What Is The Role Of Exosomal PD-L1 in Tumor Immune Escaping

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Exosomes are a group of extracellular vesicles released by cells with a size of 30–150 nm. Various human cells such as endothelial cells, mesenchymal cells, lymphocytes, dendritic cells, fibroblasts, and tumor cells can release exosomes. Exosomes are not simple cell shedding debris, but often carry a large number of nucleic acids, proteins, and carbohydrates derived from maternal cells. Recent studies have shown that PD-L1 carried by tumor-derived exosomes plays an important role in tumor immune escape and can further promote tumor proliferation and metastasis.

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In addition, tumor-derived exosomal PD-L1 was found to be related to the degree of response of patients to anti-PD1 immunotherapy, so exosomal PD-L1 is expected to become a novel marker to guide anti-PD1 immunotherapy. In the field of exosome research, a large number of studies have focused on the diagnosis and treatment value of circulating exosomal PD-L1 in malignant tumors, and it is believed that the detection of circulating exosomal PD-L1 can promote precise diagnosis and treatment.

Exosomes can transmit biological regulatory information through processes such as recognition and fusion with target cells, affecting the activity and function of target cells, while tumor cells have a strong function of secreting exosomes, and tumor-derived exosomes act on adjacent tumor cells by This leads to the progression of malignancy (Figure 1). The immune escape mechanism plays an important role in the occurrence and development of malignant tumors.

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Tumor cells can evade immune cell-killing effects through a variety of mechanisms, including concealment of tumor antigens, epithelial-mesenchymal transition, the release of inhibitory cytokines, and inhibition of immune-killer cells through direct contact. The PD1/PD-L1 signaling pathway is the most classical mechanism for suppressing the effects of cytotoxic T cells. PD-L1 molecules can be expressed on the surface of malignant tumor cells and immunosuppressive cells such as regulatory T cells, and PD-L1 molecules can bind to PD1 receptors on the surface of immune killer cells CD8+ T cells, causing CD8+ T cells Functional exhaustion makes it lose its ability to kill tumor cells.

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Tumor cells can also inhibit immune-killer cell function by releasing exosomes. Some studies have found ligands such as PD-L1 and FasL on the membrane of tumor-derived exosomes, which bind to the corresponding receptors on the immune killer cell membrane, resulting in apoptosis and functional exhaustion of target cells. In addition, exosomal PD-L1 can induce the production of immunosuppressive cells in addition to directly inhibiting cytotoxic T cell function and is believed to play a crucial role in mediating tumor immune escape.

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In conclusion, exosomal PD-L1 indirectly promotes the proliferation and metastasis of malignant tumors mainly by exerting extensive immunosuppressive effects.