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MBC in Press, published online ahead of print May 4, 2005
Mol. Biol. Cell 10.1091/mbc.E04-12-1049

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Submitted on December 3, 2004
Accepted on April 27, 2005

Vav1 and Rac Control Chemokine-promoted T Lymphocyte Adhesion Mediated by the Integrin {alpha}4{beta}1

David García-Bernal,* Natalia Wright,* Elena Sotillo-Mallo,* César Nombela-Arrieta,{dagger}{ddagger} Jens V. Stein,{dagger}{ddagger} Xosé R. Bustelo,{sect} and Joaquin Teixidó*

*Department of Immunology, Centro de Investigaciones Biológicas, CSIC, 28006 Madrid, Spain; {dagger}Department of Immunology and Oncology, Centro Nacional de Biotecnología, CSIC-Pfizer, 28049 Madrid, Spain; {sect}Centro de Investigación del Cáncer, CSIC, 37007 Salamanca, Spain

Monitoring Editor: Mark Ginsberg

The chemokine CXCL12 promotes T lymphocyte adhesion mediated by the integrin {alpha}4{beta}1. CXCL12 activates the GTPase Rac, as well as Vav1, a guanine-nucleotide exchange factor for Rac, concomitant with upregulation of {alpha}4{beta}1-dependent adhesion. Inhibition of CXCL12-promoted Rac and Vav1 activation by transfection of dominant negative Rac or Vav1 forms, or by transfection of their siRNA, remarkably impaired the increase in T lymphocyte attachment to {alpha}4{beta}1 ligands in response to this chemokine. Importantly, inhibition of Vav1 expression by RNA interference resulted in a blockade of Rac activation in response to CXCL12. Adhesions in flow chambers and soluble binding assays using these transfectants indicated that initial ligand binding and adhesion strengthening mediated by {alpha}4{beta}1 were dependent on Vav1 and Rac activation by CXCL12. Finally, CXCL12-promoted T-cell transendothelial migration involving {alpha}4{beta}1-mediated adhesion was notably inhibited by expression of dominant negative Vav1 and Rac. These results indicate that activation of Vav1-Rac signaling pathway by CXCL12 represents an important inside-out event controlling efficient upregulation of {alpha}4{beta}1-dependent T lymphocyte adhesion.

{ddagger}Present address: Theodor Kocher Institute, University of Bern, Freiestrasse 1, 3012 Bern, Switzerland.

Address correspondence to: Joaquin Teixidó (joaquint{at}cib.csic.es)




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