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Clinical and Diagnostic Laboratory Immunology, July 2003, p. 564-572, Vol. 10, No. 4
1071-412X/03/$08.00+0     DOI: 10.1128/CDLI.10.4.564-572.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

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

Diane L. Sewell,1 Emily K. Reinke,1 Dominic O. Co,1 Laura H. Hogan,1 Robert B. Fritz,2 Matyas Sandor,1 and Zsuzsa Fabry1*

Department of Pathology and Laboratory Medicine, University of Wisconsin,1 Department of Microbiology, Medical College of Wisconsin, Milwaukee, Wisconsin2

Received 5 December 2002/ Returned for modification 14 February 2003/ Accepted 2 April 2003

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-Guérin (BCG) to study this possibility. C57BL/6 mice infected with live BCG for 6 weeks were immunized with myelin oligodendroglial glycoprotein peptide (MOG35-55) 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 MOG35-55-specific green fluorescent protein-expressing cells into BCG-infected animals indicated that nervous tissue-specific (MOG35-55) 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.

* Corresponding author. Mailing address: Department of Pathology, University of Wisconsin, 1300 University Ave., 6130 MSC, Madison, WI 53706. Phone: (608) 265-8716. Fax: (608) 265-3301. E-mail: zfabry{at}facstaff.wisc.edu.

Clinical and Diagnostic Laboratory Immunology, July 2003, p. 564-572, Vol. 10, No. 4
1071-412X/03/$08.00+0     DOI: 10.1128/CDLI.10.4.564-572.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



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