Maternal and fetal antibrain antibodies in development and disease.
Recent evidence has emerged indicating that the maternal immune response can have a substantial deleterious impact on prenatal development (Croen et al., [2008]: Biol Psychiatry 64:583-588). The maternal immune response is largely sequestered from the fetus. Maternal antibodies, specifically immunoglobulin G (IgG), are passed to the fetus to provide passive immunity throughout much of pregnancy. However, both protective and pathogenic autoantibodies have equal access to the fetus (Goines and Van de Water [2010]: Curr Opin Neurol 23:111-117). If the mother has an underlying autoimmune disease or has reactivity to fetal antigens, autoantibodies produced before or during pregnancy can target tissues in the developing fetus. One such tissue is the fetal brain. The blood brainbarrier (BBB) is developing during the fetal period allowing maternal antibodies to have direct access to the brain during gestation (Diamond et al. [2009]: Nat Rev Immunol; Braunschweig et al. [2011]; Neurotoxicology 29:226-231). It has been proposed that brain injury by circulating brain-specific maternal autoantibodies might underlie multiple congenital, developmental disorders (Lee et al. [2009]: Nat Med 15:91-96). In this review, we will discuss the current state of research in the area of maternal autoantibodies and the development of autism.
Department of Internal Medicine, University of California, Davis, Davis, California 95616, USA.
Elizabeth
E
Fox
David
D
Amaral
Judy
J
Van de Water
D000818:Animals; D001321:Autistic Disorder / Q000276:immunology*; D001323:Autoantibodies / Q000009:adverse effects* / Q000276:immunology; D001921:Brain / Q000196:embryology* / Q000276:immunology*; D005260:Female; D005333:Fetus / Q000276:immunology; D006801:Humans; D008431:Maternal-Fetal Exchange / Q000276:immunology; D011247:Pregnancy
D001323:Autoantibodies