REVIEW ARTICLE
Fractalkine in rheumatoid arthritis and allied conditions
Authors
Hisanori Umehara1, Masao Tanaka1, 2, Toshioki Sawaki1, Zhe-Xiong Jin1, Cheng-Ri Huang1, Lingli Dong1, Takafumi Kawanami1, Hiromi Karasawa1, Yasufumi Masaki1, Toshihiro Fukushima1, Yuko Hirose1 and Toshirou Okazaki3
| (1) |
Division of Hematology and Immunology, Department of Internal Medicine, Kanazawa Medical University, Daigaku, Uchinada-machi, Kahoku-gun, Ishikawa 920-0293, Japan |
| (2) |
Department of Rheumatology and Clinical Immunology, Kyoto University Graduate School of Medicine, Kyoto, Japan |
| (3) |
Department of Clinical Laboratory, Medicine/Hematology, Faculty of Medicine, Tottori University, Tottori, Japan |
Received:
24 February 2006
>Accepted:
14 March 2006
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Abstract
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-α- 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-γ 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.
Key words
Chemokines - Fractalkine (CX3C) - Inflammation - Rheumatic disease - Vascular biology
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