期刊
NATURE MEDICINE
卷 15, 期 1, 页码 91-96出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/nm.1892
关键词
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资金
- US National Institutes of Health
- Alliance for Lupus Research
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [P01AI073693] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES [R01AR049126] Funding Source: NIH RePORTER
Systemic lupus erythematosus (SLE) is an autoimmune disease mediated by autoantibodies and preferentially affecting women of childbearing age. Because the offspring of mothers with SLE show a high frequency of learning disorders(1-5), we hypothesized that maternally transferred autoantibodies that bind DNA and the N-methyl-D-aspartate receptor (NMDAR)(6-12) could have a pathogenic role during fetal brain development. Here we describe a maternal SLE mouse model wherein pregnant dams harbored DNA-specific, NMDAR-specific autoantibodies throughout gestation. High titers of these autoantibodies in maternal circulation led to histological abnormalities in fetal brain and subsequent cognitive impairments in adult offspring. These data support a paradigm in which in utero exposure to neurotoxic autoantibodies causes abnormal brain development with long-term consequences. This paradigm may apply to multiple congenital neuropsychiatric disorders.
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