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. 2020 Aug 20;8(2):e000661. doi: 10.1136/jitc-2020-000661

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© Author(s) (or their employer(s)) 2020. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.

This is an open access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited, appropriate credit is given, any changes made indicated, and the use is non-commercial. See http://creativecommons.org/licenses/by-nc/4.0/.

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Diagrammatic illustration of proposed mechanism of cancer-initiated B lymphocyte-derived IgG4-mediated immune evasion. Chronic stimulation by cancer antigens induces class switch of B lymphocytes to produce IgG4. Such increased IgG4 can react to cancer-bound IgG with its Fc-Fc binding property and also to Fc receptors of immune effector cells. With its unique structural and biological property, increased IgG4 in cancer microenvironment mediates an effective immune escape for cancer. ADCC, antibody-dependent cell-mediated cytotoxicity; ADCP, antibody-dependent cellular phagocytosis; CDC, complement-dependent cytotoxicity; NK, natural killer cells.