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Biol Psychiatry. 2014 Feb 15;75(4):316-23. doi: 10.1016/j.biopsych.2013.06.010. Epub 2013 Jul 25.

Immune system disturbances in schizophrenia.

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  • 1Department of Psychiatry, Vanderbilt University, Nashville, Tennessee; Department of Psychiatry, University of Szeged, 6725 Szeged, Hungary.
  • 2Department of Psychiatry, Vanderbilt University, Nashville, Tennessee; Vanderbilt Kennedy Center for Research on Human Development, Vanderbilt University, Nashville, Tennessee; Department of Psychiatry, University of Szeged, 6725 Szeged, Hungary. Electronic address: karoly.mirnics@vanderbilt.edu.

Abstract

Epidemiological, genetic, transcriptome, postmortem, peripheral biomarker, and therapeutic studies of schizophrenia all point to a dysregulation of both innate and adaptive immune systems in the disease, and it is likely that these immune changes actively contribute to disease symptoms. Gene expression disturbances in the brain of subjects with schizophrenia show complex, region-specific changes with consistently replicated and potentially interdependent induction of serpin peptidase inhibitor, clade A member 3 (SERPINA3) and interferon inducible transmembrane protein (IFITM) family transcripts in the prefrontal cortex. Recent data suggest that IFITM3 expression is a critical mediator of maternal immune activation. Because the IFITM gene family is primarily expressed in the endothelial cells and meninges, and because the meninges play a critical role in interneuron development, we suggest that these two non-neuronal cell populations might play an important role in the disease pathophysiology. Finally, we propose that IFITM3 in particular might be a novel, appealing, knowledge-based drug target for treatment of schizophrenia.

Copyright © 2014 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved.

KEYWORDS:

Blood-brain barrier; CD14; CHI3L1; IFITM; IFITM3; SERPINA3; blood vessels; immune; meninges; pia mater; postmortem; schizophrenia

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