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. 2023 Oct 5;12(1):2261326. doi: 10.1080/2162402X.2023.2261326

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© 2023 The Author(s). Published with license by Taylor & Francis Group, LLC.

This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial License (http://creativecommons.org/licenses/by-nc/4.0/), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. The terms on which this article has been published allow the posting of the Accepted Manuscript in a repository by the author(s) or with their consent.

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Figure 8. — Proposed model of the role of the IL-17A/F:RA pathway in cancer.

The role of the IL-17A/F:RA pathway in cancer was investigated using syngeneic murine tumor models and IL-17 signaling deficient mice. Our results suggest contrasting effects of host IL-17 signaling on tumor growth, mediated by immune cell recruitment and specific anti-tumor cytotoxic CD8⁺ T responses (a,b), as well as IL-17 signaling in tumor cells (c,d) influencing tumor cell proliferation and the tumor microenvironment. Overall, IL-17 signaling in B16.SIY cells with high levels of IL-17RC activate a “canonical” pro-inflammatory IL-17 response, which, when combined with IL-17 induction of anti-tumor immunity, exerts a global anti-tumor role (c). Conversely, IL-17 signaling in EL4.SIY cells with low IL-17RC expression induces a “non-canonical” IL-17 response, promoting cell growth and inhibitory mediators of the immune response, ultimately leading to global pro-tumor effects (d). Model illustrated by @darwid_illustration.