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

Monojit Debnath, Michael Berk

Research output: Contribution to journalReview ArticleResearchpeer-review

16 Citations (Scopus)


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.

Original languageEnglish
Pages (from-to)8170-8178
Number of pages9
JournalMolecular Neurobiology
Issue number10
Publication statusPublished - Dec 2017
Externally publishedYes


  • Complement
  • Cytokines
  • Gut microbiota
  • IL-23/IL-17 axis
  • Immune
  • Inflammation
  • Schizophrenia
  • Th17 cells

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