Programmed cell death protein 1 (PD-1) is an important immunosuppressive receptor expressed mainly on T cells, B cells, natural killer cells, and other immune cells. PD-1 exerts its inhibitory function by binding to its ligands PD-L1 and PD-L2. In normal immune responses, the activation of PD-1 serves as a self-protective mechanism to prevent...
Programmed cell death protein 1 (PD-1) is an important immunosuppressive receptor expressed mainly on T cells, B cells, natural killer cells, and other immune cells. PD-1 exerts its inhibitory function by binding to its ligands PD-L1 and PD-L2. In normal immune responses, the activation of PD-1 serves as a self-protective mechanism to prevent an overactive immune system, helping to avoid attacks on self-tissues. However, during tumor immune escape, tumor cells upregulate PD-L1 expression to bind with PD-1, inhibiting T cell activity and thereby evading immune surveillance. Furthermore, abnormal activation of PD-1 also plays a significant role in autoimmune diseases. Through the interaction between PD-1 and its ligands, immune cell activity is suppressed, preventing the immune system from effectively clearing abnormal self-cells or tissues, which is an important mechanism in the development of various autoimmune diseases.
G protein-coupled receptors (GPCRs) are one of the most important signal transduction protein families in human cell membranes, regulating a wide range of physiological processes from vision and olfaction to cardiovascular function. Among them, the Angiotensin II Type 1 Receptor (AT1R) plays a central role in blood pressure regulation, fluid...
G protein-coupled receptors (GPCRs) are one of the most important signal transduction protein families in human cell membranes, regulating a wide range of physiological processes from vision and olfaction to cardiovascular function. Among them, the Angiotensin II Type 1 Receptor (AT1R) plays a central role in blood pressure regulation, fluid balance, and cardiovascular diseases. However, the activation mechanism of peptide ligand-binding GPCRs like AT1R has long been a research bottleneck, as traditional methods struggled to capture their active conformations, hindering the precise development of targeted therapeutics. A research team from Harvard Medical School, Duke University, and other institutions has successfully overcome this challenge using synthetic nanobody technology. Their findings, published in Cell, pave a new path for GPCR research and drug development.