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Cells of the Innate Immune Response01:28

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Cytotoxic T cells are a vital component of the immune system. They have the remarkable ability to identify and target antigens on infected or abnormal cells. These antigens often originate from intracellular pathogens such as viruses or abnormal proteins cancer cells produce.
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The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
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T cells are integral to our adaptive immune system, recognizing and effectively responding to foreign antigens. T cell activation and clonal selection are pivotal in orchestrating this immune response. This article elucidates these mechanisms, detailing the roles of cluster of differentiation (CD) markers, major histocompatibility complex (MHC) molecules, costimulatory signals, and the process of clonal selection.
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Measurement of Natural Killer Cell-Mediated Cytotoxicity and Migration in the Context of Hepatic Tumor Cells
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CD16A Shedding Regulates Innate Cell Engager-Induced Serial Killing by Natural Killer Cells.

Chiara Zambarda1, Karolin Guldevall1, Christian Breunig2

  • 1Department of Applied Physics, Science for Life Laboratory, KTH Royal Institute of Technology, Stockholm, Sweden.

European Journal of Immunology
|October 21, 2025
PubMed
Summary
This summary is machine-generated.

Inhibiting Fc gamma receptor IIIa (FcγRIIIA or CD16A) shedding from natural killer (NK) cells impairs serial killing. CD16A shedding is crucial for sustained anti-tumor NK cell activity, impacting therapeutic strategies.

Keywords:
CD16 sheddingNK cellsacimtamiginnate cell engagermicrochipserial killing

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Area of Science:

  • Immunology
  • Cell Biology
  • Cancer Research

Background:

  • Natural killer (NK) cells utilize activating and inhibiting receptors to eliminate tumor cells.
  • Fc gamma receptor IIIa (FcγRIIIA or CD16A) is a key activating receptor triggering antibody-dependent cellular cytotoxicity (ADCC).
  • Inhibiting CD16A shedding is explored to enhance ADCC, but results are conflicting.

Purpose of the Study:

  • To investigate the impact of inhibiting CD16A shedding on NK cell cytotoxicity dynamics.
  • To compare the efficacy of acimtamig (AFM13) versus IgG1 antibodies in ADCC.
  • To elucidate the role of CD16A shedding in NK cell serial killing and detachment.

Main Methods:

  • Microchip-based live cell-imaging was employed to observe NK cell interactions.
  • ADCC assays were performed using acimtamig and IgG1 antibodies.
  • The effects of CD16A shedding inhibition on NK cell cytotoxic function were assessed.

Main Results:

  • Acimtamig demonstrated superior ADCC compared to IgG1 antibodies.
  • Inhibition of CD16A shedding reduced NK cell serial killing capacity.
  • Impaired NK cell detachment from target cells was observed when CD16A shedding was blocked.

Conclusions:

  • CD16A shedding is an intrinsic NK cell mechanism vital for sustained anti-tumor cytotoxicity.
  • Blocking CD16A shedding negatively affects NK cell serial killing and detachment.
  • Findings have implications for engineering NK cell therapies and CD16A-targeted engagers.