During angiogenesis, vascular endothelial growth factor and basic fibroblast growth factor regulate natural killer cell adhesion to tumor endothelium
During angiogenesis, vascular endothelial growth factor and basic fibroblast growth factor regulate natural killer cell adhesion to tumor endothelium
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DOI：
10.1038/nm0996-992
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发表时间：
1996-09-01
期刊：
影响因子：
82.9
通讯作者：
Jain, RK
中科院分区：
文献类型：
--
作者：
Melder, RJ;Koenig, GC;Jain, RK
活化的自然杀伤（A-NK）细胞在生长肿瘤的微脉管系统中的定位是识别肿瘤内皮上的细胞内和血管细胞粘附分子ICAM-1和VCAM-1的结果，其由淋巴细胞功能相关蛋白LFA-1和血管淋巴细胞功能相关蛋白VLA-4介导。A-NK细胞与内皮细胞粘附的体外和体内研究表明，血管内皮生长因子（VEGF）促进粘附，而碱性成纤维细胞生长因子（bFGF）通过调节这些分子对肿瘤血管系统的影响抑制粘附。因此，一些血管生成因子可以促进淋巴细胞识别血管生成血管，而其他因子可以为这些血管提供保护它们免受细胞毒性淋巴细胞的机制。
Localization of activated natural killer (A-NK) cells in the microvasculature of growing tumors is the result of recognition of the intracellular and vascular cell-adhesion molecules ICAM-1 and VCAM-1 on the tumor endothelium, mediated by lymphocyte function-associated protein LFA-1 and vascular lymphocyte function-associated protein VLA-4. In vitro and in vivo studies of A-NK cell adhesion to endothelial cells showed that vascular endothelial growth factor (VEGF) promotes adhesion, whereas basic fibroblast growth factor (bFGF) inhibits adhesion through the regulation of these molecules on tumor vasculature. Thus, some angiogenic factors may facilitate lymphocyte recognition of angiogenic vessels, whereas others may provide such vessels with a mechanism that protects them from cytotoxic lymphocytes.