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Measurement of Natural Killer Cell-Mediated Cytotoxicity and Migration in the Context of Hepatic Tumor Cells
Published on: February 22, 2020
Insights into ectodomain shedding as a novel target in natural killer cell-based immunotherapy for cancer
Ruan Pimenta1, Jun Arai2, Luiza Ribeiro de Lima Brandao1
1The Marc and Jennifer Lipschultz Precision Immunology Institute, Icahn School of Medicine at Mount Sinai, New York, NY, United States.
Abstract:
Natural killer (NK) cells are innate lymphocytes that kill cancer cells and produce cytokines/chemokines that drive anti-tumor immune responses. NK cells are controlled by activating and inhibitory receptors, of which some, or their ligands, are regulated by ectodomain shedding, which is a post-translational modification to transform surface proteins into soluble peptides. Although ectodomain shedding is essential for normal development and physiology, it is also an immune suppression mechanism for downregulating activating receptors in NK cells or their ligands in cancer cells. The ectodomain shedding of immune receptors or ligands are therapeutic targets in cancer immunology and peculiarly relevant in NK cells, given how receptor/ligand density tips the balance to the activation or inhibition of NK cell effector functions. Two classical examples are the CD16a Fc gamma-activating receptor and the MICA/B, and B7-H6 cellular stress-induced ligands. CD16a triggers antibody-dependent cellular cytotoxicity (ADCC), but CD16a shedding by ADAM17 can prevent receptor engagement, and, therefore, CD16a shedding is a target to promote the efficacy of Fc-enabled antibodies. CD16a shedding also appears to play a dual role, not only in negatively regulating ADCC but also in terminating the immune synapse to help NK cells disengage and move to the next target cell. Furthermore, stress-induced ligands serve as "kill me" signs on the surface of cancer cells, but the shedding of such ligands enables escape from NK cell recognition. Although the shedding of stress-induced ligands is a mechanism of immune evasion in tumors, novel monoclonal antibodies that inhibit such shedding in a highly specific manner have an outstanding efficacy in preclinical tumor models, and one clone has transitioned to clinical trial phase for potently promoting anti-tumor immunity. We, therefore, review here some of the most impactful discoveries in the ectodomain shedding field with a special focus on NK cells and cancer to help inform the scientific community and help guide the development of novel immunotherapies.
Insights
Ectodomain shedding downregulates natural killer (NK) cell anti-tumor functions by shedding activating receptors and ligands. Inhibiting this shedding shows promise for enhancing cancer immunotherapies.
Area of Science:
- Immunology
- Cancer Biology
- Molecular Biology
Background:
- Natural killer (NK) cells are crucial innate immune cells that eliminate cancer cells.
- NK cell activity is regulated by a balance of activating and inhibitory receptors.
- Ectodomain shedding, a post-translational modification, alters the function of these receptors and their ligands.
Purpose of the Study:
- To review the role of ectodomain shedding in NK cell-mediated anti-tumor immunity.
- To highlight shedding as a mechanism of immune suppression and evasion in cancer.
- To discuss therapeutic strategies targeting ectodomain shedding for cancer immunotherapy.
Main Methods:
- Literature review focusing on ectodomain shedding in NK cells and cancer.
- Analysis of key receptors (e.g., CD16a) and ligands (e.g., MICA/B, B7-H6) involved in shedding.
- Examination of preclinical and clinical data on therapies targeting ectodomain shedding.
Main Results:
- Ectodomain shedding of activating receptors (e.g., CD16a) impairs NK cell cytotoxicity (ADCC).
- Shedding of stress-induced ligands (MICA/B, B7-H6) by cancer cells facilitates immune evasion.
- Inhibitors of ectodomain shedding demonstrate significant efficacy in preclinical cancer models.
Conclusions:
- Ectodomain shedding is a critical regulator of NK cell function and a target for cancer immunotherapy.
- Strategies to inhibit shedding of activating receptors and stress ligands hold therapeutic potential.
- Further development of targeted inhibitors could enhance anti-tumor immunity mediated by NK cells.
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