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. 2017 Apr 12;17:257. doi: 10.1186/s12885-017-3234-4

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© The Author(s). 2017

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. 1 — Shared immune responses to infections and cancer cells. The immune system’s action on cancer cells relies on three main steps: antigenic presentation, immune cascades and inflammation resolution. Infected cells can express TAA-like antigen which will activate DC subset. DC will prime Th cells to differentiate into Th1 cells. However, latent viruses and helminths could polarize Th cells toward a Th2 response. Finally, bacterial and fungal infections could disequilibrate inflammation resolution by activating Th17 cells that down-regulate Treg cells. (DC: dendritic cells; TAA: tumor associated antigens; Th: T helper cell; CTL: cytotoxic T cells, Treg: regulatory T cells; IFNγ: interferon γ; IL: interleukin)