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首页> 外文期刊>Cellular Signalling >S3I-201, a selective Stat3 inhibitor, restores neuroimmune function through upregulation of Treg signaling in autistic BTBR T+ Itpr3(tf)/J mice
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S3I-201, a selective Stat3 inhibitor, restores neuroimmune function through upregulation of Treg signaling in autistic BTBR T+ Itpr3(tf)/J mice

机译：S3I-201，一种选择性Stat3抑制剂，通过在自闭症BTBR T + ITPR3（TF）/ J小鼠中的Treg信号传导的上调来恢复神经影响功能

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Autism spectrum disorder (ASD) is a neurodevelopmental disorder whose symptoms include communication deficits, a lack of social skills, and stereotyped repetitive behaviors. We used BTBR T+ Itpr3(tf)/J (BTBR) mice, a model that demonstrates most of the core behavioral features of ASD, such as decreased sociability and high levels of repetitive behaviors. Currently, there is no treatment available that is able to improve most of the ASD disorder symptoms; thus, finding novel therapies is immediately required. Stat3 inhibitors are potential targets in the treatment of several immune disorders. The aim of the present study was to investigate the effects of S3I-201, a selective Stat3 inhibitor, to determine its potential mechanism in BTBR mice. In this study, we first examined the effects of S3I-201 on repetitive behavior and marble burying. We also examined the treatment of S3I-201 on Th1 (IFN-gamma and T-bet), Th17 (IL-17A, ROR gamma t, Stat3, IL-21, and IL-22), and T regulatory (Treg, Foxp3 and Helios) production in spleen CD4(+) T cells. We further assessed Th1, Th17, and Treg mRNA and protein expression levels in brain tissues. S3I-201 treatment in BTBR mice significantly prevents marble burying and repetitive behavior. Furthermore, S3I-201 administration causes a considerable decrease in IFN-gamma, T-bet, IL-17A, ROR gamma t, Stat3, IL-21, and IL-22 levels, and increases in Foxp3 and Helios production CD4(+) T cells in BTBR mice. Additionally, S3I-201 treatment also significantly decreases Th1 and Th17 levels, and increases Treg mRNA and protein expression levels. Therefore, these results suggest that S3I-201 could be considered as a therapeutic option for ASD.
机译：自闭症谱系障碍（ASD）是一种神经发育障碍，其症状包括沟通缺陷，缺乏社交技能和陈规定型的重复行为。我们使用BTBR T + ITPR3（TF）/ J（BTBR）小鼠，这是一个模型，它展示了ASD的大多数核心行为特征，例如减少社交性和高水平的重复行为。目前，没有可用的治疗，能够改善大部分ASD疾病症状;因此，需要找到新的疗法。 STAT3抑制剂是治疗多种免疫障碍的潜在靶标。本研究的目的是探讨S3I-201，选择性STAT3抑制剂的影响，以确定其BTBR小鼠的潜在机制。在这项研究中，我们首先检查了S3I-201对重复行为和大理石埋葬的影响。我们还研究了在Th1（IFN-Gamma和T-Bet），Th17（IL-17A，RORGamma T，Stat3，IL-21和IL-22）和T调节（Treg，Foxp3）上的S3I-201的治疗方法和Helios）在脾脏CD4（+）T细胞中产生。我们进一步评估了脑组织中的Th1,117和Th17和Treg mRNA和蛋白表达水平。 S3I-201在BTBR小鼠中治疗显着防止大理石埋葬和重复行为。此外，S3I-201给药导致IFN-Gamma，T-Bet，IL-17A，RORγT，STAT3，IL-21和IL-22水平相当大的降低，并增加Foxp3和Helios生产CD4（+） BTBR小鼠的T细胞。另外，S3I-201治疗也显着降低了Th1和Th17水平，并增加了Treg mRNA和蛋白质表达水平。因此，这些结果表明S3I-201可以被认为是ASD的治疗选择。

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