Agalactosyl IgG and materno-fetal transmission of autoimmune neonatal lupus

Rheumatol Int. 1996;16(3):89-94. doi: 10.1007/BF01409979.


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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Autoantibodies / blood
  • Autoantigens / immunology
  • Autoimmune Diseases / immunology*
  • Female
  • Humans
  • Immunoglobulin G / blood*
  • Infant, Newborn
  • Lupus Erythematosus, Systemic / immunology*
  • Maternal-Fetal Exchange
  • Pregnancy
  • Pregnancy Complications / immunology*
  • RNA, Small Cytoplasmic*
  • Ribonucleoproteins / immunology
  • Tetanus Toxoid / immunology


  • Autoantibodies
  • Autoantigens
  • Immunoglobulin G
  • RNA, Small Cytoplasmic
  • RO60 protein, human
  • Ribonucleoproteins
  • SS-A antigen
  • SS-B antigen
  • Tetanus Toxoid
  • agalactosyl IGG