title: Adoptively transferred EAE in mice bearing the lpr mutation.
abstract: We have recently developed approaches for the generation of encephalitogenic T cell clones from mouse strains considered resistant to experimental allergic encephalomyelitis (EAE). By allowing for the direct use of knockout and mutant strains of mice, such clones allow for the efficient characterization of the relevance of specific gene products in the effector phase of EAE. Recent studies have suggested that Fas/FasL-mediated cell death may play a role in the pathogenesis of MS. To assess the role of Fas/FasL in EAE, we have tested the ability of wild-type C57BL/6-derived, encephalitogenic T cell clones to mediate adoptively transferred EAE in Fas-deficient C57BL/6-lpr mice. We now report that mice with the lpr mutation are fully susceptible to the adoptive transfer of EAE. Our results suggest that Fas/FasL-mediated cell death in the central nervous system does not play an integral role in the effector phase of acute EAE.
authors.affiliation: Division of Rheumatic Diseases, University of Connecticut School of Medicine, Farmington 06032, USA.
authors.forename: R B
authors.initials: RB
authors.lastname: Clark
authors.forename: M
authors.initials: M
authors.lastname: Grunnet
authors.forename: E G
authors.initials: EG
authors.lastname: Lingenheld
mesh_terms: D000208:Acute Disease; D019264:Adoptive Transfer / Q000379:methods*; D000818:Animals; D004195:Disease Models, Animal; D004681:Encephalomyelitis, Autoimmune, Experimental / Q000276:immunology* / Q000473:pathology; D051379:Mice; D008810:Mice, Inbred C57BL; D019463:Mice, Inbred MRL lpr; D018345:Mice, Knockout; D013116:Spinal Cord / Q000473:pathology; D013601:T-Lymphocytes / Q000276:immunology