Decreased resistance to bacterial infection and granulocyte defects in IAP-deficient mice
Decreased resistance to bacterial infection and granulocyte defects in IAP-deficient mice
复制标题
DOI：
10.1126/science.274.5288.795
复制
发表时间：
1996-11-01
期刊：
影响因子：
56.9
通讯作者：
Brown, EJ
中科院分区：
文献类型：
--
作者：
Lindberg, FP;Bullard, DC;Brown, EJ
粒细胞[多形核白细胞（PMN）]迁移到感染部位并随后激活是宿主防御所必需的。整合素相关蛋白（IAP，也称为CD 47）基因靶向小鼠在接种时死于大肠杆菌腹膜炎，杂合子同窝出生的小鼠存活。在体内，他们有一个早期的缺陷，在感染部位的PMN积累。在体外，IAP（-/-）PMN缺乏β（3）整合素依赖性配体结合、氧化爆发活化和Fc受体介导的吞噬作用。因此，IAP在宿主防御中起着关键作用，它既参与了细菌感染引起的PMN迁移，又参与了血管外部位的PMN激活。
Granulocyte [polymorphonuclear leucocyte (PMN)] migration to sites of infection and subsequent activation is essential for host defense. Gene-targeted mice deficient for integrin-associated protein (IAP, also termed CD47) succumbed to Escherichia coli peritonitis at inoccula survived by heterozygous littermates. In vivo, they had an early defect in PMN accumulation at the site of infection. In vitro, IAP(-/-) PMNs were deficient in beta(3) integrin-dependent ligand binding, activation oi an oxidative burst, and Fc receptor-mediated phagocytosis. Thus, IAP plays a key role in host defense by participating both in PMN migration in response to bacterial infection and in PMN activation at extravascular sites.