Aggravation of experimental autoimmune neuritis in TNF-alpha receptor 1 deficient mice.

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.

• Authors: Ming-Ou Lu, Rui-Sheng Duan, Hernan Concha Quezada, Zhi-Guo Chen, Eilhard Mix, Tao Jin, Xin Yang, Hans-Gustaf Ljunggren, Jie Zhu
• Journal: Journal of neuroimmunology (J Neuroimmunol) Vol. 186 Issue 1-2 Pg. 19-26 (May 2007) ISSN: 0165-5728 [Print] Netherlands
• PMID: 17428547 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Ccr3 protein, mouse
• Histocompatibility Antigens Class II
• Myelin P0 Protein
• Receptors, CCR3
• Receptors, Chemokine
• Receptors, Tumor Necrosis Factor, Type I
• Interleukin-4
• Interferon-gamma
• Thymidine

Topics

• Animals
• Cell Proliferation
• Enzyme-Linked Immunosorbent Assay (methods)
• Flow Cytometry (methods)
• Histocompatibility Antigens Class II (metabolism)
• Immunization (methods)
• Interferon-gamma (metabolism)
• Interleukin-4 (metabolism)
• Leukocytes, Mononuclear (metabolism)
• Mice
• Mice, Inbred C57BL
• Mice, Knockout
• Myelin P0 Protein
• Neuritis, Autoimmune, Experimental (chemically induced, genetics, pathology, physiopathology)
• Receptors, CCR3
• Receptors, Chemokine (metabolism)
• Receptors, Tumor Necrosis Factor, Type I (deficiency)
• Schwann Cells (pathology)
• Severity of Illness Index
• Thymidine (pharmacokinetics)