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Immune effector receptors are a functional class of cell-surface proteins expressed on immune cells, such as T cells, Natural Killer (NK) cells, and macrophages, that initiate cytotoxic or phagocytic responses upon engagement (Advances in Antibody-Based Immune-Stimulating Drugs, 2025) [1]. Prominent examples include the CD3 epsilon subunit of the T-cell receptor complex, Fc gamma receptors (e.g., CD16), and activating receptors like NKG2D (Future Directions and Priorities for Cellular Therapy in Sarcoma, 2025) [2]. These receptors are central to the mechanism of action of various immunotherapies, including bispecific antibodies and chimeric antigen receptor (CAR) T-cell therapies, which redirect effector cell activity toward tumor-associated antigens [1, 3]. For instance, bispecific T-cell engagers (BiTEs) like blinatumomab bind to CD3 to trigger T-cell mediated lysis of target cells [1]. While highly effective, the potent activation of these receptors can lead to systemic toxicities such as cytokine release syndrome (CRS) and immune effector cell-associated neurotoxicity syndrome (ICANS) [2, 3]. Consequently, these receptors are critical therapeutic targets in oncology and infectious diseases, requiring careful management of immune activation levels [1].
Engagement and activation of immune effector cells (e.g., T cells, NK cells, or macrophages) to induce targeted cell lysis, antibody-dependent cellular cytotoxicity (ADCC), or phagocytosis.
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