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• W2074484064 abstract "Multiple sclerosis (MS) is a chronic autoimmune neurological disease characterized by infiltration of peripheral inflammatory cells to the central nervous system (CNS) and demyelination of CNS white matter. Epidemiological evidence suggests a possible infectious trigger. One potential mechanism by which an infectious agent may trigger MS is via molecular mimicry wherein T cells generated against foreign epitopes cross-react with self-myelin epitopes, such as myelin basic protein (MBP), with sufficient sequence similarity. It has been previously reported that an MBP85–99-reactive T cell clone derived from an MS patient cross-reacted with multiple bacterial-derived mimic peptides in vitro. We show that the same mimic peptides can induce clinical disease in two different strains of mice transgenic for both a human MBP85–99-specific TCR and HLA-DR2 (MHC II), albeit with different disease patterns – relapsing–remitting vs. monophasic. Interestingly, clinical disease correlates with CNS infiltration of CD4+ T cells and F4/80+ macrophages, but not with in vitro proliferative or cytokine responses of splenocytes in response to either MBP85–99 or its mimics." @default.
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• W2074484064 date "2008-12-01" @default.
• W2074484064 modified "2023-10-14" @default.
• W2074484064 title "Differential induction of experimental autoimmune encephalomyelitis by myelin basic protein molecular mimics in mice humanized for HLA-DR2 and an MBP85–99-specific T cell receptor" @default.
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• W2074484064 doi "https://doi.org/10.1016/j.jaut.2008.09.004" @default.
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