Autism spectrum disorder (ASD) is a neurodevelopmental disorder which begins in early childhood and presents itself with characteristic symptoms such as repetitive behavioral patterns and problems in speech/social interactions. Adaptive immune system is thought to be involved in the etiology of ASD. T cells orchestrate amplification of inflammation through release of inflammatory mediators; however, antioxidant defenses have not been evaluated in CD4+ T cells of ASD subjects. In this study we evaluated intracellular enzymatic antioxidant potential through measurement of major antioxidant enzymes (SOD, GPx, and GR) in ASD subjects and typically developing control (TDC) children and further assessed its role in modulation of inflammation. Our data reveal that there is an increase in antioxidant potential (SOD, GPx, GR) in CD4+ T cells of ASD subjects as compared to TDC children at both protein and activity level. Further, this antioxidant increase was associated with upregulated IL-17A levels in CD4+ T cells. This was corroborated by oxidant treatment in vitro. Pretreatment with oxidant, H₂O₂ led to attenuation of IL-17A levels along with increased oxidative stress in stimulated CD4+ T cells from ASD subjects. These data reveal that antioxidant play an essential role in modulation of inflammatory potential in CD4+ T cells of ASD subjects.

自闭症谱系障碍（ASD）是一种神经发育障碍，始于儿童早期，并表现出特征性症状，例如重复的行为模式和言语/社交互动问题。自适应免疫系统被认为与ASD的病因有关。T细胞通过释放炎症介质来协调炎症的放大；然而，尚未在ASD受试者的CD4 + T细胞中评估抗氧化剂的防御能力。在这项研究中，我们通过测量ASD受试者和通常发育为对照（TDC）儿童的主要抗氧化剂酶（SOD，GPx和GR）来评估细胞内酶抗氧化剂的潜力，并进一步评估其在炎症调节中的作用。我们的数据显示抗氧化剂的潜力有所增加（SOD，GPx，在蛋白质和活性水平上，与TDC儿童相比，ASD受试者CD4 + T细胞中的GR）。此外，这种抗氧化剂的增加与CD4 + T细胞中IL-17A水平的上调有关。氧化剂处理证实了这一点体外。用氧化剂H ₂ O ₂预处理可导致ASD受试者受刺激的CD4 + T细胞中IL-17A水平降低以及氧化应激增加。这些数据表明，抗氧化剂在调节ASD受试者CD4 + T细胞中的炎症潜能中起重要作用。