CD8-deficient SJL mice display enhanced susceptibility to Theiler's virus infection and increased demyelinating pathology

摘要: Theiler’s murine encephalomyelitis virus (TMEV) infection of the central nervous system (CNS) induces a chronic, progressive demyelinating disease in susceptible mouse strains characterized by inflammatory mononuclear infiltrates and spastic hind limb paralysis. Our lab has previously demonstrated critical role for TMEV- myelin-specific CD4+ T cells initiating perpetuating this pathology. It however, also been shown that MHC class I loci are associated with susceptibility/resistance to TMEV persistence. For reason, we investigated contribution CD8+ TMEV-induced pathology highly SJL/J strain. Here show β2M-deficient SJL mice have similar incidence rates wild-type controls, however earlier onset clinical disease, elevated vitro responses myelin proteolipid (PLP) epitopes, significantly higher levels CNS demyelination macrophage infiltration at 50 days post-infection. displayed significant elevation persisting viral titers, as well an increase macrophage-derived pro-inflammatory cytokine mRNA expression spinal cord same time point. Taken together, these results indicate not required or histologic initiation progression TMEV-infected mice. Rather, data stress capacity further emphasize potential contribute protection from demyelination.