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Rheumatol Int. 1996;16(3):89-94.

Agalactosyl IgG and materno-fetal transmission of autoimmune neonatal lupus.

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Department of Medical Microbiology, UCL Medical School, London, UK.


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.

[Indexed for MEDLINE]

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