cytokine in recall responses.
Copyright ? 2016 by The American Association of Immunologists, Inc.
PMID: 27647834 DOI: 10.4049/jimmunol.1600033
[PubMed - as supplied by publisher]
[h=1]Direct IL-6 Signals Maximize Protective Secondary CD4 T Cell Responses against Influenza.[/h] Strutt TM[SUP]1[/SUP], McKinstry KK[SUP]1[/SUP], Kuang Y[SUP]2[/SUP], Finn CM[SUP]3[/SUP], Hwang JH[SUP]3[/SUP], Dhume K[SUP]3[/SUP], Sell S[SUP]4[/SUP], Swain SL[SUP]2[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Memory T cells can often respond against pathogens that have evaded neutralizing Abs and are thus key to vaccine-induced protection, yet the signals needed to optimize their responses are unclear. In this study, we identify a dramatic and selective requirement for IL-6 to achieve optimal memory CD4 T cell recall following heterosubtypic influenza A virus (IAV) challenge of mice primed previously with wild-type or attenuated IAV strains. Through analysis of endogenous T cell responses and adoptive transfer of IAV-specific memory T cell populations, we find that without IL-6, CD4[SUP]+[/SUP], but not CD8[SUP]+[/SUP], secondary effector populations expand less and have blunted function and antiviral impact. Early and direct IL-6 signals to memory CD4 T cells are required to program maximal secondary effector responses at the site of infection during heterosubtypic challenge, indicating a novel role for a costimulatory cytokine in recall responses.
Copyright ? 2016 by The American Association of Immunologists, Inc.
PMID: 27647834 DOI: 10.4049/jimmunol.1600033
[PubMed - as supplied by publisher]