Cutting edge: STAT1 is required for IL-6-mediated Bcl6 induction for early follicular helper cell differentiation.

TitleCutting edge: STAT1 is required for IL-6-mediated Bcl6 induction for early follicular helper cell differentiation.
Publication TypeJournal Article
Year of Publication2013
AuthorsChoi YSoo, Eto D, Yang JA, Lao C, Crotty S
JournalJ Immunol
Volume190
Issue7
Pagination3049-53
Date Published04/01/2013
ISSN1550-6606
Abstract

Bcl6 is required for CD4 T cell differentiation into T follicular helper cells (Tfh). In this study, we examined the role of IL-6 in early processes of in vivo Tfh differentiation, because the timing and mechanism of action of IL-6 in Tfh differentiation have been controversial in vivo. We found that early Bcl6(+)CXCR5(+) Tfh differentiation was severely impaired in the absence of IL-6; however, STAT3 deficiency failed to recapitulate that defect. IL-6R signaling activates the transcription factor STAT1 specifically in CD4 T cells. Strikingly, we found that STAT1 activity was required for Bcl6 induction and early Tfh differentiation in vivo. IL-6 mediated STAT3 activation is important for downregulation of IL-2Rα to limit Th1 cell differentiation in an acute viral infection. Thus, IL-6 signaling is a major early inducer of the Tfh differentiation program unexpectedly mediated by both STAT3 and STAT1 transcription factors.

DOI10.4049/jimmunol.1203032
Alternate JournalJ. Immunol.
PubMed ID23447690
PubMed Central IDPMC3626564
Grant ListR01 063107 / / PHS HHS / United States
R01 072543 / / PHS HHS / United States
UM1AI100663 / AI / NIAID NIH HHS / United States
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