For Publishers
DiscoveryMetadataPeer reviewHostingPublishing
For Researchers
JoinPublishReviewCollect
Register
Blog
About
Search
Advanced search
My ScienceOpen
Search
For Publishers
For Researchers
Blog
About
1
views
66
references
 Top references
cited by
26
    
0 reviews
 Review
0
comments
 Comment
0
recommends
+1 Recommend
0 collections
    0
    shares
      313
      similar
       All similar
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      IL-6 Activities in the Tumour Microenvironment. Part 1

      review-article

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          The predominant role of IL-6 in cancer is its key promotion of tumour growth. IL-6 binds IL-6 receptor (IL-6R) and the membrane-bound glycoprotein gp130. The complex I-6/IL-6R/gp130 starts the Janus kinases (JAKs) and signal transducer and activator of transcription 3 (STAT3) or JAK/STAT3 pathway. IL-6 R exits in two forms: a membrane-bound IL-6Rα subunit (mIL-6R) that participates in classic signalling pathway and soluble IL-6R subunit (sIL-6R) engaged in trans-signalling. The pro-tumour functions of IL-6 are associated with STAT3, a major oncogenic transcription factor that triggers up-regulation of target genes responsible for tumour cell survival. IL-6 combined with TGF-β induces proliferation of pathogenic Th17 cells. The anti-tumour function of IL-6 is the promotion of anti-tumour immunity. IL-6 trans-signaling contributed to transmigration of lymphocytes in high endothelial venules (HEV). Dendritic cell (DC) secreted IL-6 in the lymph node influences the activation, distribution and polarisation of the immune response. Elevated serum levels of IL-6 and increased expression of IL-6 in tumour tissue are negative prognostic marker for patients’ survival.

          Related collections

          Most cited references66

          • Record: found
          • Abstract: found
          • Article: found
          Is Open Access

          IL-17 can promote tumor growth through an IL-6–Stat3 signaling pathway

          Lin Wang, Tangsheng Yi, Marcin Kortylewski … (2009)
          Although the Th17 subset and its signature cytokine, interleukin (IL)-17A (IL-17), are implicated in certain autoimmune diseases, their role in cancer remains to be further explored. IL-17 has been shown to be elevated in several types of cancer, but how it might contribute to tumor growth is still unclear. We show that growth of B16 melanoma and MB49 bladder carcinoma is reduced in IL-17−/− mice but drastically accelerated in IFN-γ−/− mice, contributed to by elevated intratumoral IL-17, indicating a role of IL-17 in promoting tumor growth. Adoptive transfer studies and analysis of the tumor microenvironment suggest that CD4+ T cells are the predominant source of IL-17. Enhancement of tumor growth by IL-17 involves direct effects on tumor cells and tumor-associated stromal cells, which bear IL-17 receptors. IL-17 induces IL-6 production, which in turn activates oncogenic signal transducer and activator of transcription (Stat) 3, up-regulating prosurvival and proangiogenic genes. The Th17 response can thus promote tumor growth, in part via an IL-6–Stat3 pathway.
          Article 0 comments Cited 259 times – based on 0 reviews     Review now
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Complementary DNA for a novel human interleukin (BSF-2) that induces B lymphocytes to produce immunoglobulin.

            T Hirano, K Yasukawa, H Harada … (1986)
            When stimulated with antigen, B cells are influenced by T cells to proliferate and differentiate into antibody-forming cells. Since it was reported that soluble factors could replace certain functions of helper T cells in the antibody response, several different kinds of lymphokines and monokines have been reported in B-cell growth and differentiation. Among these, human B-cell differentiation factor (BCDF or BSF-2) has been shown to induce the final maturation of B cells into immunoglobulin-secreting cells. BSF-2 was purified to homogeneity and its partial NH2-terminal amino-acid sequence was determined. These studies indicated that BSF-2 is functionally and structurally unlike other known proteins. Here, we report the molecular cloning, structural analysis and functional expression of the cDNA encoding human BSF-2. The primary sequence of BSF-2 deduced from the cDNA reveals that BSF-2 is a novel interleukin consisting of 184 amino acids.
            Article 0 comments Cited 249 times – based on 0 reviews     Review now
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Phenotype, distribution, generation, and functional and clinical relevance of Th17 cells in the human tumor environments.

              Ilona Kryczek, Mousumi Banerjee, Pui Cheng … (2009)
              Th17 cells play an active role in autoimmune diseases. However, the nature of Th17 cells is poorly understood in cancer patients. We studied Th17 cells, the associated mechanisms, and clinical significance in 201 ovarian cancer patients. Tumor-infiltrating Th17 cells exhibit a polyfunctional effector T-cell phenotype, are positively associated with effector cells, and are negatively associated with tumor-infiltrating regulatory T cells. Tumor-associated macrophages promote Th17 cells through interleukin-1beta (IL-1beta), whereas tumor-infiltrating regulatory T cells inhibit Th17 cells through an adenosinergic pathway. Furthermore, through synergistic action between IL-17 and interferon-gamma, Th17 cells stimulate CXCL9 and CXCL10 production to recruit effector T cells to the tumor microenvironment. The levels of CXCL9 and CXCL10 are associated with tumor-infiltrating effector T cells. The levels of tumor-infiltrating Th17 cells and the levels of ascites IL-17 are reduced in more advanced diseases and positively predict patient outcome. Altogether, Th17 cells may contribute to protective human tumor immunity through inducing Th1-type chemokines and recruiting effector cells to the tumor microenvironment. Inhibition of Th17 cells represents a novel immune evasion mechanism. This study thus provides scientific and clinical rationale for developing novel immune-boosting strategies based on promoting the Th17 cell population in cancer patients.
              Article 0 comments Cited 245 times – based on 0 reviews     Review now
                Bookmark
                All references

                Author and article information

                Journal
                Journal ID (nlm-ta): Open Access Maced J Med Sci
                Journal ID (iso-abbrev): Open Access Maced J Med Sci
                Title: Open Access Macedonian Journal of Medical Sciences
                Publisher: Republic of Macedonia (ID Design 2012/DOOEL Skopje )
                ISSN (Electronic): 1857-9655
                Publication date Collection: 30 July 2019
                Publication date (Electronic): 20 July 2019
                Volume: 7
                Issue: 14
                Pages: 2391-2398
                Affiliations
                [1 ]Department of Surgery, Trakia University, Medical Faculty, Stara Zagora, Bulgaria
                [2 ]Department of General and clinical pathology, Medical Faculty, Trakia University Stara Zagora, Bulgaria
                Author notes
                [* ] Correspondence: Dimitur Chavdarov Chonov. Department of Surgery, Trakia University, Medical Faculty, Stara Zagora, Bulgaria; Department of General and clinical pathology, Medical Faculty, Trakia University Stara Zagora, Bulgaria. E-mail: dimityr_chonov@ 123456abv.bg
                Article
                Publisher ID: OAMJMS-7-2391
                DOI: 10.3889/oamjms.2019.589
                PMC ID: 6765074
                PubMed ID: 31592285
                SO-VID: 5a561331-ee28-422a-b9f1-9f71e9c8c93f
                Copyright © Copyright: © 2019 Dimitur Chavdarov Chonov, Maria Magdalena Krasimirova Ignatova, Julian Rumenov Ananiev, Maya Vladova Gulubova.
                License:

                This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 International License (CC BY-NC 4.0).

                History
                Date received : 31 March 2019
                Date revision received : 09 July 2019
                Date accepted : 09 July 2019
                Categories
                Subject: Review Article

                Keywords: il-6,stat3,tumor microenvironment
                Data availability:
                Keywords: il-6, stat3, tumor microenvironment

                Comments

                Comment on this article

                scite_

                Similar content313

                See all similar

                Cited by25

                See all cited by

                Most referenced authors1,154

                See all reference authors