谷物中T-2毒素可抑制或刺激动物免疫系统，削弱或增强机体免疫机能，进而影响动物疫病的发生。前期研究我们报道：T-2毒素可同时激活STAT1和JNK1-STAT3通路；STAT1促进细胞凋亡，而JNK1-STAT3通路抑制细胞凋亡。然而，调控细胞凋亡、存活走向的STAT1和JNK1-STAT3通路平衡的分子机制仍不清楚。本项目组进一步研究发现：信号通路AKT和ITCH能调控STAT1/3表达；不同浓度T-2毒素引起STAT3磷酸化水平差异，预示潜在信号通路和毒素浓度阈值是调控此通路平衡的重要因素。在此基础上，本项目以RAW264.7细胞为模型，①深层解析维持JNK1-STAT3和STAT1通路平衡的关键因素，阐明T-2毒素诱导细胞凋亡、存活走向的信号传导机理；②明确毒素剂量阈值在细胞凋亡、存活平衡中的作用。本项目为毒素的免疫抑制和刺激形成机理提供新的分子靶点，也为动物疫病防控提供理论依据。

T-2 toxin in cereals suppresses or stimulates the immune system to weaken or enhance the immune function of animals, thus, will influence the occurrence of animal diseases. Our previous study has shown that T-2 toxin in RAW264.7 cells could activate JNK1-STAT3 and STAT1 pathways simultaneously. Moreover, STAT1 could stimulate cell apoptosis, whereas JNK1-STAT3 was able to inhibit the cell apoptosis induced by T-2 toxin. However, the mechanism underlying the balance of JNK-STAT3 and STAT1 activation to regulate the cell survival and cell apoptosis is still not clear. Our recent studies have further shown that AKT and ITCH regulated the STAT1/3 activation; T-2 toxin in different doses led to the different STAT3 phosphorylation levels, suggesting the potential signal pathways and the threshold dose of T-2 toxin are critical regulators in this balance. In this project, we aim at using RAW264.7 cell line as the model, to study the potential signal pathways in the regulation of the balance of JNK1-STAT3 and STAT1 activation, and to elucidate the mechanism of cell apoptosis and cell survival development; meanwhile, we will study the potential role of threshold dose of T-2 toxin in this balance. This project will provide a new molecular target for the underlying of the mechanism of immunosuppressant and immune stimulation, thus will provide further scientific theory for animal disease prevention and control.