Journal of Leukocyte Biology
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A more recent version of this article appeared on January 1, 2008

Published online before print October 10, 2007
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© by The Society for Leukocyte Biology
Journal of Leukocyte Biology, doi:10.1189/jlb.0407263

Received for publication April 27, 2007.
Revised August 22, 2007.
Accepted for publication September 17, 2007.

Article

Differential expression of {beta}2-integrins and cytokine production between {gamma}{delta} and {alpha}{beta} T cells in experimental autoimmune encephalomyelitis

Sherry S. Smith and Scott R. Barnum @

Departments of Microbiology and Neurology, University of Alabama at Birmingham, Birmingham, Alabama, USA

@ To whom correspondence should be addressed. E-mail: sbarnum{at}uab.edu.


  Abstract

The expression of {beta}2-integrins on {gamma}{delta} T cells in naïve mice or those with experimental autoimmune encephalomyelitis (EAE) remains poorly characterized. We compared {beta}2-integrin expression and cytokine production between {gamma}{delta} and {alpha}{beta} T cells over the acute course of EAE. We observed that unlike in {alpha}{beta} T cells, {beta}2-integrin expression on {gamma}{delta} T cells increased significantly from baseline, peaked at Day 10, and remained unchanged in the draining lymph nodes or declined in the spleen and CNS by Day 15. In addition, IFN-{gamma}- and TNF-{alpha}-producing {gamma}{delta} T cells infiltrated the CNS rapidly and produced significantly more of these cytokines than {alpha}{beta} T cells throughout the course of EAE. These results suggest unique roles for {beta}2-integrins in the trafficking of {gamma}{delta} versus {alpha}{beta} T cells during EAE and that {gamma}{delta} T cells infiltrate the CNS rapidly, producing cytokines, which modulate acute disease.

Key Words: adhesion molecules • demyelinating disease • neuroimmunology






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