谷物中T-2毒素可正负调控动物免疫机能，降低或增强动物机体对病原体防御能力，进而影响动物疫病发生。前期研究我们报道：T-2毒素可启动胞内“免疫逃避”程序，改变细胞免疫微环境，降低细胞对毒素免疫防御能力。然而，T-2毒素如何启动“免疫逃避”的分子机制尚不清楚，其在毒素免疫调控中的作用机制也未见报道。本项目组进一步研究发现，JNK1/STAT3/IDO1通路中IDO1为T-2毒素“免疫逃避”关键蛋白，且与PD-L1有潜在交联；T-2毒素诱导免疫应答因子IFN-γ、TLR-4表达具有时间动态性，预示毒素“免疫逃避”为动态活动。本项目在前期研究基础上，以RAW264.7巨噬细胞为模型，靶标IDO1–PD-L1信号轴，深层解析T-2毒素胞内“免疫逃避”分子机制；揭示“免疫逃避”在T-2毒素免疫调控中的作用机理；全面阐释T-2毒素正负免疫调控网络内涵及动态规律性，为毒素免疫调控机理提供新的分子靶点。

T-2 toxin positively and negatively regulates the immune function of animals, reduce or enhance the animal's ability to defend against pathogens, therefore to affect the occurrence of animal diseases. Our recent study showed that T-2 toxin initiated intracellular "immune evasion", inhibited the expression of immune response factors, changed the cellular immune microenvironment, and reduced the ability of cells to protect against toxins. However, the molecular mechanisms by which T-2 toxin initiates immune evasion are unclear, and its mechanism in immune regulatory networks is poorly understood. Our further research confirmed that IDO1 is the key protein of the immune evasion, and has a potential crosstalk with PD-L1; T-2 toxin regulates the expression of IFN-γ and TLR-4 with time dynamics, indicating that toxin immune evasion and immunomodulatory effects have a profile of dynamic activity. Based on our earlier work, this project will targrt the IDO1-PD-L1 signal, and will deeply analyze the intracellular "immune evasion" molecular mechanism of T-2 toxin; comprehensively explain the potential molecular roles of immune evasion in the T-2 toxin-mediated immune regulation network; fully reveals the dynamic regularity of T-2 toxin immune regulation network. This work provides a new molecular target for the immune regulation of mycotoxins.