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Signaling lymphocytic activation molecule family member 7 (SLAMF7), also known as CS1 or CD319, is a cell surface glycoprotein and a member of the signaling lymphocytic activation molecule family [1]. It is highly and consistently expressed on the surface of malignant plasma cells in multiple myeloma, while its expression in healthy tissues is limited to natural killer (NK) cells, certain T cell subsets, and mature B cells [1, 4]. In NK cells, SLAMF7 functions as an activating receptor by recruiting the adaptor protein EAT-2, which triggers downstream signaling for cytotoxicity [4]. Conversely, in multiple myeloma cells that lack EAT-2, SLAMF7 promotes cell-to-cell adhesion and survival within the bone marrow microenvironment [4, 5]. Therapeutic targeting of SLAMF7, primarily with the monoclonal antibody elotuzumab, leverages this dual role by inducing antibody-dependent cellular cytotoxicity (ADCC) against myeloma cells and directly enhancing NK cell-mediated anti-tumor activity [2, 3]. References: [1] UniProt (Q9NQ25); [2] DrugBank (DB09110); [3] Lonial S, et al. N Engl J Med. 2015; [4] Tai YT, et al. Blood. 2008; [5] StatPearls: Multiple Myeloma.
Elotuzumab binds to the SLAMF7 receptor on multiple myeloma cells, tagging them for destruction by natural killer (NK) cells through antibody-dependent cellular cytotoxicity (ADCC). Additionally, elotuzumab binds to SLAMF7 on NK cells, directly activating them via the EAT-2 signaling pathway to enhance their cytotoxic activity against tumor cells [2, 3, 4].
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