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.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Cell Proliferation
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Enzyme-Linked Immunosorbent Assay / methods
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Flow Cytometry / methods
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Histocompatibility Antigens Class II / metabolism
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Immunization / methods
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Interferon-gamma / metabolism
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Interleukin-4 / metabolism
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Leukocytes, Mononuclear / metabolism
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Mice
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Mice, Inbred C57BL
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Mice, Knockout
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Myelin P0 Protein
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Neuritis, Autoimmune, Experimental / chemically induced
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Neuritis, Autoimmune, Experimental / genetics*
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Neuritis, Autoimmune, Experimental / pathology*
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Neuritis, Autoimmune, Experimental / physiopathology*
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Receptors, CCR3
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Receptors, Chemokine / metabolism
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Receptors, Tumor Necrosis Factor, Type I / deficiency*
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Schwann Cells / pathology
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Severity of Illness Index
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Thymidine / pharmacokinetics
Substances
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Ccr3 protein, mouse
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Histocompatibility Antigens Class II
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Myelin P0 Protein
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Receptors, CCR3
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Receptors, Chemokine
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Receptors, Tumor Necrosis Factor, Type I
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Interleukin-4
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Interferon-gamma
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Thymidine