Checkpoint inhibitors and CAR-T cells are therapeutic approaches that can be used to treat cancer. Both therapies affect the function of T lymphocytes, but they have completely different mechanisms of action. On one hand, there are T cells modified with a synthetic chimeric antigen receptor (CAR), which exists in five different versions. On the other hand, there are checkpoint inhibitors, which use humanized monoclonal antibodies. CAR-T cells with the chimeric receptor independently recognize and bind to antigens, and then destroy cancer cells through the secretion of granzyme and perforin, cytokine synthesis, or the Fas/FasL pathway. With checkpoint inhibitors, anti-CTLA-4 and anti-PD-1 antibodies bind to inhibitory receptors on T cells and thus prevent the interactions of CTLA-4 and PD-1 receptors with ligands. This enables the establishment of natural effector functions and alleviates chronic T cell fatigue, thereby enhancing their anti-cancer activity. In my thesis, I will first provide a detailed overview of the CTLA-4 and PD-1 receptors and their inhibitors, as well as CAR-T cells, and then highlight the main differences in the mechanisms of action between the two therapies.
|
