| First Author | Lu MO | Year | 2007 |
| Journal | J Neuroimmunol | Volume | 186 |
| Issue | 1-2 | Pages | 19-26 |
| PubMed ID | 17428547 | Mgi Jnum | J:124562 |
| Mgi Id | MGI:3721862 | Doi | 10.1016/j.jneuroim.2007.02.004 |
| Citation | Lu MO, et al. (2007) Aggravation of experimental autoimmune neuritis in TNF-alpha receptor 1 deficient mice. J Neuroimmunol 186(1-2):19-26 |
| abstractText | 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. |
