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Functional Implications of the IL-23/IL-17 Immune Axis in Schizophrenia

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Abstract

The aetiology of schizophrenia seems to stem from complex interactions amongst environmental, genetic, metabolic, immunologic and oxidative components. Chronic low-grade inflammation has been persistently linked to schizophrenia, and this has primarily been based on the findings derived from Th1/Th2 cytokine balance. While the IL-23/IL-17 axis plays crucial role in the pathogenesis of several immune-mediated disorders, it has remained relatively unexplored in neuropsychiatric disorders. Altered levels of cytokines related to IL-23/IL-17 axis have been observed in schizophrenia patients in a few studies. In addition, other indirect factors known to confer schizophrenia risk like complement activation and altered gut microbiota are shown to modulate the IL-23/IL-17 axis. These preliminary observations provide crucial clues about the functional implications of IL-23/IL-17 axis in schizophrenia. In this review, an attempt has been made to highlight the biology of IL-23/IL-17 axis and its relevance to schizophrenia risk and pathogenesis. Given the pathogenic potential of the IL-23/IL-17 axis, therapeutic targeting of this axis may be a promising approach to benefit patients suffering from this devastating disorder.

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Acknowledgements

MB is supported by an NHMRC Senior Principal Research Fellowship 1059660.

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Correspondence to Monojit Debnath.

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Debnath, M., Berk, M. Functional Implications of the IL-23/IL-17 Immune Axis in Schizophrenia. Mol Neurobiol 54, 8170–8178 (2017). https://doi.org/10.1007/s12035-016-0309-1

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