Chromatin Remodeling Protein SMAR1 Is a Critical Regulator of T Helper Cell Differentiation and Inflammatory Diseases

被引:9
|
作者
Mirlekar, Bhalchandra [1 ,2 ]
Gautam, Dipendra [2 ]
Chattopadhyay, Samit [1 ,3 ]
机构
[1] Natl Ctr Cell Sci, Chromatin & Dis Biol Lab, Pune, Maharashtra, India
[2] Univ N Carolina, Lineberger Comprehens Canc Ctr, Chapel Hill, NC USA
[3] Indian Inst Chem Biol, Canc Biol & Inflammatory Disorder Div, Kolkata, India
来源
FRONTIERS IN IMMUNOLOGY | 2017年 / 8卷
关键词
asthma; colitis; MAR; regulatory T cells; SMAR1; T helper cells; EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS; ROR-GAMMA-T; TRANSCRIPTION FACTOR FOXP3; RECEPTOR-BETA LOCUS; GENE-EXPRESSION; LINEAGE COMMITMENT; BOWEL-DISEASE; IN-VIVO; INTERCHROMOSOMAL ASSOCIATIONS; AIRWAY INFLAMMATION;
D O I
10.3389/fimmu.2017.00072
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
T cell differentiation from naive T cells to specialized effector subsets of mature cells is determined by the iterative action of transcription factors. At each stage of specific T cell lineage differentiation, transcription factor interacts not only with nuclear proteins such as histone and histone modifiers but also with other factors that are bound to the chromatin and play a critical role in gene expression. In this review, we focus on one of such nuclear protein known as tumor suppressor and scaffold matrix attachment region-binding protein 1 (SMAR1) in CD4(+) T cell differentiation. SMAR1 facilitates Th1 differentiation by negatively regulating T-bet expression via recruiting HDAC1-SMRT complex to its gene promoter. In contrast, regulatory T (T-reg) cell functions are dependent on inhibition of Th17-specific genes mainly IL-17 and STAT3 by SMAR1. Here, we discussed a critical role of chromatin remodeling protein SMAR1 in maintaining a fine-tuned balance between effector CD4(+) T cells and T-reg cells by influencing the transcription factors during allergic and autoimmune inflammatory diseases.
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页数:11
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