期刊
SCIENCE IMMUNOLOGY
卷 5, 期 49, 页码 -出版社
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/sciimmunol.aaw2262
关键词
-
类别
资金
- NIH [R01 DK093015, R01 DK103744]
- Crohn's and Colitis Foundation of America
- UAB institutional funds
- Versus Arthritis [20770, 19796, 20305]
- Wellcome Trust [079044]
Acting in concert with TGF-beta., interleukin-6 (IL-6) signaling induces T helper 17 (T(H)17) cell development by programming T(H)17-related genes via signal transducers and activators of transcription 3 (STAT3). A role for IL-6 signaling beyond the inductive phase of T(H)17 cell development has not been defined because IL-23 signaling downstream of T(H)17 cell induction also activates STAT3 and is thought responsible for T(H)17 cell maintenance. Here, we find that IL-6 signaling is required for both induction and maintenance of mouse T(H)17 cells; IL-6R alpha-deficient T(H)17 cells rapidly lost their T(H)17 phenotype and did not cause disease in two models of colitis. Cotransfer of wild-type T(H)17 cells with IL-6R.-deficient T(H)17 cells induced colitis but was unable to rescue phenotype loss of the latter. High IL-6 expression in the colon promoted classic, or cis, rather than transreceptor signaling that was required for maintenance of T(H)17 cells. Thus, ongoing classic IL-6 signaling underpins the T(H)17 program and is required for T(H)17 cell maintenance and function.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据