The role of the immune system is to protect the body from foreign invaders. Normally, the immune system responds to tumor cells as it would to any foreign invader by destroying them. In contrast, tumor cells are often able to adapt and survive through the various stages of the tumor immune response by employing different strategies to keep the body’s immune system suppressed and unable to be killed by normal T cells. The above characteristics of tumor cells are called immune escape. What is a PD-1 inhibitor? What is a PD-L1 inhibitor? The tumor-immune cycle is mainly divided into the following seven stages: (1) tumor antigen release, (2) tumor antigen presentation, (3) initiation and activation of effector T cells, (4) migration of T cells to tumor tissue, (5) infiltration of T cells in tumor tissue, (6) recognition of tumor cells by T cells, and (7) clearance of tumor cells. Abnormalities in any of these links can lead to failure of the anti-tumor-immune cycle and immune escape. Different tumors can inhibit the effective recognition and killing of tumor cells by the immune system through abnormalities in different links, thus generating immune tolerance and even promoting the occurrence and development of tumors. What is a PD-1 inhibitor? What is PD-L1 inhibitor? In the process of tumor immunization, T cells play a central role in the immune response to tumors. After being sensitized and activated by dendritic cells in lymph nodes, T cells infiltrate into the tumor microenvironment consisting of tumor cells and infiltrating immune cells and other constructs. Activated T cells detect, bind and kill tumor cells. Programmed death receptor-1 (PD-1): an immunosuppressive molecule of CD28 superfamily members, PD-1 has two ligands, PD-L1 and PD-L2. PD-1 is mainly expressed on activated T cells, B cells, and inhibits cell activation, which is a self-stabilizing mechanism of the immune system, as excessive T cell/B cell activation can cause autoimmune diseases. Programmed death ligand-1 (PD-L1) it is an inhibitory ligand that normally plays a role in maintaining immune homeostasis. During tumor development, PD-L1 molecules highly expressed by tumor cells, PD-L1, by binding to receptor B7.1 and PD-1 on the surface of activated T cells, leads to impaired differentiation of T effector cells and T memory cells by altering T cell differentiation and differentiation into regulatory T cells (Treg) and depleted T cells (Tex), resulting in loss of cytotoxic activity of T cells and interference with This leads to the loss of cytotoxic activity of T cells and interferes with the body’s anti-tumor immune response, causing tumor cells to evade immune surveillance and killing by the body’s immune system. What is a PD-1 inhibitor? What is a PD-L1 inhibitor? Tumor immunotherapy is a therapeutic approach to control and eliminate tumors by restarting and maintaining the tumor-immune cycle and restoring the body’s normal anti-tumor immune response. PD-1 is expressed on the surface of T cells, and PD-1 inhibitors maintain the tumor-killing activity of T cells by binding to PD-1 on the surface of T cells to block the tumor immune escape pathway (PD1/PD-L1 pathway). In other words, PD-1 inhibitors affect the function of immune T cells. PD-1 inhibitors are mostly IgG4 antibodies, which have an anti-inflammatory biological function and can act against T cells. PD-L1 inhibitors work by recognizing the tumor cell surface? s PD-L1 and binding to it, blocking the tumor immune escape pathway (PD1/PD-L1 pathway) and maintaining the tumor-killing activity of T cells. Overall, PD-L1 inhibitors affect tumor cells, causing them to shed their veil of disguise as normal cells. pD-L1 inhibitors are mostly IgG1 antibodies, and IgG1 has the ability to recognize disease-causing antigens? biological role? It is able to recognize tumor cell epitopes. What is a PD-1 inhibitor? What is a PD-L1 inhibitor? PD-L1 inhibitors have the ability to block the binding of PD-L1 on the surface of tumor cells to B7.1 on the surface of T cells, which helps to maintain the anti-tumor activity of T cells for a long period of time.PD1 inhibitors block the binding of PD-1 to PD-L2, which leads to increased binding of PD-L2 to the macrophage receptor RGMb, resulting in the expansion of lung resident T cells and disrupting the respiratory tolerance balance, thus increasing the incidence of interstitial pneumonia. The incidence of interstitial pneumonia. PD-L1 inhibitors do not block the PD-L2 pathway, preserving the function of macrophage PD-L2 and avoiding the occurrence of side effects such as ILD. One study showed that patients with non-small cell lung cancer treated with PD-1 inhibitors had twice the incidence of immune-related pneumonia than those receiving PD-L1 inhibitors. In the field of lung cancer PD-1 inhibitors mainly include: pabrolizumab, naburizumab, teraplizumab, carrilizumab, sindilizumab, tirelizumab, pacumilizumab, srutilizumab PD-L1 inhibitors mainly include: dulvalizumab, atelelizumab, sugilizumab, adebrevizumab. Although PD-1/PD-L1 inhibitors mainly act on PD-1/PD-L1 pathway, the design of clinical studies and treatment of tumor species are different because PD-1/PD-L1 inhibitors have different antibody structures, different binding sites, different mechanisms of action, and different antibody modifications, so the therapeutic indications of each PD-1/PD-L1 inhibitor are different. The indications for each PD-1/PD-L1 inhibitor are also different. In the process of tumor immunization, immunotherapy is to kill tumors by activating the immune cells in the body, and T cells play a central role in the immune response against tumors. Therefore, it must be used when the basal immune status is good, because sufficient immune cells exist in the patient’s body at that time. Once it reaches the end stage, the patient’s immune system has been severely damaged and its own immune function is already weak, and the chance to restart the immune system function is smaller. Therefore, the earlier immunotherapy is used, the better, and it is never a backup drug when there are no more drugs to treat.