期刊
JOURNAL OF IMMUNOLOGY
卷 190, 期 7, 页码 3049-3053出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1203032
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资金
- National Institutes of Health National Institute of Allergy and Infectious Diseases [R01 072543, R01 063107]
- Scripps Center for HIV/AIDS Vaccine Immunology and Immunogen Discovery Award [UM1AI100663]
- La Jolla Institute for Allergy and Immunology institutional funds
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-2Ra 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. The Journal of Immunology, 2013, 190: 3049-3053.
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