Departments of Pediatrics, Microbiology/Immunology, and Pathology, Dalhousie University, Halifax, Nova Scotia, Canada
Correspondence: Dr. Thomas B. Issekutz, Department of Pediatrics, Division of Immunology, Rheumatology and Infectious Diseases, IWK Grace Health Center, 5850 University Avenue, Halifax, Nova Scotia, B3J 3G9, Canada. E-mail: tissekutz{at}iwkgrace.ns.ca
Lymphocyte infiltration in inflammation is induced by the dual actions
of chemokines and cell adhesion molecules. The role of LFA-1 and VLA-4
in chemokine-induced T cell transendothelial migration (TEM) across
cytokine-activated endothelium has not been examined. LFA-1, but not
VLA-4, mediated blood T cell TEM to RANTES, macrophage inflammatory
protein-1
(MIP-1), and stromal cell-derived factor-1 (SDF-1), and
across tumor necrosis factor (TNF-) or interferon-
(IFN-)
-stimulated endothelial cells (EC). Chemokine stimulation in
combination with TNF- activation of EC induced TEM, which was
partially mediated by VLA-4. SDF-1 increased a
ß1-integrin activation epitope on T cells and enhanced
VLA-4-mediated adhesion. Thus, LFA-1 mediates TEM under most
conditions, but VLA-4 can also mediate TEM, although, in contrast to
LFA-1, this requires exogenous chemokines and EC activation. In
addition, an LFA-1- and VLA-4-independent pathway of lymphocyte TEM can
also be induced by SDF-1.
Key Words: adhesion molecules • chemotaxis • cytokine • endothelial cells • inflammation
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