Cytokines in Autoimmune Uveitis

被引:140
作者
Horai, Reiko [1 ]
Caspi, Rachel R. [1 ]
机构
[1] NEI, Immunol Lab, NIH, Bethesda, MD 20892 USA
关键词
REGULATORY T-CELLS; GROWTH-FACTOR-BETA; NECROSIS-FACTOR-ALPHA; IFN-GAMMA; TGF-BETA; INTERFERON-GAMMA; BEHCETS-DISEASE; TH17; CELLS; OCULAR AUTOIMMUNITY; EFFECTOR MECHANISMS;
D O I
10.1089/jir.2011.0042
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
Autoimmune uveitis is a complex group of sight-threatening diseases that arise without a known infectious trigger. The disorder is often associated with immunological responses to retinal proteins. Experimental models of autoimmune uveitis targeting retinal proteins have led to a better understanding of the basic immunological mechanisms involved in the pathogenesis of uveitis and have provided a template for the development of novel therapies. The disease in humans is believed to be T cell-dependent, as clinical uveitis is ameliorated by T cell-targeting therapies. The roles of T helper 1 (Th1) and Th17 cells have been major topics of interest in the past decade. Studies in uveitis patients and experiments in animal models have revealed that Th1 and Th17 cells can both be pathogenic effectors, although, paradoxically, some cytokines produced by these subsets can also be protective, depending on when and where they are produced. The major proinflammatory as well as regulatory cytokines in uveitis, the therapeutic approaches, and benefits of targeting these cytokines will be discussed in this review.
引用
收藏
页码:733 / 744
页数:12
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