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Review
. 2023 Dec 1:12:e3109.
doi: 10.31661/gmj.v12i.3109. eCollection 2023.

Schizophrenia Etiological Factors and Their Correlation with the Imbalance of the Immune System: An Update

Affiliations
Review

Schizophrenia Etiological Factors and Their Correlation with the Imbalance of the Immune System: An Update

Noushin Lotfi et al. Galen Med J. .

Abstract

Schizophrenia (SZ) is a severe psychiatric disorder associated with a dysregulation of the immune system. Immune-related genes and environmental factors including stress, food, infections, and microbiota, alter the immune system's homeostasis and play a role in SZ pathogenesis. The most distinctive feature in the pathophysiology of the disease is a shift in the T helper 1(Th1)/Th2 balance toward Th2 dominance in the immune system. Also, microglial and Th17 cell activation cause inflammatory responses in the central nervous system (CNS). Antibodies play a role in the pathophysiology of SZ and give more evidence of a link between humoral immune reactivity and the disease. Accordingly, an imbalance in cytokine activities and neuroinfl ammation has been considered the main contributor to the pathogenesis of the SZ. Overall, the deregulation of the immune system caused by genetic, environmental, and neurochemical effects may all play a role in the etiology of SZ. This review summarized the etiological factors for SZ and discussed the role of immune responses and their interaction with genetic and environmental factors in SZ pathogenesis.

Keywords: Environmental Factors; Genes; Immune System; Inflammation; Schizophrenia.

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Conflict of interest statement

None.

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References

    1. Howell KR, Law AJ. Neurodevelopmental concepts of schizophrenia in the genome-wide association era: AKT/mTOR signaling as a pathological mediator of genetic and environmental programming during development. Schizophrenia research. 2020;(217):95–104. - PMC - PubMed
    1. Pergola G, Papalino M, Gelao B, Sportelli L, Vollerbergh W, Grattagliano I. Evocative gene-environment correlation between genetic risk for schizophrenia and bullying victimization. World psychiatry. 2019;3(18):366–366. - PMC - PubMed
    1. Torrey EF, Yolken RH. Schizophrenia as a pseudogenetic disease: A call for more gene-environmental studies. Psychiatry Res. 2019;(278):146–50. - PubMed
    1. Van Kesteren, Gremmels H, De Witte, Hol E, Van Gool, Falkai P. Immune involvement in the pathogenesis of schizophrenia: a meta-analysis on postmortem brain studies. Transl Psychiatry. 2017;3(7):e1075–e1075. - PMC - PubMed
    1. Wang L-Y, Chen S-F, Chiang J-H, Hsu C-Y, Shen Y-C. Autoimmune diseases are associated with an increased risk of schizophrenia: a nationwide population-based cohort study. Schizophr Res. 2018;(202):297–302. - PubMed

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