IL-17 expression was significantly increased in the tumor tissues and margins compared with that in the normal tissues, which was confirmed by immunohistochemical staining.
Tissues were stained with antibodies specific for pro-inflammatory molecules (cyclooxygenase 2, CXCL10, IL17), tumor-infiltrating immune cells (mature DC-LAMP<sup>+</sup> dendritic cells, CD3<sup>+</sup> T cells, CD3<sup>+</sup>Foxp3<sup>+</sup> regulatory T cells (Treg), T bet<sup>+</sup> Th1 cells, granzyme B<sup>+</sup> cytotoxic cells), and stromal cell populations (lymphatic vessels, tumor neovessels, high endothelial venules (HEV), stromal cells), which promote prostate tumor growth or are critical components of tumor-associated TLO.
In this study, the authors evaluated the dynamic change of IL-17A expression in the tumor microenvironment throughout the colorectal adenoma-carcinoma sequence.
We collected cells from pancreatic tumors of KPC mice, incubated them with IL17 or control media, measured expression of genes regulated by IL17 signaling, injected the cancer cells into immune competent mice, and measured tumor growth.
Collectively, these data demonstrate that the IL-17-CXCR2 axis facilitates the recruitment of neutrophils to the tumor sites, thus allowing them to play a cancer-promoting role in cancer progression.
Although there was no role of IL‑17A in promoting in vitro cell proliferation, IL‑17A markedly increased the tumor growth of Huh7.5 cells in both subcutaneous and orthotopic xenograft models with increased vascularization.
Finding from tumor tissue homogenate testing showed that the level of IL-17 and IFN-γ among mice immunized with TEX-SEB was significantly lower than PBS-treated group (p < 0.05).
Furthermore, IL-10 and IL-17A levels were increased in patients with a more serious clinical tumor stage and tumors that were ER<sup>-</sup> and PR<sup>-</sup>.
Further analyses revealed that anti-TNF-α treatment significantly decreased the expression of pro-inflammatory cytokines, including TNF-α (P<0.01), interleukin (IL)-1β (P<0.05), IL-6 (P<0.05) and IL-17 (P<0.05) and induced apoptosis in HCC tumors.
Ratios of IL-17 to interferon (IFN)-γ in serum level and tumor mass were higher in mice implanted with MB-IL-9 tumor clones than those observed in mice implanted with control cells.
The angiogenic factors CXCL8, MMP-2, MMP-9, and vascular endothelial growth factor detected within the tumor are possibly induced by IL-17 and indicative of poor disease prognosis.
The amplification capacity of γδ T cells was associated with the clinicopathological characteristics of patients (clinical stage, levels of AFP and albumin, duration of disease, size and number of tumors, numbers of Tregs and γδ T17 cells, and levels of IL-17A).
Our results suggested that the SNP rs2275913 of IL-17A and SNP rs763780 of IL-17F were associated with the development, as well as gender, smoking status and tumor stage of bladder cancer.
In addition, the upregulation of IL-17 both in vitro and in vivo resulted in a significant induction of invasion, migration and tumor formation ability in gastric CSCs compared with the control group, which was not treated with IL-17.
Although IL-17A and IL-17F share the highest amino acid sequence homology, they perform distinct functions; IL-17A is involved in the development of autoimmunity, inflammation, and tumors, and also plays important roles in the host defenses against bacterial and fungal infections, whereas IL-17F is mainly involved in mucosal host defense mechanisms.
Interleukin-17A (IL-17A), a pro-inflammatory cytokine secreted primarily by Th17 cells, has been proved to be involved in the microenvironment of certain inflammation-related tumors.