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Tumor cells expressing stress-induced ligands and IgG-opsonized targets

Molecular classification
Cell surface ligands, Immune complexes, MHC class I-like molecules, Immunoglobulins
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Overview

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}

Other names
NKG2D ligand-positive antibody-coated tumor cellsADCC-susceptible stressed tumor cellsNKG2DL+ IgG-opsonized targetsStress-ligand expressing cancer cells
02

Mechanism of action

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.

03

Biological functions

Immune responseAntibody-dependent cellular cytotoxicityCellular stress responseNatural killer cell activation
04

Disease associations

CancerHematologic malignanciesSolid tumors
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Safety considerations

Shedding of soluble NKG2D ligands (sMICA/B) acting as decoysOff-target activation on healthy cells expressing stress ligands due to inflammationCytokine release syndrome (CRS)Fc receptor competition with endogenous IgG
06

Interacting drugs

AFM13

6 more in the full profile.

07

Biomarkers

MICA surface expressionMICB surface expressionULBP1-6 expressionCD16A V158F polymorphismSurface IgG density

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