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More MS news articles for July 2003

Infection with Mycobacterium bovis BCG Diverts Traffic of Myelin Oligodendroglial Glycoprotein Autoantigen-Specific T Cells Away from the Central Nervous System and Ameliorates Experimental Autoimmune Encephalomyelitis

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12853387&dopt=Abstract

Clin Diagn Lab Immunol. 2003 Jul;10(4):564-72
Sewell DL, Reinke EK, Co DO, Hogan LH, Fritz RB, Sandor M, Fabry Z.
Department of Pathology and Laboratory Medicine, University of Wisconsin. Department of Microbiology, Medical College of Wisconsin, Milwaukee, Wisconsin.

Infectious agents have been proposed to influence susceptibility to autoimmune diseases such as multiple sclerosis.

We induced a Th1-mediated central nervous system (CNS) autoimmune disease, experimental autoimmune encephalomyelitis (EAE) in mice with an ongoing infection with Mycobacterium bovis strain bacillus Calmette-Guerin (BCG) to study this possibility.

C57BL/6 mice infected with live BCG for 6 weeks were immunized with myelin oligodendroglial glycoprotein peptide (MOG(35-55)) to induce EAE.

The clinical severity of EAE was reduced in BCG-infected mice in a BCG dose-dependent manner.

Inflammatory-cell infiltration and demyelination of the spinal cord were significantly lessened in BCG-infected animals compared with uninfected EAE controls.

ELISPOT and gamma interferon intracellular cytokine analysis of the frequency of antigen-specific CD4(+) T cells in the CNS and in BCG-induced granulomas and adoptive transfer of MOG(35-55)-specific green fluorescent protein-expressing cells into BCG-infected animals indicated that nervous tissue-specific (MOG(35-55)) CD4(+) T cells accumulate in the BCG-induced granuloma sites.

These data suggest a novel mechanism for infection-mediated modulation of autoimmunity.

We demonstrate that redirected trafficking of activated CNS antigen-specific CD4(+) T cells to local inflammatory sites induced by BCG infection modulates the initiation and progression of a Th1-mediated CNS autoimmune disease.