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. 2016 Oct 1;1:12. doi: 10.1186/s41199-016-0013-x

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© The Author(s) 2016

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Fig. 2 — Cetuximab-Mediated ADCC. The Fab portion of Cetuximab binds to EGFR on the surface of tumor cells, while its Fc region binds to the Fc receptor CD16/FcγRIII on the NK cell surface. This leads to NK cell activation and release of cytolytic granules containing perforin and granzyme B that result in tumor cell lysis and release of tumor antigen. This tumor antigen is subsequently presented on APCs to activate antigen-specific T-cells