Correlation between Th17 cells and tumor microenvironment

Qi, Wenhui; Huang, Xiaojuan; Wang, Junyan

doi:10.1016/j.cellimm.2013.06.001

Cited by 50 publications

(41 citation statements)

References 42 publications

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“…S9 and refs. [34][35][36][37][38][39][40]. Our findings suggest that Th17 cells act as tumor-supporting cells through Eva1-dependent intercellular association with GICs.…”

Section: Discussionmentioning

confidence: 60%

Eva1 Maintains the Stem-like Character of Glioblastoma-Initiating Cells by Activating the Noncanonical NF-κB Signaling Pathway

Ohtsu

Nakatani²,

Yamashita

et al. 2016

Cancer Research

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Glioblastoma (GBM)-initiating cells (GIC) are a tumorigenic subpopulation that are resistant to radio-and chemotherapies and are the source of disease recurrence. Therefore, the identification and characterization of GIC-specific factors is critical toward the generation of effective GBM therapeutics. In this study, we investigated the role of epithelial V-like antigen 1 (Eva1, also known as myelin protein zero-like 2) in stemness and GBM tumorigenesis. Eva1 was prominently expressed in GICs in vitro and in stem cell marker (Sox2, CD15, CD49f)-expressing cells derived from human GBM tissues. Eva1 knockdown in GICs reduced their self-renewal and tumor-forming capabilities, whereas Eva1 overexpression enhanced these properties. Eva1 deficiency was also associated with decreased expression of stemnessrelated genes, indicating a requirement for Eva1 in maintaining GIC pluripotency. We further demonstrate that Eva1 induced GIC proliferation through the activation of the RelB-dependent noncanonical NF-kB pathway by recruiting TRAF2 to the cytoplasmic tail. Taken together, our findings highlight Eva1 as a novel regulator of GIC function and also provide new mechanistic insight into the role of noncanonical NF-kB activation in GIC, thus offering multiple potential therapeutic targets for preclinical investigation in GBM.

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“…S9 and refs. [34][35][36][37][38][39][40]. Our findings suggest that Th17 cells act as tumor-supporting cells through Eva1-dependent intercellular association with GICs.…”

Section: Discussionmentioning

confidence: 60%

Eva1 Maintains the Stem-like Character of Glioblastoma-Initiating Cells by Activating the Noncanonical NF-κB Signaling Pathway

Ohtsu

Nakatani²,

Yamashita

et al. 2016

Cancer Research

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“…Comparisons were performed between the following groups: Differentiated thyroid carcinoma [(DTC) including PTCs and FTCs) (malignant neoplasm), MTC (malignant neoplasm), FTA (benign neoplasm) and goiter (non-neoplastic lesion) tissues. Fisher's exact test was used to compare two groups of data and the χ 2 test was used to analyze differences between more than three groups. Kruskal-Wallis test with Dunn's post-hoc test was used to compare the mean expression of IL-17 and IL-23 in the lymphocytes among thyroid lesions.…”

Section: Specimensmentioning

confidence: 99%

“…The tumor microenvironment is composed of stromal, endothelial and innate cells, as well as lymphocytes, which interact to form a complex system that surrounds tumor cells (1,2). The recruitment of immune effector cells to the tumor site and the intensity of specific responses are mediated by cytokines, which are secreted by immune system and tumor cells (3).…”

Section: Introductionmentioning

confidence: 99%

High IL-17 expression is associated with an unfavorable prognosis in thyroid cancer

et al. 2017

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Abstract. Previous studies have indicated that cancer may be promoted and/or exacerbated by inflammation and infection. The cytokines produced by activated innate immune cells that stimulate tumor growth and progression are considered as important components in this process. The interleukin (IL)-23/T helper (Th)17 axis, which exerts marked pro-inflammatory effects, has emerged as an important mediator in inflammation-associated cancer. Increasing clinical evidence indicates that Th17 may promote or inhibit tumor progression, however, the function of Th17 in the pathogenesis of benign and malignant thyroid neoplasms remains unclear. The present study investigated the association between the IL-23/Th17 axis and neoplastic and non-neoplastic thyroid lesions using immunohistochemistry. A total of 131 thyroid biopsy specimens were analyzed, which revealed high IL-17 and IL-23 expression in differentiated thyroid cancer and medullary thyroid cancer tissues when compared with benign lesions, including follicular thyroid adenoma and goiter tissues. Furthermore, high IL-17 expression was associated with recurrence and mortality. These results indicate that the IL-23/Th17 axis exhibits a pivotal function in the development of thyroid neoplasms.

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“…In addition, comprehensive analyses of various cytokines in plasma/serum from asbestos-exposed patients such as those with PP and MM in comparison to HV should be performed to detect other cytokines as biomarker candidates, as reported previously. Moreover, the status of function and volumes of the Th17 subtype of helper T cells should be investigated since the conversion and polarization of Treg and Th17 depends on the cytokine status surrounding these cells such as IIL-6 and TGF-β [49][50][51][52].…”

Section: Explore Biomarkers Of Asbestos Exposure and Occurrence Of MMmentioning

confidence: 99%

416 Search for biomarkers of asbestos exposure and asbestos-induced cancers in investigations of the immunological effects of asbestos

Otsuki

Lee

Matsuzaki

et al. 2018

Allergy and Immunotoxicology

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The immunological effects of asbestos exposure on various lymphocytes such as the regulatory T cell (Treg), responder CD4+ T helper cell (Tresp), CD8+ cytotoxic T lymphocytes (CTL), and natural killer (NK) cells were investigated. Results show that asbestos exposure impairs antitumor immunity through enhancement of regulatory T cell function and volume, reduction of CXCR3 chemokine receptor in responder CD4+ T helper cells, and impairment of the killing activities of CD8+ cytotoxic T lymphocytes (CTL) and NK cells. These findings were used to explore biological markers associated with asbestos exposure and asbestos-induced cancers and suggested the usefulness of serum/plasma IL-10 and TGF-β, surface CXCR3 expression in Tresp, the secreting potential of IFN-γ in Tresp, intracellular perforin level in CTL, and surface expression NKp46 in NK cells. Although other unexplored cytokines in serum/plasma and molecules in these immunological cells, including Th17, should be investigated by experimental procedures in addition to a comprehensive analysis of screening methods, biomarkers based on immunological alterations may be helpful in clinical situations to screen the high-risk population exposed to asbestos and susceptible to asbestos-related cancers such as mesothelioma.

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Correlation between Th17 cells and tumor microenvironment

Cited by 50 publications

References 42 publications

Eva1 Maintains the Stem-like Character of Glioblastoma-Initiating Cells by Activating the Noncanonical NF-κB Signaling Pathway

Eva1 Maintains the Stem-like Character of Glioblastoma-Initiating Cells by Activating the Noncanonical NF-κB Signaling Pathway

High IL-17 expression is associated with an unfavorable prognosis in thyroid cancer

416 Search for biomarkers of asbestos exposure and asbestos-induced cancers in investigations of the immunological effects of asbestos

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