Prevention of experimental autoimmune myasthenia gravis in rats by fetal alpha-fetoprotein-rich fractions.

Rats immunized with Torpedo acetylcholine receptor (AChR) developed experimental autoimmune myasthenia gravis (EAMG) manifested by an early acute phase and a late chronic phase. In the animals the acute and the chronic diseases were prevented by the administration of alpha-fetoprotein (AFP)-rich fractions obtained from human amniotic fluid and umbilical cord serum. Both the clinical and the electromyographic manifestations of EAMG was affected by AFP treatment. The anti-AChR antibody level as well as the cellular immune response to AChR were also affected by AFP. Rats immunized with Torpedo AChR and treated with AFP-rich fractions showed low levels of antibodies to rat AChR, and an inhibited proliferation response of lymphocytes to the antigen AChR. The addition of AFP in vitro to the lymphocyte culture significantly inhibited the proliferative response to AChR and to the mitogen phytohemagglutinin. AFP is present in high amounts during pregnancy, and therefore the present findings suggest that clinical remissions of myasthenia gravis during the second half of pregnancy may be attributed to the immunosuppressive effect of AFP.