STAT4: genetics, mechanisms, and implications for autoimmunity.
STAT4: genetics, mechanisms, and implications for autoimmunity.
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DOI：
10.1007/s11882-008-0077-8
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发表时间：
2008-09
影响因子：
5.5
通讯作者：
Remmers, Elaine F.
中科院分区：
文献类型：
--
作者：
Korman, Benjamin D.;Kastner, Daniel L.;Gregersen, Peter K.;Remmers, Elaine F.
遗传学和技术的最新进展使人们在理解易患自身免疫性疾病的基因方面取得了突破。信号转导和转录激活因子4(STAT4)基因的一种常见单倍型已被证明与类风湿性关节炎、系统性红斑狼疮和原发性干燥综合征的易感性有关。STAT4是一种转录因子，在T细胞和单核细胞中传递IL-12、IL-23和I型干扰素细胞因子信号，导致T辅助细胞1和T辅助细胞17分化、单核细胞活化和产生干扰素-γ。尽管这种关联的证据非常有力且重复性很好，但该基因的多态导致疾病的确切机制仍不清楚。随着对其他疾病相关基因的识别，阐明STAT4的变异形式如何调节免疫功能应该有助于更好地理解自身免疫的病理生理学。
Recent advances in genetics and technology have led to breakthroughs in understanding the genes that predispose individuals to autoimmune diseases. A common haplotype of the signal transducer and activator of transcription 4 (STAT4) gene has been shown to be associated with susceptibility to rheumatoid arthritis, systemic lupus erythematosus, and primary Sjögren’s syndrome. STAT4 is a transcription factor that transduces interleukin-12, interleukin-23, and type I interferon cytokine signals in T cells and monocytes, leading to T-helper type 1 and T-helper type 17 differentiation, monocyte activation, and production of interferon-γ. Although the evidence for this association is very strong and well replicated, the exact mechanism by which polymorphisms in this gene lead to disease remains unknown. In concert with the identification of other disease-associated loci, elucidating how the variant form of STAT4 modulates immune function should lead to an improved understanding of the pathophysiology of autoimmunity.
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