The discovery that immune dysfunction may underpin autism's most challenging symptoms represents a paradigm shift from viewing the condition as purely neurological. This finding opens new therapeutic avenues targeting the immune system rather than just behavioral interventions. Analysis of regulatory T cells from 36 children with autism spectrum disorder revealed profound alterations in these critical immune suppressors compared to 18 typically developing peers. These Tregs showed disrupted expression of 213 genes, with particular changes in cells programmed to migrate to gut tissues. Children with both autism and gastrointestinal symptoms displayed the most severe immune abnormalities, suggesting a mechanistic link between digestive problems and core autism features. The dysregulated genes clustered around chromatin organization and metabolic processes, including lipid metabolism and coenzyme A synthesis pathways. These molecular signatures indicate Tregs in autistic children may struggle to maintain normal immune tolerance, potentially allowing chronic inflammation to persist in both brain and gut tissues. This immune-gut-brain connection aligns with emerging research showing how intestinal inflammation can influence neurological development and behavior. However, the study's observational design cannot establish whether immune dysfunction causes autism symptoms or results from them. The relatively small cohort also limits generalizability across the autism spectrum's heterogeneous presentations. Still, identifying specific molecular targets within the immune system provides concrete pathways for developing immunomodulatory treatments that could address both the neurological and gastrointestinal manifestations of autism simultaneously.