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Chromatin Remodeling and T Helper Subset Differentiation
Author(s) -
Miyatake Shoichiro,
Arai Naoko,
Arai KenIchi
Publication year - 2000
Publication title -
iubmb life
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.132
H-Index - 113
eISSN - 1521-6551
pISSN - 1521-6543
DOI - 10.1080/15216540050166990
Subject(s) - gata3 , chromatin , biology , chromatin remodeling , cellular differentiation , microbiology and biotechnology , transcription factor , cytokine , t helper cell , immune system , interleukin 4 , immunology , gene , t cell , genetics
The T helper subsets Th1 and Th2 regulate specific types of immune responses by producing distinct sets of cytokines. Differentiation of the T helper subsets from their common precursors, naive CD4+ T cells, is induced by antigen stimulation and controlled by various other conditions. Of these conditions, the contributions of the cytokine environment have been the best characterized. The presence of interleukin‐4 (IL‐4) directs the differentiation towards Th2 cells, whereas IL‐12 induces Th1 differentiation. The Th2 signature cytokine genes encoding IL‐4, IL‐13, and IL‐5 are clustered, and noncoding regions such as the intergenic region of the IL‐4 and IL‐13 genes are highly conserved from mice to humans. Alteration of the chromatin structure of this Th2 cytokine cluster region is detected as nuclease‐accessible regions specific to Th2 cells. Activation of STAT6 promotes Th2 differentiation by inducing Th2‐specific transcription factors, including GATA3. Expression of GATA3 induces Th2 differentiation and enhances the Th2 cell?specific chromatin accessibility, indicating that GATA3 is a key protein that regulates differentiation through chromatin remodeling. T helper subset differentiation provides a good system to study gene expression regulation at the chromatin level.