TGF-β2 reduces demyelination, virus antigen expression, and macrophage recruitment in a viral model of multiple sclerosis

Kristen M. Drescher, Paul D. Murray, Xiaoqi Lin, Joseph A. Carlino, Moses Rodriguez

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Abstract

TGF-β2 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-β2 either before or after infection with Theiler's murine encephalomyelitis virus. Treatment continued three times weekly through day 35 postinfection. TGF-β2 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-β2 had similar levels of virus-specific IgG as infected, control-treated mice. TGF-β2 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-β2. Immunostaining with an Ab to F4/80 revealed that TGF-β2-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-β2 may control virus-induced demyelination via an immunomodulatory mechanism that reduces macrophage infiltration.

Original languageEnglish (US)
Pages (from-to)3207-3213
Number of pages7
JournalJournal of Immunology
Volume164
Issue number6
StatePublished - Mar 15 2000

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ASJC Scopus subject areas

  • Immunology

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Drescher, K. M., Murray, P. D., Lin, X., Carlino, J. A., & Rodriguez, M. (2000). TGF-β2 reduces demyelination, virus antigen expression, and macrophage recruitment in a viral model of multiple sclerosis. Journal of Immunology, 164(6), 3207-3213.