Updated Progress of Interleukin-17 in Gynecological Tumors
0
Citation
0
Reference
20
Related Paper
Abstract:
Interleukin (IL)-17 is a pro-inflammatory cytokines mainly produced by activated CD4+ T lymphocytes , which involved in the immune response, inflammation and autoimmune diseases , with biological functions of strong recruitment of neutrophils, promoting a variety of cytokines release inflammatory factors and cell proliferation. Present study found that interleukin-17 is significant in tumor development .This article focus on the relationships among interleukin-17 and ovarian cancer, cervical cancer, choriocarcinoma and other gynecological tumors.
Key words:
interleukin (IL)-17; T helper cell; cancerKeywords:
Interleukin 15
Interleukin-8(IL-8)has been proposed to play a crucial role in the angiogenesis and growth of tumor,including lung cancer.High level of IL-8 in both serum and lung cancer tissue may he correlated with the poor prognosis of disease.The secretion of IL-8 is derived from both tumor cells and inflammatory cells.The molecular mechanism of IL-8 expression might be closely associated with nuclear factor-κB and mitogen-activated protein kinase pathway.Other studies have suggested that the secretion and activation of IL-8 are common in the treatment of lung cancer,might lead to treatment failure and drug resistance of lung cancer.Thus,targeting IL-8 in lung cancer treatment might be an alternative clinical therapy.
Key words:
Interleukin-8; Chemokine receptor; Lung cancer; Therapy
Interleukin 8
Cite
Citations (0)
Interleukin-33 (IL-33) is one of the members of the IL-1 family of cytokines and a ligand of ST2 and IL-1 receptor accessory protein (IL-1RAcP) that is known to affect Th2 inflammatory response with partial effects on Th1 responses. This cytokine is released by epithelial and smooth muscle cells of the airway system during their injury by several environmental stimuli, such as allergens, viruses, helminths, and pollutants. IL-33 is an alarmin that acts as an endogenous danger signal, and it has been known to affect various types of cells, such as mast cells, basophils, eosinophils, T cells, and specific subsets of innate lymphoid cells (ILCs). In recent findings, this cytokine is believed to have a critical role in several types of cancers, such as lung cancer, liver cancer, and head and neck squamous cell cancer. The expression of IL-33/ST2 in cancer tissues shows a close association with tumor growth and tumor progression in several types of cancer, suggesting the IL-33/ST2 pathway as a potential target for therapy.
Interleukin 33
Innate lymphoid cell
Cite
Citations (34)
Objective: The tumor microenvironment has a crucial role in organizing cancer malignancy, progression, drug resistance and survival. It consists of cellular and non-cellular components. These non-cellular components such as cytokines, extracellular matrix, growth factors and metabolites are responsible for shifting the action from pro-cancer to anti-cancer effects. Twenty percent of all cancers occur in association with chronic inflammation via cytokines. Even cancers that are not caused by chronic inflammation, present high levels of cytokine expression pattern in their tumor microenvironment. Tumor necrosis factor-alpha (TNF-α) and some interleukins are characterized as pro-tumorigenic cytokines and they were involved in cancer by presenting their ability to activate the oncogenic transcription factors. The aim of this study is to evaluate the remodeling of colorectal cancer tumor microenvironment by TNF-α.
Material and Methods: TNF-α (5ng/ml) was applied to HT-29 colorectal cancer cells, then human soluble factors were determined by using Human Cytokine Group 1, 8 plex Panel (Bio-Rad Laboratories Inc. USA) and Magpix Luminex instrument and xPONENT software (version 4.2, Luminex Corp, Austin, Texas, US). The results were normalized to total protein concentration estimated via Bradford assay.
Results: Current research highlights the effect of TNF-α on the tumor microenvironment. Interleukin-6 and interleukin -8 soluble factors were higher in TNF-α treated colorectal cancer cells when compared with untreated control group.
Conclusion: The results of the study show that TNF-α is responsible for elevating the levels of interleukin-6 and interleukin-8, which are associated with inflammation in the tumor microenvironment.
Key words: Colorectal Cancer, Tumor Microenvironment, Cytokines, TNF-α, Interleukin-6, interleukin -8
Cite
Citations (4)
Tumor progression
Cite
Citations (123)
Interleukin (IL)-10, a multifunctional immune-regulatory cytokine with both immunosuppressive and anti-angiogenic functions, is produced by immune cells including macrophages, T lymphocytes, and natural killer cells. Among other effects, IL-10 promotes tumor cell proliferation and metastasis via immunosuppression. Interleukin-10-mediated immunosuppression is aided by synthesis of tumor necrosis factor, IL-1, IL-12, and chemokines, and down regulation of the surface co-stimulatory molecules CD80 and CD86 on tumors. Interleukin-10 also promotes IL-6 expression and synthesis, which causes cell proliferation via B cell lymphoma-2 (Bcl-2) upregulation and changes the proliferation/apoptosis equivalence toward neoplastic cell proliferation. Moreover, IL-10 inhibits tumorigenesis via down-regulation of VEGF, IL-1b, TNF-α, IL-6, and MMP-9. Interleukin-10 also inhibits nuclear factor-KB (NF-KB) translocation. Interleukin-10 has been reported to have both tumor-promoting and -inhibiting properties. It seems that IL-10 agonists and antagonists may have therapeutic effects via different mechanisms. Moreover, IL-10 gene polymorphisms may determine breast cancer susceptibility.
Interleukin 20
CD80
Interleukin 15
Cite
Citations (97)
The immune system can both promote and suppress cancer. Chronic inflammation and proinflammatory cytokines such as interleukin (IL)-1 and IL-6 are considered to be tumour promoting. In contrast, the exact nature of protective antitumour immunity remains obscure. Here, we quantify locally secreted cytokines during primary immune responses against myeloma and B-cell lymphoma in mice. Strikingly, successful cancer immunosurveillance mediated by tumour-specific CD4+ T cells is consistently associated with elevated local levels of both proinflammatory (IL-1α, IL-1β and IL-6) and T helper 1 (Th1)-associated cytokines (interferon-γ (IFN-γ), IL-2 and IL-12). Cancer eradication is achieved by a collaboration between tumour-specific Th1 cells and tumour-infiltrating, antigen-presenting macrophages. Th1 cells induce secretion of IL-1β and IL-6 by macrophages. Th1-derived IFN-γ is shown to render macrophages directly cytotoxic to cancer cells, and to induce macrophages to secrete the angiostatic chemokines CXCL9/MIG and CXCL10/IP-10. Thus, inflammation, when driven by tumour-specific Th1 cells, may prevent rather than promote cancer. Inflammation can result in the formation of tumours, but the immune system is also involved in the elimination of cancer cells. Here, the authors show that inflammation driven by tumour-specific CD4+T cells results in tumour regression and identify a list of cytokines associated with cancer prevention.
Proinflammatory cytokine
Immunosurveillance
Cite
Citations (284)
Interleukin 20
Cite
Citations (843)
Cite
Citations (1)
CCL5
Inflammatory breast cancer
Proinflammatory cytokine
Monocyte
Cite
Citations (10)
Interleukin-6 is a multifunctional cytokine produced by variety of cells including tumor cells. It is produced by monocytes, macrophages, B-cells and T-cells. Interleukin-6 stimulates platelet production through thrombopoietin. Interleukin-6 in surplus amount is also produced by epithelial ovarian cancer cells. Hence, it is a useful prognostic factor for ovarian cancer, and is associated with disease stage and survival period.
Pathophysiology
Interleukin 1β
Cite
Citations (0)