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Nat Med. 2009 Jan;15(1):91-6. doi: 10.1038/nm.1892. Epub 2008 Dec 14.

Neurotoxic autoantibodies mediate congenital cortical impairment of offspring in maternal lupus.

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  • 1Albert Einstein College of Medicine, Department of Microbiology & Immunology, Bronx, NY 10461, USA.

Abstract

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, we hypothesized that maternally transferred autoantibodies that bind DNA and the N-methyl-D-aspartate receptor (NMDAR) 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.

PMID:
19079257
[PubMed - indexed for MEDLINE]
PMCID:
PMC2615794
Free PMC Article

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