CD172G, also known as SIRPG or SIRPγ, is a member of the signal-regulatory protein (SIRP) family, which plays roles in immune regulation and cell-cell communication. Structurally, it belongs to the immunoglobulin (Ig) superfamily, featuring extracellular Ig domains, a transmembrane region, and a short cytoplasmic tail lacking signaling motifs. Unlike SIRPα (CD172a), which binds CD47 to mediate "don't eat me" signals, CD172G interacts with distinct ligands, though its precise binding partners remain under investigation. It is primarily expressed on T cells and natural killer (NK) cells, suggesting involvement in adaptive and innate immune responses.
CD172G is implicated in immune synapse formation, modulating T-cell activation, adhesion, and migration. Studies highlight its role in fine-tuning immune responses, potentially balancing activation and inhibition. For example, CD172G may enhance T-cell receptor signaling or synergize with co-stimulatory molecules, though its regulatory mechanisms are not fully defined. Its expression on activated T cells also links it to inflammatory conditions, autoimmune diseases, and cancer immunity.
In therapeutic contexts, CD172G is explored as a target for cancer immunotherapy. Preclinical models suggest that blocking or engaging CD172G could modulate anti-tumor immunity, either by overcoming inhibitory signals or enhancing immune cell activity. Additionally, it serves as a biomarker for immune cell subsets in translational research. Further studies are needed to clarify its ligand interactions and downstream pathways, which could unlock novel strategies for immune-related disorders.