Journal
PLOS PATHOGENS
Volume 4, Issue 2, Pages -Publisher
PUBLIC LIBRARY SCIENCE
DOI: 10.1371/journal.ppat.1000006
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Funding
- Medical Research Council [G0500617, G117/488] Funding Source: Medline
- Wellcome Trust [080340] Funding Source: Medline
- Medical Research Council [G117/488, G0500617] Funding Source: researchfish
- MRC [G0500617, G117/488] Funding Source: UKRI
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Currently, our understanding of mechanisms underlying cell-mediated immunity and particularly of mechanisms that promote robust T cell memory to respiratory viruses is incomplete. Interleukin (IL)-6 has recently re-emerged as an important regulator of T cell proliferation and survival. Since IL-6 is abundant following infection with influenza virus, we analyzed virus-specific T cell activity in both wild type and IL-6 deficient mice. Studies outlined herein highlight a novel role for IL-6 in the development of T cell memory to influenza virus. Specifically, we find that CD4(+) but not CD8(+) T cell memory is critically dependent upon IL-6. This effect of IL-6 includes its ability to suppress CD4(+)CD25(+) regulatory T cells (Treg). We demonstrate that influenza-induced IL-6 limits the activity of virus-specific Tregs, thereby facilitating the activity of virus-specific memory CD4(+) T cells. These experiments reveal a critical role for IL-6 in ensuring, within the timeframe of an acute infection with a cytopathic virus, that antigen-specific Tregs have no opportunity to down-modulate the immune response, thereby favoring pathogen clearance and survival of the host.
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