The Mechanism Of T Cells Apoptosis Induced By Different Galectins

Cancer has become one of the most serious global public health problems,killing about 5 million people each year.Therefore,exploring the mechanism of cancer development has great significance for the treatment of tumors from the perspective of immunology.Galectins(Gals)is a class of proteins that specifically recognize and bind β-D-galactoside through the carbohydrate recognition domain(CRD).A total of 16 family members have been found to participate in the development of tumorigenesis,including T cell apoptosis and tumor immune escape.At present,galectin-induced apoptosis of T cells is only anchored to a single family member.This paper aims to compare the strength and mechanism of various galectin-induced T cell apoptosis.This article first extracted and purified Gal-1,Gal-2,Gal-3,Gal-7,Gal-8,Gal-10,and Gal-13 seven galectins.After incubating T cells at different concentrations we detected apoptosis via Western Blotting and flow cytometry.The results showed that Gal-1,Gal-3,Gal-7,and Gal-8 can induce apoptosis in Jurkat T cells,and the concentration of Gal-8 to induce apoptosis is the lowest;Gal-3 and Gal-8 can also induce CCRF-CEM T cell apoptosis.On this basis,we studied the mechanism of galectin-induced apoptosis in T cells.Since Gal-3 induces T cell apoptosis through ROS--ERK and PKC--ERK signaling pathways,this study first examined the effects of various galectins on ERK,PKC and ROS release,and then used them separately.The inhibitors of ERK,ROS,and PKC inhibited the expression of the corresponding molecules and detected changes in apoptosis.The results showed that Gal-1,Gal-3,Gal-7 and Gal-8 all induced Jurkat T cell apoptosis via ROS--ERK pathway.Gal-3 and Gal-8 can also activate PKC--ERK pathway to induce Jurkat T cell apoptosis.Gal-1 and Gal-7 induced apoptosis of Jurkat T cells by activating PKC,but the downstream PKC molecule was not ERK.In exploring the molecular mechanism of galectin-induced CEM T cell apoptosis,we found Gal-3 can induce CEM T cell apoptosis via ROS--ERK and PKC--ERK pathways,while activated ROS and PKC do not participate in Gal-8 Induced apoptosis of CEM T cells.This study systematically compared the mechanism of galectin-induced T cell apoptosis and found that Gal-1,Gal-3,Gal-7,and Gal-8 can induce T cell apoptosis via ROS--ERK pathway.The ROS-ERK pathway may be the key for galectins to participate in tumor immune escape.The results of this study will help to understand the role of various galectins in tumor immune escape.