| First Author | Goluszko E | Year | 2001 |
| Journal | J Neuroimmunol | Volume | 113 |
| Issue | 1 | Pages | 109-18 |
| PubMed ID | 11137582 | Mgi Jnum | J:102964 |
| Mgi Id | MGI:3608277 | Doi | 10.1016/s0165-5728(00)00420-3 |
| Citation | Goluszko E, et al. (2001) Lymphotoxin-alpha deficiency completely protects C57BL/6 mice from developing clinical experimental autoimmune myasthenia gravis. J Neuroimmunol 113(1):109-18 |
| abstractText | A complete prevention of clinical experimental autoimmune myasthenia gravis (EAMG) was observed in lymphotoxin (LT)-alpha deficient (LT-alpha(-/-)) mice compared to LT-alpha(+/+) mice when immunized with acetylcholine receptor. However, only a partial prevention of clinical EAMG incidence was observed in LT-beta(-/-) mice compared to LT-beta(+/+) mice. LT-alpha(-/-)and LT-beta(-/-) mice had lower mean titers of total IgG, IgG(1), IgG(2a) and IgG(2b) and higher or equal mean titers of IgM anti-AChR antibodies compared to controls. Therefore, LT-alpha(-/-)and LT-beta(-/-) AChR immunized mice are capable of mounting a primary (IgM) humoral immune response to AChR, but are less capable of switching to the pathogenic anti-AChR IgG isotypes. LT could play a significant role in the pathogenesis of myasthenia gravis. |
