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Published online before print October 10, 2007
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and
β T cells in experimental autoimmune encephalomyelitis
,1
Departments of
* Microbiology and
Neurology, University of Alabama at Birmingham, Birmingham, Alabama, USA
1 Correspondence: Department of Microbiology, University of Alabama at Birmingham, 845 19th St. S., BBRB/842, Birmingham, AL 35294, USA. E-mail: sbarnum{at}uab.edu
ABSTRACT
The expression of β2-integrins on 
T cells in naïve mice or those with experimental autoimmune encephalomyelitis (EAE) remains poorly characterized. We compared β2-integrin expression and cytokine production between 
and
β T cells over the acute course of EAE. We observed that unlike in
β T cells, β2-integrin expression on 
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-
- and TNF-
-producing 
T cells infiltrated the CNS rapidly and produced significantly more of these cytokines than
β T cells throughout the course of EAE. These results suggest unique roles for β2-integrins in the trafficking of 
versus
β T cells during EAE and that 
T cells infiltrate the CNS rapidly, producing cytokines, which modulate acute disease.
Key Words: adhesion molecules demyelinating disease neuroimmunology
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