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The signaling suppressor CIS controls proallergic T cell development and allergic airway inflammation. Nat Immunol 2013 Jul;14(7):732-40

Date

06/04/2013

Pubmed ID

23727894

Pubmed Central ID

PMC4084713

DOI

10.1038/ni.2633

Scopus ID

2-s2.0-84879355943   76 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.

Author List

Yang XO, Zhang H, Kim BS, Niu X, Peng J, Chen Y, Kerketta R, Lee YH, Chang SH, Corry DB, Wang D, Watowich SS, Dong C

Author

Demin Wang PhD Assistant Professor in the Microbiology and Immunology department at Medical College of Wisconsin




MESH terms used to index this publication - Major topics in bold

Animals
Asthma
Cell Differentiation
Histocytochemistry
Immunoblotting
Inflammation
Mice
Mice, Inbred C57BL
Mice, Knockout
Phosphorylation
RNA
Real-Time Polymerase Chain Reaction
STAT Transcription Factors
Signal Transduction
Suppressor of Cytokine Signaling Proteins
T-Lymphocytes, Regulatory
jenkins-FCD Prod-469 c3fc8ab87196149f9b23743c01b947d47e7319e5