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首页> 外文期刊>Cellular Signalling >Adenosine A2A receptor modulates neuroimmune function through Th17/ retinoid-related orphan receptor gamma t (ROR gamma t) signaling in a BTBR T+ Itpr3(tf)/J mouse model of autism
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Adenosine A2A receptor modulates neuroimmune function through Th17/ retinoid-related orphan receptor gamma t (ROR gamma t) signaling in a BTBR T+ Itpr3(tf)/J mouse model of autism

机译：腺苷A2A受体通过Th17 /无素相关的孤儿受体γT（RORγT）信号传导在BTBR T + ITPR3（TF）/ J小鼠模型中通过Th17 /无碱相关孤儿函数γt（RORγT）信号传导来调节神经影响功能

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Autism spectrum disorder (ASD) is a complex neurodevelopmental disorder characterized by abnormal social interactions, repetitive behaviors that impair social communication, and circumscribed interests. BTBR T + tf/J (BTBR) inbred mice are generally used as a model for ASD, as they show repetitive behaviors and social deficits that resemble signs of ADS in humans. Adenosine A2A receptors (A2ARs) are considered as potential targets in the treatment of immune, inflammatory, and neurodegenerative diseases. In this study, we investigated the potential effects of the A2A adenosine receptor (A2AR) antagonist SCH 5826 (SCH) and agonist CGS 21680 (CGS) on behavior (self-grooming), hot plate test results, and expression levels of IL-17A(+), ROR gamma t(+), Foxp3(+), and IL-10(+) in CD4(+) T spleen cells in BTBR and C57BL/6 (B6) mice. We also assessed IL-17A, ROR gamma t, Stat3, pStat3, Foxp3, and IL-10 mRNA and protein expression levels in the brain tissue. The CGS-treated mice showed a significantly altered self-grooming score and a reduced response to the hot plate test. The results further revealed that the SCH efficiently increased the IL-17A(+) and ROR gamma t(+) expression levels and decreased the Foxp3(+) and IL-10(+) expression levels in CD4(+) cells. However, the treatment with CGS significantly reversed these effects. In addition, CGS significantly decreased the IL-17A, ROR gamma t, Stat3, and pStat3 levels and increased the Foxp3 and IL-10 mRNA and protein expression levels as compared with the BTBR control and SCH treatments. Our results clearly indicate that the CGS A2AR agonist may represent a unique target for future therapeutic strategies for neuroimmune dysfunction.
机译：自闭症谱系障碍（ASD）是一种复杂的神经发育障碍，其具有异常的社会互动，损害社交沟通的重复行为，以及受到限制的兴趣。 BTBR T + TF / J（BTBR）近额小鼠通常用作ASD的模型，因为它们显示了类似人类广告迹象的重复行为和社会缺陷。腺苷A2A受体（A2ARs）被认为是治疗免疫，炎症和神经变性疾病的潜在靶标。在这项研究中，我们研究了A2A腺苷受体（A2AR）拮抗剂SCH 5826（SCH）和激动剂CGS 21680（CGS）对IL-17A的表达水平（SCH）和激动剂CGS 21680（CGS）的潜在影响（+），在BTBR和C57BL / 6（B6）小鼠中CD4（+）T脾细胞中的rORγt（+），FoxP3（+）和IL-10（+）。我们还评估了脑组织中的IL-17A，RORγT，STAT3，PSTAT3，FOXP3和IL-10 mRNA和蛋白表达水平。 CGS处理的小鼠显示出显着改变的自我修饰得分和对热板测试的响应减少。结果进一步揭示了SCH有效地增加了IL-17A（+）和RORγT（+）表达水平并降低了CD4（+）细胞中的FoxP3（+）和IL-10（+）表达水平。然而，CGS的治疗显着逆转了这些效果。此外，与BTBR对照和SCH处理相比，CGS显着降低了IL-17a，RORγ，STAT3和PSTAT3水平，并增加了Foxp3和IL-10 mRNA和蛋白表达水平。我们的结果清楚地表明，CGS A2AR激动剂可以代表未来治疗功能障碍的未来治疗策略的独特目标。

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