Abstract
Interleukin-23 (IL-23) is a survival factor for a newly described population of T lymphocytes, namely Th-17 cells, that secrete IL-17, tumor necrosis factor- alpha (TNFα) and IL-6. It has been shown that Th-17 cells are a pathogenic T cell subset involved in autoimmune and chronic inflammatory diseases. Based on the increasing evidence of immune dysfunction in autism, including possible autoimmune and inflammatory processes, we hypothesized that Th-17 cells, a T cell lineage that has not been previously examined in this disorder, may be altered in autism. To assess the potential role, if any, of Th-17 cells in autism, we analyzed plasma samples obtained from children ranging in age from 2-5 years with a diagnosis of autism and age-matched typically developing controls for the presence of IL-17 and IL-23 cytokines. Plasma samples from 40 children with autism including 20 children with a regressive form of autism, 20 with early onset and no regression and 20 typically developing age-matched control children were analyzed for IL-17 and IL-23, under the hypothesis that altered number and function of Th-17 cells would directly correlate with altered levels of IL-17 and IL-23 in the plasma. In this study, we were able to demonstrate that IL-23 cytokine levels were significantly different in children with autism compared with age-matched controls, a finding primarily driven by children with early onset autism. In contrast, there were no statistical differences in IL-17 levels autism compared with age-matched typically developing controls. This is the first study to report altered IL-23 production in autism. The decreased plasma IL-23 production observed in children with autism warrants further research as to its affect on the generation and survival of Th-17 cells, a subset important in neuroinflammatory conditions that may include autism.
Highlights
Autism (AU) is a neurodevelopmental disorder This suggests that the immune system in some children presenting in early childhood with specific social and with autism may be dysregulated
The occurrence and timing of regression has led to an interest in early life infectious and environmental exposures that occur within this same period and have been hypothesized to abnormalities include increased inflammatory cytokines in the plasma and CNS, neuroinflammatory cytokine interleukin-6 (IL-6)[4, 5], proinflammatory cytokine tumor necrosis factor alpha (TNF )[4,5,6] and play a role in the genesis of autism disorder
Since IFN, which is increased in many chronic inflammatory and autoimmune disease models, induces production of IL-12, Th1 cells were interpreted as playing a decisive role in disease pathogenesis; a more pivotal role may be attributable to IL-23 production[17, 26, 27]
Summary
Autism (AU) is a neurodevelopmental disorder This suggests that the immune system in some children presenting in early childhood with specific social and with autism may be dysregulated. Recent evidence suggests that Th-17 cells may be involved in development of autoimmune and inflammatory disease and its potential role in autism warrants investigation. Th-17 cells produce the cytokines IL-6 and TNF , which have been shown to be increased in subjects with autism[4,5,6].
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