| In the process of chronic infection or cancer, T cells are exposed to persistentantigen stimulation or inflammatory signals for a long time , resulting in the gradual lossof effector functions of T cells in a graded manner, commonly known as T cellexhaustion. The high expres sion and co-expres sion of inhibitory receptors such as PD-1, CTLA-4, LAG-3, Tim-3 and BTLA on T cells is one of the main characteristics ofexhausted T cells. In our previous study, secretory autophagosomes have beensucces sfully recruited from the culture supernatant of a variety of mouse / human tumorcells and from the hydrothorax/ascites of tumor patients by differential centrifugation,and named as tumor cell-released autophagosome (TRAP). It was further found thatTRAPs could induce B cells to differentiate IL-10+ Bregs with immunosuppressivefunction in tumor microenvironment; induce macrophages to polarize to M2-like, andhighly express PD-L1; promote neutrophil apoptosis by triggering neutrophils toproduce ROS and inducing caspase-3 activation, also induce CD4+ T cells to secreteIL-6 to inhibit T cell function and promote tumor growth and metastasis . However, it isnot clear whether TRAPs is involved in inducing the expres sion of inhibitory receptorson T cells and its mechanism. |
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