Author/Authors :
Hisanori Umehara، نويسنده , , EdaT. Bloom، نويسنده , , Toshiro Okazaki، نويسنده , , Naochika Domae، نويسنده , , Toshio Imai، نويسنده ,
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 CX3C-chemokine, fractalkine, is expressed on activated endothelial cells, and its receptor, CX3CR1, 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.