Comparison of microglia regulatory cytokines and T-helper cytokine levels in children with autism spectrum disorder with healthy controls

Objective: In this study, in order to investigate the role of neuroinflammation in the etiopathogenesis of Autism Spectrum Disorder (ASD), we aimed to evaluate serum levels of IL-34 and CSF-1, IL-12, IFN-γ, IL-4, IL-10, TGF-β, IL-17 and IL-23 and to examine the relationship between these parameters and ASD disease severity. Material and Methods: The sample of this study consisted of 42 children diagnosed with ASD and 40 age- and gender-matched healthy children. Symptom severity of children diagnosed with ASD was evaluated using the Childhood Autism Rating Scale. Serum levels of IL-34, CSF-1, IL-12, IFN-γ, IL-4, IL-10, TGF-β, IL-17 and IL-23 were measured by ELISA. Results: IL-34, CSF-1, IFN-γ, IL-4, IL-10 and IL-17 serum levels were significantly higher in the patient group compared to the control group. IL-34, CSF-1, IFN-γ, IL-4, IL-10 and IL-17 were found to have significant discriminatory power in differentiating ASD (p<0.05). According to the ROC analysis, the highest AUC value belonged to IL-10 (AUC=0.743; p<0.001) and according to the Delong test results, it was found to have a statistically significant stronger discriminative power compared to other parameters. No correlation was found between the analyzed parameters and disease severity. Conclusion: In our study, IL-34 and CSF-1, which are the main regulators of microglial functions, and IFN-γ, IL-4, which are T-helper-associated cytokines that are mostly associated with peripheral inflammation but have recently been reported to have important roles in neuronal functions, The fact that IL-10 and IL-17 were found to be significantly higher in the patient group and that these cytokines showed positive correlations with each other suggests that a complex immune profile may play a role in the etiopathogenesis of ASD and suggests that they may be potential therapeutic targets or biological parameters that can be used in disease follow-up with longitudinal studies. Keywords: ASD, neuroinflammation, microglia, cytokines, t helper, IL-34, CSF-1