Abstract
The role of tumor necrosis factor (TNF)-α 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-α might have anti-inflammatory effect preventing the development of EAN in this mouse model.
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