FIP-Fve,一种来自金针菇的真菌子实体蛋白,具有潜在的免疫调节特性。这里,我们通过进行细胞活力测定和IL-2释放测定,研究了FIP-fve在JurkatE6-1细胞中的免疫调节机制。激酶抑制剂实验和蛋白质组学分析也参与了机制研究。发现FIP-fve在JurkatE6-1细胞中以剂量依赖性方式刺激细胞增殖并增强IL-2分泌。无偏高通量蛋白质组学分析表明,4种T细胞免疫激活标记,包括ZAP-70,CD69,CD82和KIF23在FIP-fve治疗后表达上调.进一步的通路分析表明MAP2K3/p38通路相关蛋白,包括MAP2K,p38,ELK,AATF,FOS,还有JUN-B,不受管制。此外,losmapimod(p38抑制剂)和gossypetin(MAP2K3抑制剂)抑制FIP-fve增强JurkatE6-1细胞中的细胞增殖和IL-2释放。我们的结果表明,FIP-fve通过激活MAP2K3/p38α刺激细胞增殖并增强IL-2的分泌。
FIP-fve, a fungal fruiting body protein from Flammulina velutipes, has potential immunomodulatory properties. Here, we investigated the immunomodulation mechanism of FIP-fve in Jurkat E6-1 cells by conducting a cell viability assay and IL-2 release assay. Kinase inhibitors experiment and proteomics analysis were also involved in the mechanism study. It was found that FIP-fve stimulated cell proliferation and enhanced IL-2 secretion in a dose-dependent manner in Jurkat E6-1 cells. Unbiased high-throughput proteomics analysis showed that 4 T cell immune activation markers, including ZAP-70, CD69, CD82, and KIF23, were upregulated in response to FIP-fve treatment. Further pathway analysis indicated that MAP2K3/p38 pathway-related proteins, including MAP2K, p38, ELK, AATF, FOS, and JUN-B, were unregulated. In addition, losmapimod (p38 inhibitor) and gossypetin (MAP2K3 inhibitor) inhibited FIP-fve enhanced cell proliferation and IL-2 release in Jurkat E6-1 cells. Our results demonstrate that FIP-fve stimulates cell proliferation and enhances IL-2 secretion through MAP2K3/p38α activation.