Therapeutic mechanisms involving elotuzumab and Anti-SLAMF3 in multiple myeloma (MM)

The therapeutic mechanisms involving elotuzumab and Anti-SLAMF3 in multiple myeloma (MM). Elotuzumab engages with various receptors and pathways to coordinate an immune response. It targets signaling lymphocytic activation molecule family receptor (SLAMF7) on both natural killer (NK) cells and MM cells, activating NK cells through EAT-2 and inducing antibody-dependent cellular cytotoxicity (ADCC) via Fc component interaction with CD16. The antibody also disrupts the homotypic interactions between SLAMF7 on MM cells and bone marrow stromal cells (BMSCs), inhibiting adhesion. The signaling cascade initiated by elotuzumab enhances cytotoxicity through the ERK pathway, polarizes cytolytic granules, and enables macrophage-mediated antibody-dependent cellular phagocytosis (ADCP). In the context of MM, SLAMF3 molecules also play a role by forming connections that trigger the ERK signaling pathway and activate distinct transcription factors. The potential for limiting malignancy growth exists through antibodies targeting SLAMF3. Collectively, these mechanisms activate innate immune responses against MM cells and enhance the therapeutic efficacy of both elotuzumab and Anti-SLAMF3.

Publication

SLAM Modification as an Immune-Modulatory Therapeutic Approach in Cancer (2023) Alireza Tojjari, et al. Cancers (Basel). 2023 Oct;15(19):4808. Figure: F1. Homo sapiens

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