Diverse targets of the transcription factor STAT3 contribute to T cell pathogenicity and homeostasis

Lydia Durant, Wendy T. Watford, Haydeé L. Ramos, Arian Laurence, Golnaz Vahedi, Lai Wei, Hayato Takahashi, Hong Wei Sun, Yuka Kanno, Fiona Powrie, John J. O'Shea

研究成果: Article査読

492 被引用数 (Scopus)

抄録

STAT3, an essential transcription factor with pleiotropic functions, plays critical roles in the pathogenesis of autoimmunity. Despite recent data linking STAT3 with inflammatory bowel disease, exactly how it contributes to chronic intestinal inflammation is not known. Using a T cell transfer model of colitis, we found that STAT3 expression in T cells was essential for the induction of both colitis and systemic inflammation. STAT3 was critical in modulating the balance of T helper 17 (Th17) and regulatory T (Treg) cells, as well as in promoting CD4+ T cell proliferation. We used chromatin immunoprecipitation and massive parallel sequencing (ChIP-Seq) to define the genome-wide targets of STAT3 in CD4+ T cells. We found that STAT3 bound to multiple genes involved in Th17 cell differentiation, cell activation, proliferation, and survival, regulating both expression and epigenetic modifications. Thus, STAT3 orchestrates multiple critical aspects of T cell function in inflammation and homeostasis.

本文言語English
ページ(範囲)605-615
ページ数11
ジャーナルImmunity
32
5
DOI
出版ステータスPublished - 2010 5月
外部発表はい

ASJC Scopus subject areas

  • 免疫アレルギー学
  • 免疫学
  • 感染症

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