http://www.ncbi.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12133983&dopt=Abstract

J Immunol 2002 Aug 1;169(3):1550-5
Haring JS, Pewe LL, Perlman S.
Departments of. Microbiology and Pediatrics, University of Iowa, Iowa City, IA 52242.

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.