内皮在炎症和肿瘤转移中的作用。

G Siegel, M Malmsten
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引用次数: 37

摘要

在炎症中,细胞通过特定的细胞表面受体和粘附分子的时空干预模式与细胞外基质或邻近细胞相互作用。损伤组织的常驻细胞通过细胞因子和直接的细胞间接触与循环效应细胞交流。这些细胞因子刺激内皮细胞表面粘附分子ICAM-1、VCAM-1、E-和p -选择素的表达,并上调管腔白细胞上的β 2整合素和ICAM-1。白细胞粘附在活化的内皮细胞上,通过血管壁迁移,穿透感染区或组织损伤区。细胞免疫应答的基础是由T淋巴细胞和抗原呈递细胞之间的相互作用形成的,抗原呈递细胞通过粘附分子lfa -1,2,3与ICAM-1结合而扩增。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The role of the endothelium in inflammation and tumor metastasis.

In inflammation, cells interact with extracellular matrices or neighboring cells by a spatio-temporal intervention pattern of specific cell surface receptors and adhesion molecules. Resident cells of the injured tissue communicate with circulating effector cells by cytokines and direct cell-cell contact. These cytokines stimulate expression of the adhesion molecules ICAM-1, VCAM-1, and E- and P-selectin on endothelial cell surfaces and upregulate beta 2-integrins and ICAM-1 on luminal leukocytes. White blood cells then adhere to the activated endothelial cells, migrate through the vessel wall, and penetrate areas of infection or tissue damage. The basis for a cellular immune response is formed by the interaction between T lymphocytes and antigen-presenting cells amplified by adhesion molecule LFA-1,2,3 to ICAM-1 binding.

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