Immune system disturbances in schizophrenia

Szatmár Horváth, Károly Mirnics

Research output: Contribution to journalReview article

83 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)316-323
Number of pages8
JournalBiological Psychiatry
Volume75
Issue number4
DOIs
StatePublished - Feb 15 2014

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Keywords

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

ASJC Scopus subject areas

  • Biological Psychiatry

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