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Fractalkine and vascular injury
H Umehara1, E Bloom, T Okazaki
1Dept of Rheumatology and Clinical Immunology, Kyoto University Graduate School of Medicine, 54 Kawahara-cho, Sho-goin, Sakyo-ku, Kyoto 606-8507, Japan. umehara@kuhp.kyoto-u.ac.jp
Abstract:
The vascular endothelium plays a central role in the recruitment and migration of circulating effector cells into sites of inflammation and immune responses. The unique CX(3)C-chemokine, fractalkine, is expressed on activated endothelial cells, and its receptor, CX(3)CR1, is expressed on natural killer cells, monocytes and some CD8+ T cells, all of which possess cytolytic function. Accumulating evidence that fractalkine is expressed on endothelial cells during glomerulonephritis and cardiac allograft rejection, as well as on cardiac endothelial cells activated by pro-inflammatory cytokines, might provide insight into the pathogenesis of vascular injury. Here, we propose a model in which fractalkine mediates vascular injury through the accumulation and activation of killer cells.