Inhibition of Th17 cells and induction of regulatory T cells is mediated by SOCS-1 in the tumor microenvironment of breast cancer patients

Abstract

Event Abstract Back to Event Inhibition of Th17 cells and induction of regulatory T cells is mediated by SOCS-1 in the tumor microenvironment of breast cancer patients Arash Pourgholaminejad1, 2*, Rahil Eftekhari1, Keivan Majidzadeh3 and Jamshid Hadjati1 1 School of Medicine- Tehran University of Medical Sciences, Department of Immunology, Iran 2 Faculty of Medical Sciences- Tarbiat Modares University, Department of Immunology, Iran 3 Iranian Center for Breast Cancer (ICBC); Academic Center for Education, Culture and Research (ACECR), Iran Introduction: Suppressors of cytokine signaling (SOCS) are important negative feedback regulators of the JAK/STAT signaling pathway, and have been recently investigated for their role in the development of different cancers. It has been shown that SOCS-1 negatively regulates STAT-3 activation in breast cancer tissues and therefore it may be a regulator of Th17 cells in tumor area. In the preset study, we demonstrated that SOCS-1 is in associated with decrease of Th17 cells and increase of Tregs in breast cancer patients. Methods and Materials: In this study, we examined the expression of SOCS-1 gene in normal and breast cancer tissue and correlated this with factors related to Th17 cells and Tregs. Human breast cancer tissues from 4 stages and normal tissues were collected. Afterward, mRNA was extracted from the tissues and cDNA was synthesized. Subsequently, the mRNA expression of genes related to Th17 cells (IL-17, RORc, STAT-3) and Tregs (FoxP3, IL-10, CTLA-4) and also SOCS-1 were determined by Quantitative Real-time PCR. Results: The results showed that the expression of SOCS-1 gene is increased in breast cancer and it negatively associated with IL-17, RORc and STAT-3 gene expression significantly and also factors related to regulatory T cells such as IL-10, FoxP3 and CTLA-4 is decreased. Conclusion: We concluded that regulatory T cell responses increase in the tumor microenvironment and that inversely correlates with Th17 cells as a potent anti-tumor immune response. It seems that SOCS-1 inhibits Th17 and also induces Tregs in breast cancer patients with advanced stages. Keywords: SOCS-1, Th17, Treg, breast cancer, Tumor Microenvironment Conference: 15th International Congress of Immunology (ICI), Milan, Italy, 22 Aug - 27 Aug, 2013. Presentation Type: Abstract Topic: Immune-mediated disease pathogenesis Citation: Pourgholaminejad A, Eftekhari R, Majidzadeh K and Hadjati J (2013). Inhibition of Th17 cells and induction of regulatory T cells is mediated by SOCS-1 in the tumor microenvironment of breast cancer patients. Front. Immunol. Conference Abstract: 15th International Congress of Immunology (ICI). doi: 10.3389/conf.fimmu.2013.02.00088 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 08 Mar 2013; Published Online: 22 Aug 2013. * Correspondence: Mr. Arash Pourgholaminejad, School of Medicine- Tehran University of Medical Sciences, Department of Immunology, Tehran, Iran, arash_pgn@yahoo.com Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Arash Pourgholaminejad Rahil Eftekhari Keivan Majidzadeh Jamshid Hadjati Google Arash Pourgholaminejad Rahil Eftekhari Keivan Majidzadeh Jamshid Hadjati Google Scholar Arash Pourgholaminejad Rahil Eftekhari Keivan Majidzadeh Jamshid Hadjati PubMed Arash Pourgholaminejad Rahil Eftekhari Keivan Majidzadeh Jamshid Hadjati Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.