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      Improved Detection of in vivo Human NK Cell-Mediated Antibody-Dependent Cellular Cytotoxicity Using a Novel NOG-FcγR-Deficient Human IL-15 Transgenic Mouse

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          Abstract

          We generated an NOD/Shi- scid-IL2Rγ null (NOG) mouse deficient for the Fcer1g and Fcgr2b genes (NOG-FcγR −/− mice), in which monocytes/macrophages do not express activating (FcγRI, III, and IV) or inhibitory (FcγRIIB) Fcγ receptors. Antibody-dependent cellular cytotoxicity (ADCC) by innate immune cells was strongly reduced in this strain. Thus, while the growth of xenogeneic human tumors engrafted in conventional NOG mice was suppressed by innate cells upon specific antibody treatment, such growth inhibition was abrogated in NOG-FcγR −/− mice. Using this novel strain, we further produced NOG-FcγR −/−-mice expressing human IL-15 (NOG-FcγR −/−-hIL-15 Tg). The mice inherited unique features from each strain, i.e., the long-term sustenance of human natural killer (NK) cells, and the elimination of mouse innate cell-mediated ADCC. As a result, segregation of human NK cell-mediated ADCC from mouse cell-mediated ADCC was possible in the NOG-FcγR −/−-hIL-15 Tg mice. Our results suggest that NOG-FcγR −/−-hIL-15 Tg mice are useful for validating the in vivo function of antibody drug candidates.

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          Bispecific antibodies: a mechanistic review of the pipeline

          Aran F Labrijn, Maarten Janmaat, Janice M. Reichert … (2019)
          The term bispecific antibody (bsAb) is used to describe a large family of molecules designed to recognize two different epitopes or antigens. BsAbs come in many formats, ranging from relatively small proteins, merely consisting of two linked antigen-binding fragments, to large immunoglobulin G (IgG)-like molecules with additional domains attached. An attractive bsAb feature is their potential for novel functionalities - that is, activities that do not exist in mixtures of the parental or reference antibodies. In these so-called obligate bsAbs, the physical linkage of the two binding specificities creates a dependency that can be temporal, with binding events occurring sequentially, or spatial, with binding events occurring simultaneously, such as in linking an effector to a target cell. To date, more than 20 different commercialized technology platforms are available for bsAb creation and development, 2 bsAbs are marketed and over 85 are in clinical development. Here, we review the current bsAb landscape from a mechanistic perspective, including a comprehensive overview of the pipeline.
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            Humanized mice for immune system investigation: progress, promise and challenges.

            Leonard D. Shultz, Michael A Brehm, J. Garcia-Martinez … (2012)
            Significant advances in our understanding of the in vivo functions of human cells and tissues and the human immune system have resulted from the development of 'humanized' mouse strains that are based on severely immunodeficient mice with mutations in the interleukin-2 receptor common γ-chain locus. These mouse strains support the engraftment of a functional human immune system and permit detailed analyses of human immune biology, development and functions. In this Review, we discuss recent advances in the development and utilization of humanized mice, the lessons learnt, the remaining challenges and the promise of using humanized mice for the in vivo study of human immunology.
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              Anti-CD47 antibody synergizes with rituximab to promote phagocytosis and eradicate non-Hodgkin lymphoma.

              Christine P Chao, R Malumbres, Chad Tang … (2010)
              Monoclonal antibodies are standard therapeutics for several cancers including the anti-CD20 antibody rituximab for B cell non-Hodgkin lymphoma (NHL). Rituximab and other antibodies are not curative and must be combined with cytotoxic chemotherapy for clinical benefit. Here we report the eradication of human NHL solely with a monoclonal antibody therapy combining rituximab with a blocking anti-CD47 antibody. We identified increased expression of CD47 on human NHL cells and determined that higher CD47 expression independently predicted adverse clinical outcomes in multiple NHL subtypes. Blocking anti-CD47 antibodies preferentially enabled phagocytosis of NHL cells and synergized with rituximab. Treatment of human NHL-engrafted mice with anti-CD47 antibody reduced lymphoma burden and improved survival, while combination treatment with rituximab led to elimination of lymphoma and cure. These antibodies synergized through a mechanism combining Fc receptor (FcR)-dependent and FcR-independent stimulation of phagocytosis that might be applicable to many other cancers. Copyright 2010 Elsevier Inc. All rights reserved.
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                Author and article information

                Contributors
                Journal
                Journal ID (nlm-ta): Front Immunol
                Journal ID (iso-abbrev): Front Immunol
                Journal ID (publisher-id): Front. Immunol.
                Title: Frontiers in Immunology
                Publisher: Frontiers Media S.A.
                ISSN (Electronic): 1664-3224
                Publication date (Electronic): 07 October 2020
                Publication date Collection: 2020
                Volume: 11
                Electronic Location Identifier: 532684
                Affiliations
                [1] 1Laboratory Animal Research Department, Central Institute for Experimental Animals (CIEA) , Kawasaki, Japan
                [2] 2Pathological Analysis Center, Central Institute for Experimental Animals (CIEA) , Kawasaki, Japan
                Author notes

                Edited by: Tim Willinger, Karolinska Institutet, Sweden

                Reviewed by: Anthony Rongvaux, Fred Hutchinson Cancer Research Center, United States; Nicholas D. Huntington, Walter and Eliza Hall Institute of Medical Research, Australia

                *Correspondence: Takeshi Takahashi takeshi-takahashi@ 123456ciea.or.jp

                This article was submitted to Cancer Immunity and Immunotherapy, a section of the journal Frontiers in Immunology

                Article
                DOI: 10.3389/fimmu.2020.532684
                PMC ID: 7577188
                PubMed ID: 33117338
                SO-VID: 7c514a9a-0686-4b14-a483-cea5a5ecd8e1
                Copyright © Copyright © 2020 Katano, Ito, Kawai and Takahashi.
                License:

                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.

                History
                Date received : 05 February 2020
                Date accepted : 07 September 2020
                Page count
                Figures: 3, Tables: 0, Equations: 0, References: 37, Pages: 9, Words: 5820
                Funding
                Funded by: Japan Society for the Promotion of Science 10.13039/501100001691
                Award ID: 18H02368
                Funded by: Japan Agency for Medical Research and Development 10.13039/100009619
                Categories
                Subject: Immunology
                Subject: Original Research

                ScienceOpen disciplines: Immunology
                Keywords: humanized mice,nk cell,fcγr,adcc,mouse innate immunity
                Data availability:
                ScienceOpen disciplines: Immunology
                Keywords: humanized mice, nk cell, fcγr, adcc, mouse innate immunity

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