Immune checkpoint inhibitors (ICIs) are a group of drugs that inhibit the activity and function of inhibitory immune checkpoint molecules, such as programmed cell death protein 1 (PD-1), programmed death ligand 1 (PD-L1), cytotoxic T lymphocyte-associated protein 4 (CTLA-4), lymphocyte activation gene 3 (LAG3), and T-cell immunoglobulin and mucin domain-containing protein 3 (TIM3). Under physiological conditions, inhibitory immune checkpoint molecules play an important role in maintaining self-tolerance, preventing autoimmune reactions, and minimizing tissue damage by regulating the duration and intensity of immune responses. However, abnormal expression and excessive activation of immune checkpoint molecules can cause many diseases, including cancer. In particular, inhibitory immune checkpoint molecules are upregulated in various cells within the tumor microenvironment, forming various pairings and limiting the normal antitumor function of immune cells. In contrast, the use of ICIs can restore the function of immune cells hijacked by cancer cells, resulting in an enhanced immunosurveillance with a cytotoxic T lymphocyte (CTL) response. ICIs (e.g., pembrolizumab, nivolumab, cemiplimab, and atezolizumab) have changed the landscape of cancer treatment and become a new hope for cancer patients after the failure of regular chemotherapy or radiotherapy. |