| First Author | Wang L | Year | 2012 |
| Journal | J Exp Med | Volume | 209 |
| Issue | 6 | Pages | 1083-9 |
| PubMed ID | 22565825 | Mgi Jnum | J:189050 |
| Mgi Id | MGI:5444101 | Doi | 10.1084/jem.20111986 |
| Citation | Wang L, et al. (2012) Female mouse fetal loss mediated by maternal autoantibody. J Exp Med 209(6):1083-9 |
| abstractText | 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. |
