» Articles » PMID: 34733609

Relationship Between Th17 Immune Response and Cancer

Abstract

Cancer is the second leading cause of death worldwide and epidemiological projections predict growing cancer mortality rates in the next decades. Cancer has a close relationship with the immune system and, although Th17 cells are known to play roles in the immune response against microorganisms and in autoimmunity, studies have emphasized their roles in cancer pathogenesis. The Th17 immune response profile is involved in several types of cancer including urogenital, respiratory, gastrointestinal, and skin cancers. This type of immune response exerts pro and antitumor functions through several mechanisms, depending on the context of each tumor, including the protumor angiogenesis and exhaustion of T cells and the antitumor recruitment of T cells and neutrophils to the tumor microenvironment. Among other factors, the paradoxical behavior of Th17 cells in this setting has been attributed to its plasticity potential, which makes possible their conversion into other types of T cells such as Th17/Treg and Th17/Th1 cells. Interleukin (IL)-17 stands out among Th17-related cytokines since it modulates pathways and interacts with other cell profiles in the tumor microenvironment, which allow Th17 cells to prevail in tumors. Moreover, the IL-17 is able to mediate pro and antitumor processes that influence the development and progression of various cancers, being associated with variable clinical outcomes. The understanding of the relationship between the Th17 immune response and cancer as well as the singularities of carcinogenic processes in each type of tumor is crucial for the identification of new therapeutic targets.

Citing Articles

The bidirectional interplay between T cell-based immunotherapies and the tumor microenvironment.

Pherez-Farah A, Boncompagni G, Chudnovskiy A, Pasqual G Cancer Immunol Res. 2025; .

PMID: 39786986 PMC: 7617322. DOI: 10.1158/2326-6066.CIR-24-0857.


Interleukin-6 Modulation in Ovarian Cancer Necessitates a Targeted Strategy: From the Approved to Emerging Therapies.

Amer H, Kampan N, Itsiopoulos C, Flanagan K, Scott C, Kartikasari A Cancers (Basel). 2025; 16(24.

PMID: 39766086 PMC: 11674514. DOI: 10.3390/cancers16244187.


Unveiling the influence of tumor and immune signatures on immune checkpoint therapy in advanced lung cancer.

Kim N, Park S, Jo A, Eum H, Kim H, Lee K Elife. 2024; 13.

PMID: 39514276 PMC: 11548875. DOI: 10.7554/eLife.98366.


Role and functional mechanisms of IL‑17/IL‑17R signaling in pancreatic cancer (Review).

Liu W, Wang X, Wu W Oncol Rep. 2024; 52(5).

PMID: 39219271 PMC: 11378154. DOI: 10.3892/or.2024.8803.


Anakinra-Loaded Sphingomyelin Nanosystems Modulate In Vitro IL-1-Dependent Pro-Tumor Inflammation in Pancreatic Cancer.

Abal-Sanisidro M, De Luca M, Roma S, Ceraolo M, Fuente M, De Monte L Int J Mol Sci. 2024; 25(15).

PMID: 39125655 PMC: 11312284. DOI: 10.3390/ijms25158085.


References
1.
Miossec P, Korn T, Kuchroo V . Interleukin-17 and type 17 helper T cells. N Engl J Med. 2009; 361(9):888-98. DOI: 10.1056/NEJMra0707449. View

2.
Zhong W, Xu X, Zhu Z, Du Q, Du H, Yang L . Increased expression of IRF8 in tumor cells inhibits the generation of Th17 cells and predicts unfavorable survival of diffuse large B cell lymphoma patients. Oncotarget. 2017; 8(30):49757-49772. PMC: 5564805. DOI: 10.18632/oncotarget.17693. View

3.
Ferrarini I, Rigo A, Zamo A, Vinante F . Classical Hodgkin lymphoma cells may promote an IL-17-enriched microenvironment. Leuk Lymphoma. 2019; 60(14):3395-3405. DOI: 10.1080/10428194.2019.1636983. View

4.
Witowski J, Pawlaczyk K, Breborowicz A, Scheuren A, Wisniewska J, Polubinska A . IL-17 stimulates intraperitoneal neutrophil infiltration through the release of GRO alpha chemokine from mesothelial cells. J Immunol. 2000; 165(10):5814-21. DOI: 10.4049/jimmunol.165.10.5814. View

5.
Chang C, Qiu J, OSullivan D, Buck M, Noguchi T, Curtis J . Metabolic Competition in the Tumor Microenvironment Is a Driver of Cancer Progression. Cell. 2015; 162(6):1229-41. PMC: 4864363. DOI: 10.1016/j.cell.2015.08.016. View