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Review
. 2017 Apr;95(4):347-355.
doi: 10.1038/icb.2017.6. Epub 2017 Feb 21.

Antibody-dependent cell cytotoxicity: immunotherapy strategies enhancing effector NK cells

Maria Carmen Ochoa  1   2 , Luna Minute  1   2 , Inmaculada Rodriguez  1   2   3   4 , Saray Garasa  1   2 , Elisabeth Perez-Ruiz  5 , Susana Inogés  1   3   4 , Ignacio Melero  1   2   3   4 , Pedro Berraondo  1   2   3   4
Affiliations
Review

Antibody-dependent cell cytotoxicity: immunotherapy strategies enhancing effector NK cells

Maria Carmen Ochoa et al. Immunol Cell Biol. 2017 Apr.

Abstract

Antibody-dependent cellular cytotoxicity (ADCC) is a set of mechanisms that target cells coated with IgG antibodies of the proper subclasses (IgG1 in the human) to be the prey of cell-to-cell cytolysis executed by immune cells expressing FcRIIIA (CD16A). These effectors include not only natural killer (NK) cells but also other CD16+ subsets such as monocyte/macrophages, NKT cells or γδ T cells. In cancer therapy, ADCC is exploited by antibodies that selectively recognize proteins on the surface of malignant cells. An approach to enhance antitumor activity is to act on effector cells so they are increased in their numbers or enhanced in their individual (on a cell per cell basis) ADCC performance. This enhancement can be therapeutically attained by cytokines (that is, interleukin (IL)-15, IL-21, IL-18, IL-2); immunostimulatory monoclonal antibodies (that is, anti-CD137, anti-CD96, anti-TIGIT, anti-KIR, anti-PD-1); TLR agonists or by adoptive infusions of ex vivo expanded NK cells which can be genetically engineered to become more efficient effectors. In conjunction with approaches optimizing IgG1 Fc affinity to CD16, acting on effector cells offers hope to achieve synergistic immunotherapy strategies.

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References

    1. Clin Cancer Res. 2013 Mar 1;19(5):1126-38 - PubMed
    1. Clin Pharmacol Ther. 2017 Jan;101(1):81-88 - PubMed
    1. Nat Commun. 2016 Oct 04;7:13019 - PubMed
    1. Front Oncol. 2016 Oct 31;6:232 - PubMed
    1. Blood. 2002 Feb 1;99(3):754-8 - PubMed

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