Lymphocyte transcellular migration occurs through recruitment of endothelial ICAM-1 to caveola- and F-actin-rich domains

被引:307
作者
Millán, J
Hewlett, L
Glyn, M
Toomre, D
Clark, P
Ridley, AJ
机构
[1] Royal Free & Univ Coll Sch Med, Ludwig Inst Canc Res, London W1W 7BS, England
[2] UCL, Dept Biochem & Mol Biol, London WC1E 6BT, England
[3] UCL, MRC, Mol Cell Biol Lab, London WC1E 6BT, England
[4] Univ London Imperial Coll Sci Technol & Med, Natl Heart & Lung Inst, London SW7 2AZ, England
[5] Yale Univ, Sch Med, Dept Cell Biol, Ludwig Inst Canc Res, New Haven, CT 06520 USA
关键词
D O I
10.1038/ncb1356
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
During inflammation, leukocytes bind to the adhesion receptors ICAM-1 and VCAM-1 on the endothelial surface before undergoing transendothelial migration, also called diapedesis. ICAM-1 is also involved in transendothelial migration, independently of its role in adhesion, but the molecular basis of this function is poorly understood. Here we demonstrate that, following clustering, apical ICAM-1 translocated to caveolin-rich membrane domains close to the ends of actin stress fibres. In these F-actin- rich areas, ICAM-1 was internalized and transcytosed to the basal plasma membrane through caveolae. Human T-lymphocytes extended pseudopodia into endothelial cells in caveolin- and F-actin-enriched areas, induced local translocation of ICAM-1 and caveolin-1 to the endothelial basal membrane and transmigrated through transcellular passages formed by a ring of F-actin and caveolae. Reduction of caveolin-1 levels using RNA interference (RNAi) specifically decreased lymphocyte transcellular transmigration. We propose that the translocation of ICAM-1 to caveola- and F-actin-rich domains links the sequential steps of lymphocyte adhesion and transendothelial migration and facilitates lymphocyte migration through endothelial cells from capillaries into surrounding tissue.
引用
收藏
页码:113 / U5
页数:15
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