Abstract
Neither the incidence nor the severity of neonatal autoimmune disease correlates with maternal or neonatal autoantibody titres. However, there is now evidence that the agalactosyl [Gal(0)] fractions of autoantibodies are the most pathogenic. We found that systemic lupus erythematosus (SLE) mothers whose infants developed congenital heart block (CHB) had higher %Gal(0) at the end of pregnancy than did mothers of unaffected infants (P < 0.05) or control mothers (P < 0.01). Similarly, affected infants had higher %Gal(0) than control infants (P < 0.01). Then we studied the Gal(0) content of the anti-Ro and we found that it was higher in affected neonates than in unaffected neonates (P < 0.05), though there was no difference between the corresponding groups of mothers by this criterion. We propose that agalactosyl IgG may have a regulatory or effector role and that the risk of neonates developing maternal autoantibody-mediated disorders may be related to the quantity of agalacotsyl autoantibody present at birth, rather than to its absolute titre.
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