Abstract
Chemokines trigger rapid integrin-dependent lymphocyte arrest to vascular endothelium. We show that the chemokines SLC, ELC, and SDF-1alpha rapidly induce lateral mobility and transient increase of affinity of the beta2 integrin LFA-1. Inhibition of phosphatidylinositol 3-OH kinase (PI(3)K) activity blocks mobility but not affinity changes and prevents lymphocyte adhesion to ICAM-1 immobilized at low but not high densities, suggesting that mobility enhances the frequency of encounters between high-affinity integrin and ligand but that at higher ligand density affinity changes are sufficient for arrest. Thus, chemokines trigger, through distinct signaling pathways, both a high-affinity state and lateral mobility of LFA-1 that can coordinately determine the vascular arrest of circulating lymphocytes under physiologic conditions.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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CD18 Antigens / metabolism
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Cell Adhesion
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Cell Membrane / metabolism
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Cell Movement / physiology*
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Cells, Cultured
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Chemokine CCL19
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Chemokine CCL21
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Chemokine CXCL12
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Chemokines, CC / metabolism*
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Chemokines, CC / pharmacology
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Chemokines, CXC / metabolism*
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Chemokines, CXC / pharmacology
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Endopeptidases / metabolism
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Endothelium, Vascular / metabolism
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Humans
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Intercellular Adhesion Molecule-1 / metabolism
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Lymphocyte Function-Associated Antigen-1 / metabolism*
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Lymphocytes / cytology
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Lymphocytes / drug effects
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Lymphocytes / metabolism
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Lymphocytes / physiology*
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Mice
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Models, Biological
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Peyer's Patches / metabolism
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Phosphatidylinositol 3-Kinases / metabolism
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Time Factors
Substances
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CCL19 protein, human
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CCL21 protein, human
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CD18 Antigens
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CXCL12 protein, human
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Ccl19 protein, mouse
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Ccl21c protein, mouse
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Chemokine CCL19
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Chemokine CCL21
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Chemokine CXCL12
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Chemokines, CC
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Chemokines, CXC
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Cxcl12 protein, mouse
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Lymphocyte Function-Associated Antigen-1
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Intercellular Adhesion Molecule-1
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Phosphatidylinositol 3-Kinases
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Endopeptidases