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Maternal Antibodies and the Placental–Fetal IgG Transfer Theory

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Autism

Part of the book series: Current Clinical Neurology ((CCNEU))

Abstract

We hypothesize that maternal autoimmunity is a contributing factor to etiology in up to 40% of pregnancies that lead to autism. More specifically, we propose that the transplacental transfer of maternal antibodies to the fetus alters fetal brain development, and, on a background of genetic susceptibility, ultimately leads to the postnatal emergence of autism. Circumstantial evidence for this hypothesis includes human studies showing that maternal autoimmune disorders can adversely affect fetal brain development, as well as studies of human leukocyte antigens (HLA). To date, two groups of investigators have identified differential patterns of specific antibodies directed to human fetal brain in sera from mothers of children with autistic disorder (MCAD) as compared with mothers of unaffected children. In both studies, specific maternal antibodies correlated with the presence of developmental regression in offspring. Lastly, the pregnant dam mouse model has shown that MCAD IgG can cross the placenta, enter embryonic brain, induce an immune response, and cause behavioral changes. In this chapter, we review circumstantial and direct evidence for, and future requirements necessary to confirm, the placental–fetal IgG transfer theory.

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Morris, C.M., Pletnikov, M., Zimmerman, A.W., Singer, H.S. (2008). Maternal Antibodies and the Placental–Fetal IgG Transfer Theory. In: Autism. Current Clinical Neurology. Humana Press. https://doi.org/10.1007/978-1-60327-489-0_14

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  • DOI: https://doi.org/10.1007/978-1-60327-489-0_14

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