IL-35可通过调节失控性炎症对ARDS发挥保护作用，是调控Treg细胞炎症抑制功能所需细胞因子。我们前期研究表明：ARDS时氨基酸代谢微环境(L-精氨酸降低)影响Treg细胞分化，而IL-35能促进NaïveCD4T细胞向Treg细胞分化；且GCN2-CHOP/mTORC1信号网络是精氨酸缺乏时T细胞分化关键调控环节。基于此，我们提出“IL-35通过调控GCN2-CHOP/mTORC1信号网络，启动蛋白质翻译、减少细胞死亡，促进Treg细胞分化，抑制ARDS失控性炎症”的科学假说，并拟以NaïveCD4T、肺血管内皮等细胞(株)和IL-35(KO)、GCN2(KO)、B-NSG等基因敲除小鼠模型，腺病毒载体RNA干扰、氨基酸饥饿、细胞共培养、T细胞过继回输等技术与方法，从分子-细胞-动物-临床整体论证并阐明ARDS新机制，为以Treg细胞作为代谢检测点设计ARDS潜在治疗靶标提供新方向。

IL-35 can protect ARDS by regulating uncontrollable inflammation, and IL-35 is an important cytokine required to regulate the inflammatory suppressive function of Treg cells. Our previous studies showed that amino acid metabolism microenvironment, such as L-arginine decreased, can affect the Treg cell differentiation in ARDS. And we had illustrated that IL-35 can promote the differentiation from Naïve CD4 T cells into Treg cells. Simultaneously, the GCN2-CHOP/mTORC1 signaling network is one of the key regulatory element of T cell differentiation during arginine deficiency. Based on theories and results from the above, we proposed a scientific hypothesis that IL-35 could initiate protein translation and reduce cell death through regulation of the GCN2-CHOP/mTORC1 signaling network, and then promote Treg cells differentiation and suppress uncontrolled inflammatory reaction of ARDS through regulating the GCN2-CHOP/mTORC1 signaling. Naïve CD4 T cells, pulmonary vascular endothelial cells and other knockout mouse models, including IL-35(KO) mice, GCN2(KO) mice and B-NSG mice were used; adenovirus vector RNA interference, amino acid starvation, cells co-culture and adoptive transfusion of T cells were carried out to explore a new mechanism of ARDS, which could contribute to use the Treg cells as the metabolic check point to provide a promising strategy for identifying potential therapeutic targets of ARDS.