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J Exp Med. 2012 Jun 4;209(6):1083-9. doi: 10.1084/jem.20111986. Epub 2012 May 7.

Female mouse fetal loss mediated by maternal autoantibody.

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  • 1Center for Autoimmune and Musculoskeletal Diseases, The Feinstein Institute for Medical Research, NorthShore–Long Island Jewish Health System, Manhasset, NY 11030, USA.


Systemic lupus erythematosus (SLE), a disease of women during childbearing years, is characterized by the production of double-stranded DNA antibodies. A subset of these antibodies, present in 40% of patients, cross-reacts with the NR2A and NR2B subunits of the N-methyl-d-aspartate receptor (NMDAR). In this study, we show that, in mouse models, these antibodies cause a loss of female fetus viability by inducing apoptosis of NR2A-expressing neurons within the brainstem late in fetal development; gender specificity derives from a time-dependent increased expression of NR2A in female brainstem or increased vulnerability of female fetal neurons to signaling through NR2A-containing NMDARs. This paradigm is consistent with available data on the sex ratio of live births of women with SLE. It represents a novel mechanism by which maternal autoantibodies can severely affect fetal health in a gender-specific fashion and raises the question of how many maternal antibodies affect brain development or exhibit gender-specific fetal effects.

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