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From CD16a Biology to Antibody-Dependent Cell-Mediated Cytotoxicity Improvement
Antibody-dependent cell-mediated cytotoxicity (ADCC) is a potent cytotoxic mechanism that is mainly mediated in humans by natural killer (NK) cells. ADCC mediates the clinical benefit of several widely used cytolytic monoclonal antibodies (mAbs), and increasing its efficacy would improve cancer immu...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Frontiers Media S.A.
2022
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9203678/ https://www.ncbi.nlm.nih.gov/pubmed/35720368 http://dx.doi.org/10.3389/fimmu.2022.913215 |
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author | Coënon, Loïs Villalba, Martin |
author_facet | Coënon, Loïs Villalba, Martin |
author_sort | Coënon, Loïs |
collection | PubMed |
description | Antibody-dependent cell-mediated cytotoxicity (ADCC) is a potent cytotoxic mechanism that is mainly mediated in humans by natural killer (NK) cells. ADCC mediates the clinical benefit of several widely used cytolytic monoclonal antibodies (mAbs), and increasing its efficacy would improve cancer immunotherapy. CD16a is a receptor for the Fc portion of IgGs and is responsible to trigger NK cell-mediated ADCC. The knowledge of the mechanism of action of CD16a gave rise to several strategies to improve ADCC, by working on either the mAbs or the NK cell. In this review, we give an overview of CD16a biology and describe the latest strategies employed to improve antibody-dependent NK cell cytotoxicity. |
format | Online Article Text |
id | pubmed-9203678 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-92036782022-06-18 From CD16a Biology to Antibody-Dependent Cell-Mediated Cytotoxicity Improvement Coënon, Loïs Villalba, Martin Front Immunol Immunology Antibody-dependent cell-mediated cytotoxicity (ADCC) is a potent cytotoxic mechanism that is mainly mediated in humans by natural killer (NK) cells. ADCC mediates the clinical benefit of several widely used cytolytic monoclonal antibodies (mAbs), and increasing its efficacy would improve cancer immunotherapy. CD16a is a receptor for the Fc portion of IgGs and is responsible to trigger NK cell-mediated ADCC. The knowledge of the mechanism of action of CD16a gave rise to several strategies to improve ADCC, by working on either the mAbs or the NK cell. In this review, we give an overview of CD16a biology and describe the latest strategies employed to improve antibody-dependent NK cell cytotoxicity. Frontiers Media S.A. 2022-06-03 /pmc/articles/PMC9203678/ /pubmed/35720368 http://dx.doi.org/10.3389/fimmu.2022.913215 Text en Copyright © 2022 Coënon and Villalba https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Immunology Coënon, Loïs Villalba, Martin From CD16a Biology to Antibody-Dependent Cell-Mediated Cytotoxicity Improvement |
title | From CD16a Biology to Antibody-Dependent Cell-Mediated Cytotoxicity Improvement |
title_full | From CD16a Biology to Antibody-Dependent Cell-Mediated Cytotoxicity Improvement |
title_fullStr | From CD16a Biology to Antibody-Dependent Cell-Mediated Cytotoxicity Improvement |
title_full_unstemmed | From CD16a Biology to Antibody-Dependent Cell-Mediated Cytotoxicity Improvement |
title_short | From CD16a Biology to Antibody-Dependent Cell-Mediated Cytotoxicity Improvement |
title_sort | from cd16a biology to antibody-dependent cell-mediated cytotoxicity improvement |
topic | Immunology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9203678/ https://www.ncbi.nlm.nih.gov/pubmed/35720368 http://dx.doi.org/10.3389/fimmu.2022.913215 |
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