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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.

Publication ,  Journal Article
Sewell, DL; Reinke, EK; Co, DO; Hogan, LH; Fritz, RB; Sandor, M; Fabry, Z
Published in: Clinical and diagnostic laboratory immunology
July 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 (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.

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Published In

Clinical and diagnostic laboratory immunology

DOI

EISSN

1098-6588

ISSN

1071-412X

Publication Date

July 2003

Volume

10

Issue

4

Start / End Page

564 / 572

Related Subject Headings

  • Tuberculosis
  • Tuberculoma
  • Th1 Cells
  • Peptide Fragments
  • Myelin-Oligodendrocyte Glycoprotein
  • Myelin-Associated Glycoprotein
  • Myelin Proteins
  • Mycobacterium bovis
  • Microbiology
  • Mice, Inbred C57BL
 

Citation

APA
Chicago
ICMJE
MLA
NLM
Sewell, D. L., Reinke, E. K., Co, D. O., Hogan, L. H., Fritz, R. B., Sandor, M., & Fabry, Z. (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. Clinical and Diagnostic Laboratory Immunology, 10(4), 564–572. https://doi.org/10.1128/cdli.10.4.564-572.2003
Sewell, Diane L., Emily K. Reinke, Dominic O. Co, Laura H. Hogan, Robert B. Fritz, Matyas Sandor, and Zsuzsa Fabry. “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.Clinical and Diagnostic Laboratory Immunology 10, no. 4 (July 2003): 564–72. https://doi.org/10.1128/cdli.10.4.564-572.2003.
Sewell, Diane L., et al. “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.Clinical and Diagnostic Laboratory Immunology, vol. 10, no. 4, July 2003, pp. 564–72. Epmc, doi:10.1128/cdli.10.4.564-572.2003.

Published In

Clinical and diagnostic laboratory immunology

DOI

EISSN

1098-6588

ISSN

1071-412X

Publication Date

July 2003

Volume

10

Issue

4

Start / End Page

564 / 572

Related Subject Headings

  • Tuberculosis
  • Tuberculoma
  • Th1 Cells
  • Peptide Fragments
  • Myelin-Oligodendrocyte Glycoprotein
  • Myelin-Associated Glycoprotein
  • Myelin Proteins
  • Mycobacterium bovis
  • Microbiology
  • Mice, Inbred C57BL