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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 (TNF) 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.
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