The signaling suppressor CIS controls proallergic T cell development and allergic airway inflammation

Xuexian O. Yang, Huiyuan Zhang, Byung Seok Kim, Xiaoyin Niu, Juan Peng, Yuhong Chen, Romica Kerketta, Young Hee Lee, Seon Hee Chang, David B. Corry, Demin Wang, Stephanie S. Watowich, Chen Dong

Research output: Contribution to journalArticle

79 Scopus citations

Abstract

Transcription factors of the STAT family are critical in the cytokine-mediated functional differentiation of CD4 + helper T cells. Signaling inhibitors of the SOCS family negatively regulate the activation of STAT proteins; however, their roles in the differentiation and function of helper T cells are not well understood. Here we found that the SOCS protein CIS, which was substantially induced by interleukin 4 (IL-4), negatively regulated the activation of STAT3, STAT5 and STAT6 in T cells. CIS-deficient mice spontaneously developed airway inflammation, and CIS deficiency in T cells led to greater susceptibility to experimental allergic asthma. CIS-deficient T cells showed enhanced differentiation into the TH2 and TH9 subsets of helper T cells. STAT5 and STAT6 regulated IL-9 expression by directly binding to the Il9 promoter. Our data thus demonstrate a critical role for CIS in controlling the proallergic generation of helper T cells.

Original languageEnglish (US)
Pages (from-to)732-740
Number of pages9
JournalNature immunology
Volume14
Issue number7
DOIs
StatePublished - Jul 2013

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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