NEUTROPHIL MAC-1 AND MEL-14 ADHESION PROTEINS INVERSELY REGULATED BY CHEMOTACTIC FACTORS
NEUTROPHIL MAC-1 AND MEL-14 ADHESION PROTEINS INVERSELY REGULATED BY CHEMOTACTIC FACTORS
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DOI：
10.1126/science.2551036
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发表时间：
1989-09-15
期刊：
影响因子：
56.9
通讯作者：
BUTCHER, EC
中科院分区：
文献类型：
--
作者：
KISHIMOTO, TK;JUTILA, MA;BUTCHER, EC
中性粒细胞Mac-1和gp 100 MEL-14粘附蛋白参与炎症过程中的中性粒细胞外渗。中性粒细胞活化后Mac-1的表达和活性均显著增加。相反，中性粒细胞脱落gp 100 MEL-14从细胞表面4分钟内用趋化因子或佛波醇酯激活后，释放96千道尔顿的抗原片段到上清液中。免疫组织学显示，gp 100 MEL 14在已经外渗到发炎组织中的中性粒细胞上下调。gp 100 MEL-14粘附蛋白可能参与未活化的中性粒细胞与内皮的结合; gp 100 MEL-14的快速脱落可能防止活化的中性粒细胞外渗到正常组织中并损伤正常组织。
The neutrophil Mac-1 and gp100MEL-14 adhesion proteins are involved in neutrophil extravasation during inflammation. Both the expression and activity of Mac-1 are greatly increased after neutrophil activation. In contrast, neutrophils shed gp100MEL-14 from the cell surface within 4 minutes after activation with chemotactic factors or phorbol esters, releasing a 96-kilodalton fragment of the antigen into the supernatant. Immunohistology showed that gp100MEL14 was downregulated on neutrophils that had extravasated into inflamed tissue. The gp100MEL-14 adhesion protein may participate in the binding of unactivated neutrophils to the endothelium; rapid sheddding of gp100MEL-14 may prevent extravasation into and damage of normal tissues by activated neutrophils.