Frontiers in Immunology (Jun 2022)

Aberrant IL-17 Levels in Rodent Models of Autism Spectrum Disorder: A Systematic Review

  • Alexandra Jade Thawley,
  • Luciana Peixoto Veneziani,
  • Luciana Peixoto Veneziani,
  • Luciana Peixoto Veneziani,
  • Luciana Peixoto Veneziani,
  • Francisco Diego Rabelo-da-Ponte,
  • Francisco Diego Rabelo-da-Ponte,
  • Ingo Riederer,
  • Ingo Riederer,
  • Ingo Riederer,
  • Ingo Riederer,
  • Daniella Areas Mendes-da-Cruz,
  • Daniella Areas Mendes-da-Cruz,
  • Daniella Areas Mendes-da-Cruz,
  • Daniella Areas Mendes-da-Cruz,
  • Victorio Bambini-Junior,
  • Victorio Bambini-Junior,
  • Victorio Bambini-Junior

DOI
https://doi.org/10.3389/fimmu.2022.874064
Journal volume & issue
Vol. 13

Abstract

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Autism spectrum disorder (ASD) is a heterogeneous neurodevelopmental disorder characterised by stereotyped behaviours, specific interests, and impaired communication skills. Elevated levels of pro-inflammatory cytokines, such as interleukin-17A (IL-17A or IL-17), have been implicated as part of immune alterations that may contribute to this outcome. In this context, rodent models have helped elucidate the role of T-cell activation and IL-17 secretion in the pathogenesis of ASD. Regarding the preclinical findings, the data available is contradictory in offspring but not in the pregnant dams, pointing to IL-17 as one of the main drivers of altered behaviour in some models ASD, whilst there are no alterations described in IL-17 levels in others. To address this gap in the literature, a systematic review of altered IL-17 levels in rodent models of ASD was conducted. In total, 28 studies that explored IL-17 levels were included and observed that this cytokine was generally increased among the different models of ASD. The data compiled in this review can help the choice of animal models to study the role of cytokines in the development of ASD, seeking a parallel with immune alterations observed in individuals with this condition.Systematic Review RegistrationPROSPERO, identifier CRD42022306558.

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