Umehara H, Bloom E, Okazaki T, Domae N, Imai T
Dept of Rheumatology and Clinical Immunology, Kyoto University Graduate School of Medicine, 54 Kawahara-cho, Sho-goin, Sakyo-ku, Kyoto 606-8507, Japan.
Trends Immunol. 2001 Nov;22(11):602-7. doi: 10.1016/s1471-4906(01)02051-8.
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.
血管内皮在循环效应细胞募集和迁移至炎症和免疫反应部位的过程中发挥核心作用。独特的CX(3)C趋化因子——fractalkine,在活化的内皮细胞上表达,其受体CX(3)CR1在自然杀伤细胞、单核细胞和一些具有细胞溶解功能的CD8 + T细胞上表达。越来越多的证据表明,fractalkine在肾小球肾炎和心脏移植排斥反应期间在内皮细胞上表达,以及在由促炎细胞因子激活的心脏内皮细胞上表达,这可能为血管损伤的发病机制提供见解。在此,我们提出一个模型,其中fractalkine通过杀伤细胞的积聚和激活介导血管损伤。