Regulation of nuclear factor-κB in autoimmunity

被引:244
|
作者
Sun, Shao-Cong [1 ,2 ]
Chang, Jae-Hoon [1 ]
Jin, Jin [1 ]
机构
[1] Univ Texas MD Anderson Canc Ctr, Dept Immunol, Houston, TX 77030 USA
[2] Univ Texas Houston, Grad Sch Biomed Sci, Houston, TX 77030 USA
基金
美国国家卫生研究院;
关键词
NF-kappa B; autoimmunity; inflammation; ubiquitination; regulatory T cells; DENDRITIC CELL ACTIVATION; T-CELLS; DIFFERENTIAL REQUIREMENT; LINEAR POLYUBIQUITIN; FOXP3; EXPRESSION; C-REL; A20; PREVENTS; DEFICIENCY; NIK;
D O I
10.1016/j.it.2013.01.004
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Nuclear factor (NF)-kappa B transcription factors are pivotal regulators of innate and adaptive immune responses, and perturbations of NF-kappa B signaling contribute to the pathogenesis of immunological disorders. NF-kappa B is a well-known proinflammatory mediator, and its deregulated activation is associated with the chronic inflammation of autoimmune diseases. Paradoxically, NF-kappa B plays a crucial role in the establishment of immune tolerance, including both central tolerance and the peripheral function of regulatory T (Treg) cells. Thus, defective or deregulated activation of NF-kappa B may contribute to autoimmunity and inflammation, highlighting the importance of tightly controlled NF-kappa B signaling. This review focuses on recent progress regarding NF-kappa B regulation and its association with autoimmunity.
引用
收藏
页码:282 / 289
页数:8
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