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pubmed-article:17428547pubmed:abstractTextThe role of tumor necrosis factor (TNF)-alpha and its receptors in the pathogenesis of experimental autoimmune neuritis (EAN) induced by P0 peptide 180-199 in TNFR1 (p55) deficient (TNFR1-/-) mice was investigated. Compared to wild type EAN mice, TNFR1-/- EAN mice developed significantly more severe clinical signs, in parallel with enhanced numbers of inflammatory infiltrating cells in peripheral nerves and splenic P0-reactive T cell proliferation, as well as increased obviously MHC class II and CCR3 expression on the macrophages in the cauda equina. Our data indicated that TNF-alpha might have anti-inflammatory effect preventing the development of EAN in this mouse model.lld:pubmed
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pubmed-article:17428547pubmed:articleTitleAggravation of experimental autoimmune neuritis in TNF-alpha receptor 1 deficient mice.lld:pubmed
pubmed-article:17428547pubmed:affiliationDivision of Neurodegeneration and Neuroinflammation, Karolinska Institute, Karolinska University Hospital Huddinge, Stockholm, Sweden.lld:pubmed
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