NORMAL AND PATHOLOGIC MECHANISMS OF INFLAMMATION AND REPAIR

炎症和免疫反应的演变取决于 循环中的白细胞向损伤部位的募集和迁移 或抗原沉积。白细胞的蓄积不是依赖于 不仅取决于发炎部位发出的趋化信号，而且还 促进血管内皮生长因子表达的炎性介质的释放 黏附分子。黏附分子上调促进细胞- 基质相互作用促进循环细胞靶向病变 地点。最近的证据表明，转化生长因子β 为启动趋化反应提供了极强的信号， 这些研究解决了转化生长因子-β影响血管生成的能力。 白细胞与内皮细胞和细胞外基质的必要黏附 在他们前往发炎地点的旅途中。粘附力是通过 代表细胞表面蛋白家族的整合素的表达 介导细胞与其他细胞和细胞外基质的黏附。 这些分子已被证明对血小板聚集、创伤至关重要 愈合、免疫激活、组织修复和肿瘤侵袭。

Evolution of inflammatory and immune reactions is dependent upon the recruitment and migration of circulating leukocytes to the site of injury or antigen deposition. The accumulation of leukocytes is dependent not only on chemotactic signals emanating from the inflammatory site, but also on the release of inflammatory mediators which enhance expression of adhesion molecules. Upregulation of adhesion molecules facilitates cell- matrix interactions to promote targeting of circulating cells to the lesion site. Recent evidence indicates that transforming growth factor beta provides an extremely potent signal for initiating a chemotactic response, and these studies have addressed the ability of TGF-beta to influence the requisite adhesion of leukocytes to endothelium and to extracellular matrix in their journey to the site of inflammation. Adhesion occurs through the expression of integrins which represent a family of cell surface proteins that mediate cell adhesion to other cells and to the extracellular matrix. The molecules have been shown to be vital to platelet aggregation, wound healing, immune activation, tissue repair and in tumor invasion.