期刊
JOURNAL OF EXPERIMENTAL MEDICINE
卷 200, 期 12, 页码 1571-1580出版社
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.20040965
关键词
inflammation; diapedesis; integrins; adhesion molecules; imaging
资金
- NHLBI NIH HHS [R01 HL072124, HL58467, HL72124, HL-53995, HL54229, R01 HL054229] Funding Source: Medline
- NIDDK NIH HHS [K01 DK062894, DK61379, DK62894, R24 DK064399, DK64399, R01 DK061379] Funding Source: Medline
The leukocyte integrin lymphocyte function-associated antigen 1 (LFA-1) and its endothelial ligand intercellular adhesion molecule (ICAM)-1 play an important role in transmigration as demonstrated by in vivo and in vitro models of inflammation. Despite the prominent role, little is known concerning the distribution and dynamic behavior of these adhesion molecules during leukocyte transmigration. Therefore, we examined the spatial and temporal distribution of LFA-1 on neutrophils actively transmigrating tumor necrosis factor-alpha-activated human umbilical vein endothelial monolayers under shear flow. Upon neutrophil arrest, LFA-1 was evenly distributed. However, once neutrophils initiated transmigration, LFA-1 rapidly redistributed to form a ringlike cluster at the neutrophil-endothelial junctional interface through which transmigration occurred. As transmigration was completed, LFA-1 redistributed to the neutrophil uropod. Endothelial ICAM-1 and JAM-A both colocalized with the ringlike LFA-1 cluster. Further analysis of PMA-stimulated neutrophils, which increase mobility of LFA-1, showed a rapid redistribution of LFA-1 and ICAM-1, but not endothelial JAM-A. Thus, endothelial JAM-A does not appear to contribute to adhesion or transmigration in this system. This is the first demonstration that neutrophil LFA-1 rapidly redistributes to form a ringlike structure that coclusters with endothelial ICAM-1 as the neutrophil transmigrates.
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