NDLI: Transmigration of neutrophils across inflamed endothelium is signaled through LFA-1 and Src family kinase.

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Transmigration of neutrophils across inflamed endothelium is signaled through LFA-1 and Src family kinase.

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Transmigration of neutrophils across inflamed endothelium is signaled through LFA-1 and Src family kinase.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Sarantos, Melissa R. Zhang, Hong Lowell, Clifford A. Schaff, Ulrich Y. Hayenga, Heather N. Simon, Scott I. Dixit, Neha
Description	Country affiliation: United States Author Affiliation: Sarantos MR ( Department of Biomedical Engineering, University of California, Davis, CA 95616, USA.)
Abstract	Leukocyte capture on inflamed endothelium is facilitated by a shift in LFA-1 from low to high affinity that supports binding to ICAM-1. LFA-1 bonds help anchor polymorphonuclear leukocytes (PMN) to inflamed endothelium in shear flow, and their redistribution to the leading edge guides pseudopod formation, migration, and extravasation. These events can be disrupted at the plasma membrane by stabilizing LFA-1 in a low- or intermediate-affinity state with allosteric small molecules. We hypothesized that a minimum dimeric bond formation between high-affinity LFA-1 and ICAM-1 under shear stress is necessary to catalyze transmembrane signaling of directed cell migration. Microspheres and substrates were derivatized with monomeric or dimeric ICAM-1 to simulate the surface of inflamed endothelium under defined ligand valence. Binding to dimeric ICAM-1, and not monomeric ICAM-1, was sufficient to elicit assembly of F-actin and phosphorylation of Src family kinases that colocalized with LFA-1 on adherent PMN. Genetic deletion or small molecule inhibition of Src family kinases disrupted their association with LFA-1 that correlated with diminished polarization of arrested PMN and abrogation of transmigration on inflamed endothelium. We conclude that dimeric bond clusters of LFA-1/ICAM-1 provide a key outside-in signal for orienting cytoskeletal dynamics that direct PMN extravasation at sites of inflammation.
ISSN	00221767
e-ISSN	15506606
Journal	The Journal of Immunology
Issue Number	12
Volume Number	181
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2008-12-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Cell Movement Immunology Endothelium, Vascular Pathology Inflammation Mediators Physiology Lymphocyte Function-associated Antigen-1 Neutrophils Signal Transduction Src-family Kinases Actins Blood Metabolism Animals Cell Adhesion Cell Aggregation Cell Line Cells, Cultured Dimerization Enzymology Intercellular Adhesion Molecule-1 Mice Mice, Inbred C57bl Mice, Knockout Phosphorylation Protein Binding Research Support, N.i.h., Extramural Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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