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Tumor cells expressing stress-induced ligands and IgG-opsonized targets describes a specific cellular phenotype that serves as a primary target for Natural Killer (NK) cell-mediated immunity [1, 3]. This target state involves the expression of stress-induced ligands, such as MICA, MICB, and ULBPs, which are recognized by the NKG2D activating receptor on NK cells [2, 5]. Simultaneously, these cells are opsonized or coated with IgG antibodies, which are recognized by the CD16 (FcγRIIIa) receptor, triggering antibody-dependent cellular cytotoxicity (ADCC) [1, 7]. The}
Synergistic activation of Natural Killer (NK) cells through the simultaneous engagement of the NKG2D receptor (by stress-induced ligands) and the CD16A/FcγRIIIa receptor (by the Fc portion of IgG antibodies), leading to enhanced antibody-dependent cellular cytotoxicity (ADCC) and tumor cell lysis.
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