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Related Experiment Video

Updated: Jun 6, 2026

Derivation, Expansion, Cryopreservation and Characterization of Brain Microvascular Endothelial Cells from Human Induced Pluripotent Stem Cells

Derivation, Expansion, Cryopreservation and Characterization of Brain Microvascular Endothelial Cells from Human Induced Pluripotent Stem Cells

Published on: November 19, 2020

Immune System and Schizophrenia.

Norbert Müller¹, Markus J Schwarz

¹Department of Psychiatry and Psychotherapy Ludwig-Maximilians-Universität Munchen, Germany.

Current Immunology Reviews

|November 9, 2010

Summary

This summary is machine-generated.

Schizophrenia involves immune dysfunction, specifically altered tryptophan metabolism leading to increased kynurenic acid. Antipsychotics may rebalance this immune imbalance, and COX-2 inhibitors show promise for treating schizophrenia.

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Area of Science:

Neuroimmunology
Psychiatry

Background:

Immune dysfunction and infectious agents are implicated in schizophrenia pathophysiology.
A blunted type-1 immune response and dysregulated indoleamine 2,3-dioxygenase (IDO) activity characterize schizophrenia.
This leads to altered tryptophan-kynurenine metabolism and increased kynurenic acid production.

Purpose of the Study:

To explore the role of immune dysregulation in schizophrenia.
To investigate the link between tryptophan metabolism, kynurenic acid, and glutamatergic neurotransmission.
To assess the immunological effects of antipsychotics and the potential of COX-2 inhibitors.

Main Methods:

Analysis of immune response in schizophrenia.
Examination of tryptophan-kynurenine metabolism and kynurenic acid levels.
Review of antipsychotic effects and clinical trials of COX-2 inhibitors.

Main Results:

Schizophrenia is associated with a blunted type-1 immune response and dysregulated IDO, increasing kynurenic acid.
Increased kynurenic acid contributes to glutamatergic neurotransmission imbalance and NMDA antagonism.
Antipsychotics partially restore immune balance and reduce kynurenic acid overproduction.
Inflammatory state with increased prostaglandin E(2) (PGE(2)) and cyclo-oxygenase-2 (COX-2) expression is observed.

Conclusions:

Immune imbalance and altered kynurenine pathway are key in schizophrenia.
Targeting COX-2 may offer a novel therapeutic strategy for schizophrenia.