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Science. 2011 Nov 11;334(6057):825-9. doi: 10.1126/science.1208421. Epub 2011 Sep 29.

Late interleukin-6 escalates T follicular helper cell responses and controls a chronic viral infection.

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1
Division of Biological Sciences, University of California San Diego, La Jolla, CA 92093, USA.

Abstract

Multiple inhibitory molecules create a profoundly immunuosuppressive environment during chronic viral infections in humans and mice. Therefore, eliciting effective immunity in this context represents a challenge. Here, we report that during a murine chronic viral infection, interleukin-6 (IL-6) was produced by irradiation-resistant cells in a biphasic manner, with late IL-6 being absolutely essential for viral control. The underlying mechanism involved IL-6 signaling on virus-specific CD4 T cells that caused up-regulation of the transcription factor Bcl6 and enhanced T follicular helper cell responses at late, but not early, stages of chronic viral infection. This resulted in escalation of germinal center reactions and improved antibody responses. Our results uncover an antiviral strategy that helps to safely resolve a persistent infection in vivo.

PMID:
21960530
PMCID:
PMC3388900
DOI:
10.1126/science.1208421
[Indexed for MEDLINE]
Free PMC Article
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