SLAMF7, also known as CRACC, CS1, CD319, is an Ig-like receptor expressed on various immune cells including macrophages, B cells, T cells, NK cells, etc. It plays a crucial role in regulating immune responses, especially in macrophage activation, phagocytosis, and B-cell and NK-cell functions. It is associated with pathways such as TLR-dependent MAPK and NF-κB signaling, and its regulation impacts cytokine production and cell-cell interactions [1,4,5,6].

In multiple myeloma, SLAMF7 is overexpressed and serves as an attractive immunotherapeutic target [2,7]. In hepatocellular carcinoma, loss of Slamf7 in liver-specific knockout mice led to increased carcinogenesis, metastasis, and immunosuppressive macrophage infiltration, highlighting its role in macrophage regulation and as a potential biomarker for immunotherapy response [3]. In CNS autoimmunity, SLAMF7-/-mice were more susceptible to experimental autoimmune encephalomyelitis (EAE), indicating its role in modulating B cells and adaptive immunity [5].

In conclusion, SLAMF7 is a key regulator in immune-related biological processes. Studies using gene knockout mouse models have revealed its importance in multiple diseases, including multiple myeloma, hepatocellular carcinoma, and CNS autoimmunity. These findings provide insights into disease mechanisms and potential therapeutic strategies targeting SLAMF7.