| First Author | Goluszko E | Year | 2002 |
| Journal | J Neuroimmunol | Volume | 122 |
| Issue | 1-2 | Pages | 85-93 |
| PubMed ID | 11777546 | Mgi Jnum | J:102961 |
| Mgi Id | MGI:3608274 | Doi | 10.1016/s0165-5728(01)00474-x |
| Citation | Goluszko E, et al. (2002) Tumor necrosis factor receptor p55 and p75 deficiency protects mice from developing experimental autoimmune myasthenia gravis. J Neuroimmunol 122(1-2):85-93 |
| abstractText | The precise pathogenic role of proinflammatory cytokines belonging to the tumor necrosis factor (TNF) family has not been investigated yet in antibody-mediated myasthenia gravis (MG) and experimental autoimmune myasthenia gravis (EAMG). In this study we report that TNF receptor p55(-/-) p75(-/-) mice were resistant to the development of clinical EAMG induced by acetylcholine receptor (AChR) immunizations. The resistance was associated with reduced serum levels of IgG, IgG(1), IgG(2a), and IgG(2b) anti-AChR antibody isotypes. However, IgM anti-AChR antibodies were not reduced, suggesting defective anti-AChR IgG class switching in TNF receptor p55(-/-) p75(-/-) mice. We thus demonstrate the genetic evidence for the role of TNF receptor p55 and p75 in EAMG pathogenesis, and their requirement for the generation of anti-AChR IgG antibodies. |
