Abstract
Drug resistance has become an obstacle to the further development of immunotherapy in clinical applications and experimental studies. In the current review, the acquired resistance to immunotherapy was examined. The mechanisms of acquired resistance were based on three aspects as follows: The change of the tumor functions, the upregulated expression of inhibitory immune checkpoint proteins, and the effects of the tumor microenvironment. The combined use of immunotherapy and other therapies is performed to delay acquired resistance. A comprehensive understanding of acquired drug resistance may provide ideas for solving this dilemma.
Highlights
Tumorigenesis and immunity have been extensively studied, and immunotherapy against cancer is undoubtedly becoming a research hotspot
A review estimated the objective response rate for patients who treated with Pembrolizumab in melanoma, non-small cell lung cancer (NSCLC), renal cell carcinoma (RCC), Hodgkin lymphoma, urothelial carcinoma, esophageal cancer, and head and neck squamous cell carcinoma were 52%, 42%, 36%, 72%, 29%, 10%, and 17%, respectively [2]
Compensatory upregulation of the expression levels of inhibitory immune checkpoints (ICs) used in immunotherapy the uses of anti-PD-1/L1 and anti-CTLA-4 antibodies have been approved by the U.S Food and Drug Administration (FDA), it has been shown that LAG-3, TIM-3, TIGIT, VISTA have the potential to be upregulated in patients with tumor recurrence following anti-PD-1/L1 or anti-CTLA-4, which implies another mechanism for the acquired resistance
Summary
Tumorigenesis and immunity have been extensively studied, and immunotherapy against cancer is undoubtedly becoming a research hotspot. Downregulation or loss of β2M expression was detected in patients with lung cancer or melanoma who had been treated with ICI therapy and subsequently developed acquired resistance [18, 21].
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