Induction of relapsing paralysis in experimental autoimmune encephalomyelitis by bacterial superantigen

摘要: THE role of infection in the pathogenesis clinical relapses that occur most autoimmune diseases, including multiple sclerosis, remains to be established1,2. Experimental encephalomyelitis (EAE) serves as a model for with episodes relapsing paralysis3–9. In certain strains mice, T-lym-phocytes expressing V/β8 T-cell receptor (TCR)6–8 engage amino-terminal epitope Ac 1–11 myelin basic protein, leading EAE. The bacterial superantigen staphylococcal enterotoxin B (SEB) activates V/β8-expressing T cells. Here we show after immunization 1–11, or transfer encephalitogenic lines clones reactive Acl-11, SEB induces exacerbation paralytic disease mice are remission following an initial episode paralysis, and triggers paralysis subclinical disease. Tumour necrosis factor has critical mechanism underlying SEB-induced disease, because anti-tumour antibody given vivo delays onset triggered by SEB. On reactivation autoaggressive cells through their receptor, superantigens may induce