Demyelination induced by T cell lines and clones specific for myelin basic protein in mice.

Neuropathological studies were performed in order to investigate experimental allergic encephalomyelitis induced by long-term cultured T cell lines and clones specific for myelin basic protein, which were established from SJL/J and DDD/1 mice. All antigen-activated T line or clone cells induced similar disease in euthymic and athymic mice with a common I-A haplotype. The lesion was characterized by perivascular and parenchymal infiltration of mononuclear cells with abundant polymorphonuclear cells located mainly in the lower spinal cord. Axons were severely affected and decreased in number. However, demyelination was present in all cases and was especially marked when recipient mice were: given whole-body X-ray irradiation, I-A compatible other strains, or were congenitally athymic. Topographically, demyelinated axons were most prominent in the root exit and entry zones of the lower spinal cord. Repeated transfer or relapse did not seem to be the factor responsible for enhancing demyelination. We conclude that: inflammation with axonal damage is the main feature of murine experimental allergic encephalomyelitis induced by myelin basic protein-specific T cell lines and clones, demyelination definitely occurs under certain conditions and in certain areas especially at the root exit and entry zones in nude mice, and a single T cell clone induces experimental allergic encephalomyelitis lesions associated with demyelination without the aid of interaction with another recipient-derived T cell population.