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      STAT3 regulates cytokine-mediated generation of inflammatory helper T cells.

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          Abstract

          Interleukin-17 (IL-17)-producing helper T (TH) cells, named as TH(IL-17), TH17, or inflammatory TH (THi), have been recently identified as a novel effector lineage. However, how cytokine signals mediate THi differentiation is unclear. We found that IL-6 functioned to up-regulate IL-23R and that IL-23 synergized with IL-6 in promoting THi generation. STAT3, activated by both IL-6 and IL-23, plays a critical role in THi development. A hyperactive form of STAT3 promoted THi development, whereas this differentiation process was greatly impaired in STAT3-deficient T cells. Moreover, STAT3 regulated the expression of retinoic acid receptor-related orphan receptor gamma-T (RORgamma t), a THi-specific transcriptional regulator; STAT3 deficiency impaired RORgamma t expression and led to elevated expression of T-box expressed in T cells (T-bet) and Forkhead box P3 (Foxp3). Our data thus demonstrate a pathway whereby cytokines regulate THi differentiation through a selective STAT transcription factor that functions to regulate lineage-specific gene expression.

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          Author and article information

          Journal
          J Biol Chem
          The Journal of biological chemistry
          American Society for Biochemistry & Molecular Biology (ASBMB)
          0021-9258
          0021-9258
          Mar 30 2007
          : 282
          : 13
          Affiliations
          [1 ] Department of Immunology, M.D. Anderson Cancer Center, Houston, Texas 77030.
          [2 ] Blood Research Institute, Blood Center of Wisconsin, Milwaukee, Wisconsin 53226.
          [3 ] Department of Immunology, M.D. Anderson Cancer Center, Houston, Texas 77030. Electronic address: cdong@mdanderson.org.
          Article
          S0021-9258(19)33588-4
          10.1074/jbc.C600321200
          17277312
          2a7a047f-30ce-46c4-8c77-f6f15df99306
          History

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