The immune escape mechanism of nasopharyngeal carcinoma

Tumor cells are known for being able to evade immune system surveillance, a hallmark of malignancy. Complicated immune escape mechanisms in the tumor microenvironment (TME) provide favorable conditions for tumor invasion, metastasis, treatment resistance, and recurrence. Epstein-Barr virus (EBV) infection is closely related to the pathogenesis of nasopharyngeal carcinoma (NPC), and the co-existence of EBV-infected NPC cells and tumor-infiltrating lymphocytes represents a distinctive, highly heterogeneous, and suppressive TME that supports immune escape and promotes tumorigenesis. Understanding the complex interaction between EBV and NPC host cells and focusing on the immune escape mechanism of TME may help to identify specific immunotherapy targets and to develop effective immunotherapy drugs.

Automated summary

Tumor cells are capable of evading immune system surveillance, favoring tumor invasion, metastasis, treatment resistance, and recurrence. Epstein-Barr virus (EBV) infection in nasopharyngeal carcinoma (NPC) contributes to a suppressive tumor microenvironment (TME), characterized by the co-existence of EBV-infected NPC cells and tumor-infiltrating lymphocytes. Understanding the interaction between EBV and NPC host cells and the immune escape mechanisms in the TME could lead to the identification of specific immunotherapy targets and the development of effective immunotherapy drugs.