Interleukin‐17 is associated with expression of programmed cell death 1 ligand 1 in ovarian carcinoma

Aotsuka, Aeri; Matsumoto, Yōko; Arimoto, Takahide; Kawata, Akihiro; Ogishima, Juri; Taguchi, Ayumi; Sone, Kenbun; Mori‐Uchino, Mayuyo; Tsuruga, Tetsushi; Oda, Katsutoshi; Kawana, Kei; Osuga, Yutaka; Fujii, Tomoyuki

doi:10.1111/cas.14174

Cited by 27 publications

(22 citation statements)

References 48 publications

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“…Neutrophils can modulate and suppress the activity of T cells in the OvCA microenvironment [80,81] and can facilitate the immune escape of OvCA cells by upregulating the expression of PD-L1 [80] (Figure 1). Another recent study confirmed that NLR ratio positively correlates with increased Th17/IL-17 levels and expression of PD-L1 in ovarian carcinoma [82].…”

Section: Neutrophilsmentioning

confidence: 69%

The Ovarian Cancer Tumor Immune Microenvironment (TIME) as Target for Therapy: A Focus on Innate Immunity Cells as Therapeutic Effectors

Baci

Bosi

Gallazzi

et al. 2020

IJMS

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Ovarian cancer (OvCA) accounts for one of the leading causes of death from gynecologic malignancy. Despite progress in therapy improvements in OvCA, most patients develop a recurrence after first-line treatments, dependent on the tumor and non-tumor complexity/heterogeneity of the neoplasm and its surrounding tumor microenvironment (TME). The TME has gained greater attention in the design of specific therapies within the new era of immunotherapy. It is now clear that the immune contexture in OvCA, here referred as tumor immune microenvironment (TIME), acts as a crucial orchestrator of OvCA progression, thus representing a necessary target for combined therapies. Currently, several advancements of antitumor immune responses in OvCA are based on the characterization of tumor-infiltrating lymphocytes, which have been shown to correlate with a significantly improved clinical outcome. Here, we reviewed the literature on selected TIME components of OvCA, such as macrophages, neutrophils, γδ T lymphocytes, and natural killer (NK) cells; these cells can have a role in either supporting or limiting OvCA, depending on the TIME stimuli. We also reviewed and discussed the major (immune)-therapeutic approaches currently employed to target and/or potentiate macrophages, neutrophils, γδ T lymphocytes, and NK cells in the OvCA context.

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Section: Neutrophilsmentioning

confidence: 69%

The Ovarian Cancer Tumor Immune Microenvironment (TIME) as Target for Therapy: A Focus on Innate Immunity Cells as Therapeutic Effectors

Baci

Bosi

Gallazzi

et al. 2020

IJMS

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“…In addition, the association between IL-17 and PD-1/PD-L1 has been observed in several kinds of carcinoma. Aotsuka et al (36) demonstrated that IL-17A induced the expression of PD-L1 in ovarian cancer cell lines. Wang et al (37) observed that IL-17A upregulated PD-L1 protein levels in human prostate cancer and human colon cancer cell lines.…”

Section: Discussionmentioning

confidence: 99%

Estrogen Receptor Downregulates Expression of PD-1/PD-L1 and Infiltration of CD8+ T Cells by Inhibiting IL-17 Signaling Transduction in Breast Cancer

et al. 2020

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Background: The relationship between the interleukin 17 (IL-17) family of cytokines and breast cancer has been widely studied in recent years. Many studies have revealed increased levels of the cytokine IL-17A in estrogen receptor (ER)-negative or triple-negative breast cancer. Upregulation of IL-17A signaling is associated with increased expression of programmed cell death protein 1 (PD-1) and programmed death-ligand 1 (PD-L1) in breast cancer with low ER expression and may elevate the infiltration of CD8 + T cells in tumor tissue. This study aims to determine whether ER downregulates the expression of PD-1/PD-L1, reduces the infiltration of CD8 + T cells, and affects the immune microenvironment by decreasing T-helper 17 (Th17) cell infiltration and inhibiting IL-17 signaling in breast cancer. Methods: Samples in The Cancer Genome Atlas Breast Cancer dataset were grouped by ER status and the PAM50 intrinsic subtype. The expression of IL-17 family cytokines and Th17 cell signature cytokines were compared between groups. IL-17 signaling pathway-related genes that were differentially expressed according to the ER level were identified. The PD-1 and PD-L1 levels were compared between breast cancer samples with different ER statuses and IL-17A/IL-17F expression levels. Correlation analyses of the expression of PD-1/PD-L1 and IL-17 signaling pathway-related genes were performed. The associations of the expression of IL-17 signaling pathway-related genes with the immune microenvironment were investigated. Results: High levels of ER decreased the expression of IL-17A, IL-17C, and IL-17F but increased the expression of IL-17E (IL25), which acts as a suppressor of IL-17 signaling. The expression levels of Th17 cell signature cytokines were significantly increased in ER-negative breast cancer. The expression levels of genes encoding downstream products of IL-17A/IL-17F signaling were downregulated in breast cancer with high ER expression. Increased expression of PD-1/PD-L1 was associated with ER-negative status, IL-17A-positive status, IL-17F-positive status, and upregulation of IL-17 signaling pathway-related genes in breast cancer. Enhanced IL-17 signal transduction was Shuai et al. Effect of ER in BC associated with the elevation of CD8 + T cell infiltration and variation of the immune microenvironment of breast cancer. Conclusion: High estrogen receptor levels decrease PD-1/PD-L1 expression and CD8 + T cell infiltration by suppressing Th17 cell infiltration and IL-17 signal transduction in breast cancer.

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“…In addition, they have abilities to recognize different tumor cells in a major histocompatibility complex (MHC)-unrestricted manner and lyse cancer cells by producing chemokines and cytokines, or by direct contact with cancer cells through the death receptor signal (19,20), which suggests that γδ T cells may have a potential role in antitumor immunotherapy. However, accumulating evidence suggests that γδ T cells also play a protumor role mainly by expressing interleukin-17 (IL-17) in several cancers (17,(21)(22)(23)(24)(25)(26).…”

Section: Introductionmentioning

confidence: 99%

Immune Effects of γδ T Cells in Colorectal Cancer: A Review

Yuan

Guo

et al. 2020

Front. Immunol.

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Gamma delta (γδ) T cells can effectively recognize and kill colorectal cancer (CRC) cells, thereby suppressing tumor progression via multiple mechanisms. They also have abilities to exert a protumor effect via secreting interleukin-17 (IL-17). γδ T cells have been selected as potential immunocytes for antitumor treatment because of their significant cytotoxic activity. Immunotherapy is another potential anti-CRC strategy after an operation, chemotherapy, and radiotherapy. γδ T cell-based immunotherapy for CRC shows fewer side effects and better toleration. This review will outline the immune functions and the mechanisms of γδ T cells in the growth and progression of CRC in recent years, and summarize the immunotherapies based on γδ T cells, thus providing a direction for future γδ T cells in CRC research.

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Interleukin‐17 is associated with expression of programmed cell death 1 ligand 1 in ovarian carcinoma

Cited by 27 publications

References 48 publications

The Ovarian Cancer Tumor Immune Microenvironment (TIME) as Target for Therapy: A Focus on Innate Immunity Cells as Therapeutic Effectors

The Ovarian Cancer Tumor Immune Microenvironment (TIME) as Target for Therapy: A Focus on Innate Immunity Cells as Therapeutic Effectors

Estrogen Receptor Downregulates Expression of PD-1/PD-L1 and Infiltration of CD8+ T Cells by Inhibiting IL-17 Signaling Transduction in Breast Cancer

Immune Effects of γδ T Cells in Colorectal Cancer: A Review

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