Influence of alpha-fetoprotein on the in vitro and in vivo immune response to acetylcholine receptor.

Alpha-fetoprotein (AFP) derived from amniotic fluid and both maternal and umbilical cord sera but not from hepatoma, blocks the binding of serum acetylcholine receptor (AChR) antibody from patients with myasthenia gravis (MG) and animals with experimental autoimmune MG (EAMG) to AChR preparations as measured by a radioimmunoassay. AFP also inhibits the AChR and mitogen induced in vitro proliferative response of lymphocytes obtained from animals with EAMG. Laboratory animals repeatedly injected with AFP fail to develop EAMG in response to sensitization with AChR. Animals with established EAMG show clinical improvement in response to AFP treatment. AChR antibodies are suppressed in such AFP-treated animals. AFP is present in increased amounts during pregnancy and thus could contribute to remissions during the second half of pregnancy in patients with MG. The rapid decrease in levels of AFP during the post-partum period may also be partly responsible for relapses seen during this period. AFP may also be responsible for the appearance of transitory neonatal MG only sometime after birth and in only a minority of cases.