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. 2022 Dec 1;14(23):5954. doi: 10.3390/cancers14235954

Figure 1.

Figure 1

Mechanism of action of PD-1/PD-L1 and CTLA4 inhibitors. Antigen presentation occurs on the surfaces of antigen-presenting cells (APCs) via T-cell receptors (TCR) and major histocompatibility complex (MHC). There are stimulatory and inhibitory signals, such as cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) and programmed cell death-1 (PD-1). Some of the upregulators of T-cells and their cognate ligands are CD27-CD70 and CD28-B7. Inhibitory T-cell receptors and their ligands include LAG3-MHC, CTLA4-B7 and PD1-PDL1. CTLA-4 reduces signaling via its co-stimulatory receptor, CD28, by binding to CD80 and CD86 on APC. CTLA-4 sends an inhibitory signal to T-cells. A CTLA-4 inhibitor (ipilimumab) stops autoreactive T-cells. PD-1 binds to programmed death-ligand 1 (PD-L1), which results in cancer evasion from the immune system. Blockade of PD-1 (via pembrolizumab, nivolumab, cemiplimab or dostarlimab) or PD-L1 (via atezolizumab, durvalumab or avelumab) increases anti-tumor immune activity. The image used has been modified from a prior submission [11].