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Journal of Biomedicine and Biotechnology
Volume 2010 (2010), Article ID 576318, 12 pages
Review Article

Evidence for Maternal-Fetal Genotype Incompatibility as a Risk Factor for Schizophrenia

Departments of Psychiatry, and Biobehavioral Sciences and Human Genetics, UCLA Semel Institute, 760 Westwood Plaza, Room 47-422, Los Angeles, CA 90095, USA

Received 17 September 2009; Revised 9 February 2010; Accepted 20 February 2010

Academic Editor: Robert Elston

Copyright © 2010 Christina G. S. Palmer. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Prenatal/obstetric complications are implicated in schizophrenia susceptibility. Some complications may arise from maternal-fetal genotype incompatibility, a term used to describe maternal-fetal genotype combinations that produce an adverse prenatal environment. A review of maternal-fetal genotype incompatibility studies suggests that schizophrenia susceptibility is increased by maternal-fetal genotype combinations at the RHD and HLA-B loci. Maternal-fetal genotype combinations at these loci are hypothesized to have an effect on the maternal immune system during pregnancy which can affect fetal neurodevelopment and increase schizophrenia susceptibility. This article reviews maternal-fetal genotype incompatibility studies and schizophrenia and discusses the hypothesized biological role of these ‘‘incompatibility genes’’. It concludes that research is needed to further elucidate the role of RHD and HLA-B maternal-fetal genotype incompatibility in schizophrenia and to identify other genes that produce an adverse prenatal environment through a maternal-fetal genotype incompatibility mechanism. Efforts to develop more sophisticated study designs and data analysis techniques for modeling maternal-fetal genotype incompatibility effects are warranted.