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Functional implications of the IL-23/IL-17 immune axis in schizophrenia
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.
History
Journal
Molecular neurobiologyVolume
54Issue
10Pagination
8170 - 8178Publisher
SpringerLocation
Berlin, GermanyPublisher DOI
eISSN
1559-1182Language
engPublication classification
C Journal article; C1 Refereed article in a scholarly journalCopyright notice
2016, SpringerUsage metrics
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Categories
Keywords
ComplementCytokinesGut microbiotaIL-23\/IL-17 axisImmuneInflammationSchizophreniaTh17 cellsScience & TechnologyLife Sciences & BiomedicineNeurosciencesNeurosciences & NeurologyHELPER 17 CELLSINFLAMMATORY MARKERSDOUBLE-BLINDBACTERIAL TRANSLOCATIONANKYLOSING-SPONDYLITISN-ACETYLCYSTEINECYTOKINE PROFILEATOPIC DISORDERSTH17 PATHWAY