HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Drescher, K. M. Articles by Rodriguez, M. Search for Related Content PubMed PubMed Citation Articles by Drescher, K. M. Articles by Rodriguez, M.

TGF-ß2 Reduces Demyelination, Virus Antigen Expression, and Macrophage Recruitment in a Viral Model of Multiple Sclerosis¹

Kristen M. Drescher^2,*,, Paul D. Murray, Xiaoqi Lin^3,*,, Joseph A. Carlino and Moses Rodriguez^4,*,

Departments of ^* Neurology and Immunology, Mayo Clinic/Foundation, Rochester, MN 55905; and Celtrix Pharmaceuticals, Santa Clara, CA 95052

TGF-ß2 is a potent immunoregulatory mediator that influences B cell, T cell, and macrophage function. To test whether this cytokine alters pathology in a model of virus-induced demyelinating disease, we treated SJL/J mice with TGF-ß2 either before or after infection with Theiler’s murine encephalomyelitis virus. Treatment continued three times weekly through day 35 postinfection. TGF-ß2 administration resulted in significantly smaller lesions and fewer virus Ag-positive cells in the spinal cords of infected SJL/J mice. Mice treated with TGF-ß2 had similar levels of virus-specific IgG as infected, control-treated mice. TGF-ß2 administration significantly increased the level of non-virus-specific activated CTLs, but had no effect on virus-specific CTLs. TUNEL revealed a decrease in the number of apoptotic nuclei in the spinal cord white matter of mice treated in vivo with TGF-ß2. Immunostaining with an Ab to F4/80 revealed that TGF-ß2-treated mice had significantly fewer F4/80-positive cells in the white matter of the spinal cord as compared with infected control-treated mice. These data suggest that TGF-ß2 may control virus-induced demyelination via an immunomodulatory mechanism that reduces macrophage infiltration.