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Bystander CD8 T cell-mediated demyelination after viral infection of the central nervous system
Journal article   Peer reviewed

Bystander CD8 T cell-mediated demyelination after viral infection of the central nervous system

Jodie S Haring, Lecia L Pewe and Stanley Perlman
Journal of immunology (Baltimore, Md. : 1950), Vol.169(3), pp.1550-1555
08/01/2002
DOI: 10.4049/jimmunol.169.3.1550
PMID: 12133983

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Abstract

Multiple sclerosis, a chronic inflammatory disease of the CNS, is characterized by immune-mediated demyelination. Many patients have a remitting-relapsing course of disease with exacerbations often following unrelated microbial illnesses. The relationship between the two events remains obscure. One possibility is that T cells specific for the inciting microbial pathogen are able to effect demyelination at a site of ongoing inflammation within the CNS. This possibility was examined in mice infected with mouse hepatitis virus, a well-described model of virus-induced demyelination. Using transgenic TCR/recombination activation gene 2(-/-) mice with only non-mouse hepatitis virus-specific T cells, we show that CD8 T cells are able to cause demyelination in the absence of cognate Ag in the CNS, but only if specifically activated. These findings demonstrate a novel mechanism for immune-mediated neuropathology and show that activated CD8 T cells may serve as important mediators of bystander demyelination during times of infection, including in patients with multiple sclerosis.
Central Nervous System Viral Diseases - complications Chemokines - biosynthesis Lymphocyte Activation Mice, Inbred C57BL Bystander Effect Demyelinating Autoimmune Diseases, CNS - immunology Murine hepatitis virus Animals Coronavirus Infections - complications Demyelinating Autoimmune Diseases, CNS - etiology Mice Multiple Sclerosis - etiology CD8-Positive T-Lymphocytes - immunology Homeodomain Proteins - physiology Cytokines - biosynthesis

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