CXCR3, Inflammation, and Autoimmune Diseases
CXCR3, Inflammation, and Autoimmune Diseases
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DOI：
10.1111/j.1749-6632.2009.04813.x
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发表时间：
2009-01-01
期刊：
影响因子：
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通讯作者：
Dumortier, Helene
中科院分区：
文献类型：
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作者：
Lacotte, Stephanie;Brun, Susana;Dumortier, Helene
CXCR 3是G蛋白偶联的七跨膜受体，其结合CXC家族的三种IFN-γ诱导型趋化因子CXCL 9、CXCL 10和CXCL 11并被其激活。这些趋化因子不是组成型表达的，而是在促炎细胞因子环境中上调。因此，它们的主要功能是在炎症部位选择性地招募免疫细胞，但它们也在血管生成机制中发挥作用。在过去的几年中，已经获得了强有力的实验和临床证据，支持CXCR 3途径参与自身免疫性疾病的发展的观点，特别是通过在靶器官中产生炎症的局部放大环，从而诱导临床表现的恶化。本文简要回顾了我们今天所知道的CXCR 3的性质和功能，特别强调其参与两种主要的风湿性系统性自身免疫性疾病，即类风湿性关节炎和系统性红斑狼疮。
CXCR3 is a G protein-coupled, seven-transmembrane receptor that binds and is activated by the three IFN-gamma-inducible chemokines of the CXC family named CXCL9, CXCL10, and CXCL11. These chemokines are not constitutively expressed but are up-regulated in a proinflammatory cytokine milieu. Consequently, their major function is to selectively recruit immune cells at inflammation sites, but they also play a role in angiogenesis mechanisms. In the last few years, strong experimental and clinical evidence has been obtained supporting the idea that the CXCR3 pathway is involved in the development of autoimmune diseases, especially by creating local amplification loops of inflammation in target organs, thereby inducing worsening of clinical manifestations. This article briefly reviews what we know today about the nature and functions of CXCR3, with special emphasis on its involvement in two main rheumatic systemic autoimmune diseases, namely rheumatoid arthritis and systemic lupus erythematosus.