Npgrj_ni_1194 497..506
نویسندگان
چکیده
It is widely believed that rolling lymphocytes require successive chemokine-induced signaling for lymphocyte function– associated antigen 1 (LFA-1) to achieve a threshold avidity that will mediate lymphocyte arrest. Using an in vivo model of lymphocyte arrest, we show here that LFA-1-mediated arrest of lymphocytes rolling on high endothelial venules bearing LFA-1 ligands and chemokines was abrupt. In vitro flow chamber models showed that endothelium-presented but not soluble chemokines triggered instantaneous extension of bent LFA-1 in the absence of LFA-1 ligand engagement. To support lymphocyte adhesion, this extended LFA-1 conformation required immediate activation by its ligand, intercellular adhesion molecule 1. These data show that chemokine-triggered lymphocyte adhesiveness involves a previously unrecognized extension step that primes LFA-1 for ligand binding and firm adhesion.
منابع مشابه
Topology Proceedings 4 (1979) pp. 497-506: SHRINKABLE DECOMPOSITIONS, CRITERIA AND GENERALIZATIONS
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تاریخ انتشار 2005