| First Author | Kalush F | Year | 1992 |
| Journal | Am J Reprod Immunol | Volume | 28 |
| Issue | 3-4 | Pages | 264-8 |
| PubMed ID | 1285898 | Mgi Jnum | J:4731 |
| Mgi Id | MGI:53214 | Doi | 10.1111/j.1600-0897.1992.tb00811.x |
| Citation | Kalush F, et al. (1992) Neonatal lupus erythematosus in offspring of mothers with experimental systemic lupus erythematosus. Am J Reprod Immunol 28(3-4):264-8 |
| abstractText | Neonatal lupus erythematosus (NLE) syndrome is a result of the transfer of autoantibodies produced by the mother, across the placenta, to the fetus. NLE is characterized by a transient dermatitis, a variety of systemic and hematological abnormalities, and isolated cases of congenital heart block. The latter has been reported to be due to the presence of autoantibodies specific to La (SS-B) and/or Ro (SS-A). As female mice with experimental SLE, induced by immunization with the monoclonal anti-DNA 16/6 Id, produce a variety of autoantibodies including anti-Ro and anti-La antibodies, we examined the relevance of NLE in the murine system. Offspring of SLE-afflicted BALB/c mothers possessed antibody titers to the 16/6 Id, ssDNA, and nuclear extract, which gradually declined until reduced to normal levels by day 60 after delivery. Antibody titers in the sera of the mothers remained elevated throughout this period. Electrocardiograms were recorded from groups of neonates from mothers with experimental SLE. The results indicated that a high percentage of the offspring had defects in their conduction system including first, second, and third degree heart block; significant bradycardia; and wide QRS complex. Normal patterns were observed in offspring of healthy mothers. Experiments done with mice that were exposed to SLE-related autoantibodies early in their development indicated that offspring to mothers with experimental SLE were neither protected nor more susceptible to disease induction by the 16/6 Id. |
