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. 2021 Feb 9;124(8):1411–1420. doi: 10.1038/s41416-021-01272-6

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© The Author(s), under exclusive licence to Cancer Research UK 2021

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as 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 images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 5 — Three receptors of IgG, FcγRI, FcγRII and FcγRIII (a) were analysed in T cells, HROC277, HROC285, HROC370 and HROC374. Compared to T cells, the colon cancer cells expressed a significantly higher level of FcγRI (b), FcγRII (c) and FcγRIII (d). In addition, after incubation with PRIVIGEN^® IgG for 24 h, we observed that PRIVIGEN^® IgG not only binds to the receptors (e, g, i and k), it is also internalised by cancer cells (f, h, j and l). Of note, cells stained without PRIVIGEN incubation and thus displaying the intrinsic and cancer cell-derived IgG of the respective HROC cells (individual levels can be depicted from Supplementary Fig. 3) were set as the blank reference. The P-values were determined by Mann–Whitney U test. N = 9 for (e), (f), (h), (j), (l); N = 8 for (b–d and g); N = 7 (i); N = 5 for (k).