Cd84, also known as SLAMF5, is a member of the SLAM family of cell-surface immunoreceptors. It functions as a homophilic adhesion molecule, and its signaling can either activate or inhibit leukocyte function depending on the cell type and its activation or differentiation stage. Cd84-mediated signaling is involved in diverse immunological processes such as T cell cytokine secretion, natural killer cell cytotoxicity, monocyte activation, autophagy, T:B interactions, and B cell tolerance at the germinal center checkpoint [1].

In multiple myeloma, CD84-deficient mice show reduced MDSC accumulation, elevated T cell activity, and reduced tumor load, suggesting that CD84 regulates the immunosuppressive microenvironment in this disease [2]. In Mycobacterium tuberculosis-infected CD84-deficient C57BL/6 mice, there is improved M. tuberculosis clearance and longer survival, indicating that CD84 suppresses T and B cell activation during M. tuberculosis pathogenesis [3]. In acute myeloid leukemia, down-regulation of CD84 in human cell lines, patient-derived xenograft cells, and MLL-AF9 and inv(16) AML mouse models disrupts leukemia cell proliferation, clonogenicity, and engraftment capabilities [4].

In conclusion, Cd84 plays a crucial role in regulating immunological processes and is involved in various disease conditions such as autoimmune disorders, multiple myeloma, tuberculosis, and acute myeloid leukemia. Studies using gene knockout mouse models have been instrumental in revealing its functions in these diseases, providing potential therapeutic targets for treatment.