Neonatal autoimmune diseases are thought to be due to the transfer of
maternal autoantibodies. However, there is a puzzling lack of correlat
ion between maternal autoantibody titres and disease in the neonate. S
o far, no factor reliably predictive of neonatal disease has been Foun
d. Agalactosyl IgG is a variable feature of normal IgG. Preliminary st
udies 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 d
isease we sought to determine whether this relationship holds true in
a neonatal autoimmune disease. We measured the % agalactosyl IgG in pa
ired 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 tha
n in unaffected neonates. Moreover % agalactosyl IgG was higher in ser
a of affected neonates than in serum from their mothers, while unaffec
ted infants of mothers with myasthenia had %Gal(0) lower than their mo
thers, mimicking the normal situation. This suggests that in affected
neonates a high proportion of the IgG is synthesised by the baby itsel
f rather than derived from the mother. This agrees with previous evide
nce based on the presence of idiotypes not found in the mother which i
mplied that the neonates with neonatal myasthenia gravis produce their
own autoantibodies.