Lymphotoxin-alpha deficiency completely protects C57BL/6 mice from developing clinical experimental autoimmune myasthenia gravis

A complete prevention of clinical experimental autoimmune myasthenia gravis (EAMG) was observed in lymphotoxin (LT)-α deficient (LT-α −/−) mice compared to LT-α +/+ mice when immunized with acetylcholine receptor. However, only a partial prevention of clinical EAMG incidence was observed in LT-β −/− mice compared to LT-β +/+ mice. LT-α −/−and LT-β −/− 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-α −/−and LT-β −/− 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.