In the immune system, T lymphocytes undergo rapid clonal expansion upon pathogen infection. Following pathogen clearance, most of proliferated T cells will be eliminated by the apoptosis pathway to keep the balance of immune cells. FASLG, by interacting with its cognate receptor FAS, plays a major role in controlling the T cell death. FASLG is a type II transmembrane protein, with its C-terminal extracellular domain responsible for interacting with FAS. The N-terminal cytosolic region, despite short and intrinsically disordered, plays critical roles on the protein stability and transportation. The correct localization, either on the plasma membrane or secreted with exosome, or shed into the extracellular region after protease cleavage, has a great impact on the proper function of FASLG. Following synthesis, FASLG is transported by intracellular vesicle transportation system to the final destination. In this report, ALG2, a molecule identified in the T cell apoptosis and shown to be involved in vesicle trafficking previously, was found to interact with FASLG and regulate FASLG transportation. Therefore, we identified a new regulating factor for FASLG function within T cells and also revealed a new pathway for ALG2 involvement in T cell apoptosis.

中文翻译：

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ALG2通过调节FASLG细胞内运输影响T细胞凋亡。

在免疫系统中，T淋巴细胞在病原体感染后会经历快速的克隆扩增。清除病原体后，大多数增殖的T细胞将通过凋亡途径消除，以保持免疫细胞的平衡。FASLG通过与其同源受体FAS相互作用，在控制T细胞死亡中起主要作用。FASLG是II型跨膜蛋白，其C端胞外域负责与FAS相互作用。N-末端胞质区，尽管短而内在地无序，但是在蛋白质的稳定性和运输中起着关键的作用。正确的定位，无论是在质膜上还是由外泌体分泌，或者在蛋白酶切割后掉入细胞外区域，对FASLG的正常功能都有很大的影响。综合之后 FASLG通过细胞内囊泡运输系统运输到最终目的地。在该报告中，发现了在T细胞凋亡中鉴定出的分子ALG2，该分子以前参与了小泡运输，被发现与FASLG相互作用并调节FASLG的运输。因此，我们确定了T细胞内FASLG功能的新调节因子，并揭示了ALG2参与T细胞凋亡的新途径。