The SWI/SNF Chromatin-remodeling Complex Modulates Peripheral T Cell Activation and Proliferation by Controlling AP-1 Expression

被引:25
|
作者
Jeong, Seung Min
Lee, Changjin
Lee, Sung Kyu
Kim, Jieun
Seong, Rho Hyun [1 ]
机构
[1] Seoul Natl Univ, Dept Biol Sci, Inst Mol Biol & Genet, Seoul 151742, South Korea
基金
新加坡国家研究基金会;
关键词
NF-KAPPA-B; KINASE-C-THETA; EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS; GLUCOCORTICOID-INDUCED APOPTOSIS; MULTIPLE-SCLEROSIS LESIONS; TUMOR-NECROSIS-FACTOR; PKC-THETA; TRANSCRIPTION FACTORS; SRG3; EXPRESSION; BAF COMPLEX;
D O I
10.1074/jbc.M109.026997
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The SWI/SNF chromatin-remodeling complex has been implicated in the activation and proliferation of T cells. After T cell receptor signaling, the SWI/SNF complex rapidly associates with chromatin and controls gene expression in T cells. However, the process by which the SWI/SNF complex regulates peripheral T cell activation has not been elucidated. In this study, we show that the SWI/SNF complex regulates cytokine production and proliferation of T cells. During T cell activation, the SWI/SNF complex is recruited to the promoter of the transcription factor AP-1, and it increases the expression of AP-1. Increased expression of the SWI/SNF complex resulted in enhanced AP-1 activity, cytokine production, and proliferation of peripheral T cells, whereas knockdown of the SWI/SNF complex expression impaired the AP-1 expression and reduced the activation and proliferation of T cells. Moreover, mice that constitutively expressed the SWI/SNF complex in T cells were much more susceptible to experimentally induced autoimmune encephalomyelitis than the normal mice were. These results suggest that the SWI/SNF complex plays a critical role during T cell activation and subsequent immune responses.
引用
收藏
页码:2340 / 2350
页数:11
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