Neonatal
autoimmune diseases are thought to be due to the transfer of maternal
autoantibodies. However, there is a puzzling lack of correlation between maternal
autoantibody titres and disease in the neonate. So far, no factor reliably predictive of
neonatal disease has been found.
Agalactosyl IgG is a variable feature of normal
IgG. Preliminary studies indicated that the percentage of
agalactosyl IgG is lower in the serum of normal neonates, than in the serum of the mother at delivery. Since raised %
agalactosyl IgG is often associated with
autoimmune disease we sought to determine whether this relationship holds true in a neonatal
autoimmune disease. We measured the %
agalactosyl IgG in paired maternal-cord sera from patients with
myasthenia gravis, some of whom had offspring with
neonatal myasthenia gravis. We found that the percentage of
agalactosyl IgG was significantly higher in affected than in unaffected neonates. Moreover %
agalactosyl IgG was higher in sera of affected neonates than in serum from their mothers, while unaffected infants of mothers with myasthenia had %Gal(0) lower than their mothers, mimicking the normal situation. This suggests that in affected neonates a high proportion of the
IgG is synthesised by the baby itself rather than derived from the mother. This agrees with previous evidence based on the presence of idiotypes not found in the mother which implied that the neonates with
neonatal myasthenia gravis produce their own
autoantibodies.