Schematic of the distinct mechanisms of five classes of immunotherapeutic drugs: programmed death-1/programmed death-ligand 1 (PD-1/PD-L1) inhibitors specifically bind to PD-1 or PD-L1, blocking their interaction (IMAGE)
Caption
This releases the inhibitory state of T cells, restoring their activity so they can recognize and attack tumor cells once again. After specifically recognizing and binding to antigens on the surface of tumor cells, the antibody-drug conjugate (ADC) is internalized into the tumor cell. Within the cell, the ADC is degraded, releasing the cytotoxic drug that damages the tumor cell’s DNA or inhibits its division. Another portion can penetrate the cell membrane and diffuse into surrounding tumor cells, targeting those that do not express or express low levels of the target antigen. Chimeric antigen receptor T cells (CAR-T) can specifically recognize and bind to tumor antigens. Activated T cells can also release cytokines such as interferon-gamma (IFN-γ), thereby helping to activate a small number of innate immune cells and enhance immune responses. Bispecific antibodies (BsAbs) directly recruit immune cells to the vicinity of tumor cells, enabling more precise killing. Simultaneously, they activate immune cells such as natural killer (NK) cells to release cytokines, enhancing their cytotoxic function and promoting their proliferation. Dendritic cells (DCs) present tumor antigens to T cells, activating specific T cell immune responses and inducing the production of large numbers of cytotoxic T lymphocytes (CTLs) capable of recognizing tumors. These cells then kill tumor cells. IL, interleukin; MHC I, major histocompatibility complex class I; TCR, T-cell receptor; TRAIL, TNF-related apoptosis-inducing ligand.
Credit
Zengzheng Li, Tonghua Yang, Hongjun Guo
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