Umehara Hisanori, Tanaka Masao, Sawaki Toshioki, Jin Zhe-Xiong, Huang Cheng-Ri, Dong Lingli, Kawanami Takafumi, Karasawa Hiromi, Masaki Yasufumi, Fukushima Toshihiro, Hirose Yuko, Okazaki Toshirou
Division of Hematology and Immunology, Department of Internal Medicine, Kanazawa Medical University, Daigaku, Uchinada-machi, Kahoku-gun, Ishikawa, 920-0293, Japan.
Mod Rheumatol. 2006;16(3):124-30. doi: 10.1007/s10165-006-0471-9.
Leukocyte adhesion and trafficking at the endothelium requires both adhesion molecules and chemotactic factors. Fractalkine (CX3C) is a unique chemokine, and is expressed on tumor necrosis factor-alpha- and interleukin-1-activated endothelial cells (ECs). Fractalkine receptor, CX3CR1, is expressed on NK cells, monocytes, and some portion of CD4- and CD8-positive T cells. Interactions between fractalkine and CX3CR1 can mediate not only chemotaxis, but also cell adhesion in the absence of substrates for other adhesion molecules. Furthermore, fractalkine activates NK cells, leading to increased cytotoxicity and interferon-gamma production. Recently, accumulating evidence has shown that fractalkine is involved in the pathogenesis of rheumatoid arthritis and allied conditions. This review examines new concepts underlying fractalkine-mediated leukocyte migration and tissue damage, focusing primarily on the pathophysiological roles of fractalkine in rheumatic diseases.
白细胞在内皮细胞处的黏附和迁移需要黏附分子和趋化因子。趋化因子（CX3C）是一种独特的趋化因子，在肿瘤坏死因子-α和白细胞介素-1激活的内皮细胞（ECs）上表达。趋化因子受体CX3CR1在自然杀伤细胞、单核细胞以及部分CD4和CD8阳性T细胞上表达。趋化因子与CX3CR1之间的相互作用不仅可以介导趋化作用，还可以在缺乏其他黏附分子底物的情况下介导细胞黏附。此外，趋化因子可激活自然杀伤细胞，导致细胞毒性增加和干扰素-γ产生。最近，越来越多的证据表明趋化因子参与类风湿关节炎及相关病症的发病机制。本综述探讨了趋化因子介导白细胞迁移和组织损伤的新概念，主要关注趋化因子在风湿性疾病中的病理生理作用。
