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The Journal of Immunology, 2001, 167: 2824-2830.
Copyright © 2001 by The American Association of Immunologists

The Affinity of Integrin {alpha}4{beta}1 Governs Lymphocyte Migration1

David M. Rose*, Valentin Grabovsky{dagger}, Ronen Alon{dagger} and Mark H. Ginsberg2,*

* Department of Vascular Biology, The Scripps Research Institute, La Jolla, CA 92037; and {dagger} Department of Immunology, Weizmann Institute of Science, Rehovot, Israel

The interaction of integrin {alpha}4{beta}1 with endothelial VCAM-1 controls the trafficking of lymphocytes from blood into peripheral tissues. Cells actively regulate the affinity of {alpha}4{beta}1 for VCAM-1 (activation). To investigate the biological function of {alpha}4{beta}1 activation, we isolated Jurkat T cell lines with defective {alpha}4{beta}1 activation. Using these cells, we found that {alpha}4{beta}1-stimulated {alpha}L{beta}2-dependent cell migration was dramatically reduced in cells with defects in {alpha}4{beta}1 activation. These cells required 20 times more VCAM-1 to promote {alpha}L{beta}2-dependent cell migration. This defect was at the level of {alpha}4{beta}1 affinity as an activating {alpha}4{beta}1 Ab rescued {alpha}4{beta}1-stimulated {alpha}L{beta}2-dependent migration. In contrast, migration of {alpha}4{beta}1 activation-defective cells on VCAM-1 alone was enhanced at higher VCAM-1 densities. Thus, {alpha}4{beta}1 activation determines a set point or threshold at which VCAM-1 can regulate {alpha}L{beta}2-dependent as well as {alpha}4{beta}1-dependent cell migration. Changes in this set point may specify preferred anatomical sites of integrin-dependent leukocyte emigration from the bloodstream.




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