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Updated: Jul 15, 2026
Induction of Experimental Autoimmune Encephalomyelitis in Mice and Evaluation of the Disease-dependent Distribution of Immune Cells in Various Tissues
Published on: May 8, 2016
Aggravation of experimental autoimmune neuritis in TNF-alpha receptor 1 deficient mice
Ming-Ou Lu1, Rui-Sheng Duan, Hernan Concha Quezada
1Division of Neurodegeneration and Neuroinflammation, Karolinska Institute, Karolinska University Hospital Huddinge, Stockholm, Sweden.
Abstract:
The 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.
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