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.