ArticleCancer immunology research2025
The FcγRIIIA (CD16) L48-H/R Polymorphism Enhances NK Cell-Mediated Antibody-Dependent Cellular Cytotoxicity by Promoting Serial Killing.
Article in Cancer immunology research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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The trial behind it
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Who cites it
12 citing papers in PubMed.
- Advances in natural killer cell immunotherapy for hematologic malignancies.Cancer biology & therapy · 2026Review
- The membrane distal domain of CD16a allosterically regulates NK cell ADCC.bioRxiv : the preprint server for biology · 2026Article
- High levels of circulating miR-19a-3p in patients with metastatic HER2 + breast cancer are associated with a favorable prognosis and anti-tumor immune responses.Breast cancer research : BCR · 2026Article
- Natural Killer Cell Therapy in Ovarian Cancer: From Preclinical Potentials to Clinical Applications and Combination Strategies.International journal of biological sciences · 2026Review
- A fully human IgG1 antibody targeting MICA α1 domain inhibits interaction with NKG2D and activates immune effector functions against MICA-expressing cells.Frontiers in immunology · 2026Article
- HSV-2 gE2/gI2 are immune evasion molecules that bind IgG Fc to inhibit antibody-dependent cellular cytotoxicity.Frontiers in immunology · 2026Article
- Review
- Reprogramming natural killer cells in the tumor microenvironment: Challenges and therapeutic opportunities.Cytokine & growth factor reviews · 2025Review
- The role of NK cells in regulating tumorimmunity: current state, challenges and future strategies.Cancer cell international · 2025Review
- Review
- From Molecular Precision to Clinical Practice: A Comprehensive Review of Bispecific and Trispecific Antibodies in Hematologic Malignancies.International journal of molecular sciences · 2025Review
- Application and prospects of genetic engineering in CAR-NK cell therapy.Frontiers in immunology · 2025Review
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Authors and funding
6 authors.
Funding
Abstract
Many tumor-specific monoclonal antibody therapies stimulate antibody-dependent cellular cytotoxicity (ADCC) by natural killer (NK) cells through FcγRIIIa (CD16). The efficacy of these ADCC-based immunotherapies is potentiated in patients with the common CD16 polymorphic variant F158-V that increases the binding affinity between the receptor and the IgG Fc domain. However, other CD16 variants are less well characterized. Here, we report that CD16 L48-H and L48-R variants both significantly enhance in vitro ADCC responses in primary NK cells and NK-92 cells. During ADCC responses, NK cells expressing CD16 48-H killed and disengaged from target cells faster than those expressing CD16 48-L, resulting in improved serial killing of tumor cells. We found that CD16 48-H also formed an immunologic synapse with a more compact interface, as well as more robust intracellular calcium signaling and quicker polarization of cytolytic vesicles. The ADCC response observed occurs due to increased cytolytic signaling and target cell disengagement, which drives NK cell-mediated serial killing of tumor cells. The L48-H/R polymorphism has potential to benefit patient responses to cancer antibody therapies and may also potentiate antitumor ADCC responses if incorporated into adoptive NK cell therapeutic platforms.
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