Major histocompatibility complex i in brain development and schizophrenia

Research output: Contribution to journalArticle

65 Citations (Scopus)

Abstract

Although the etiology of schizophrenia (SZ) remains unknown, it is increasingly clear that immune dysregulation plays a central role. Genome-wide association studies reproducibly indicate an association of SZ with immune genes within the major histocompatibility complex (MHC). Moreover, environmental factors that increase risk for SZ, such as maternal infection, alter peripheral immune responses as well as the expression of immune molecules in the brain. MHC class I (MHCI) molecules might mediate both genetic and environmental contributions to SZ through direct effects on brain development in addition to mediating immunity. MHCI molecules are expressed on neurons in the central nervous system throughout development and into adulthood, where they regulate many aspects of brain development, including neurite outgrowth, synapse formation and function, long-term and homeostatic plasticity, and activity-dependent synaptic refinement. This review summarizes our current understanding of MHCI expression and function in the developing brain as well as its involvement in maternal immune activation, from the perspective of how these roles for MHCI molecules might contribute to the pathogenesis of SZ.

Original languageEnglish (US)
Pages (from-to)262-268
Number of pages7
JournalBiological Psychiatry
Volume75
Issue number4
DOIs
StatePublished - Feb 15 2014

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Major Histocompatibility Complex
Schizophrenia
Brain
Mothers
Genome-Wide Association Study
Synapses
Immunity
Central Nervous System
Neurons
Infection
Genes

Keywords

  • Cytokines
  • infection
  • maternal immune activation
  • neuroimmunology
  • synapse formation
  • synaptic plasticity

ASJC Scopus subject areas

  • Biological Psychiatry

Cite this

Major histocompatibility complex i in brain development and schizophrenia. / Usrey, A Kimberley.

In: Biological Psychiatry, Vol. 75, No. 4, 15.02.2014, p. 262-268.

Research output: Contribution to journalArticle

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