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Mediators of Inflammation
Volume 2014, Article ID 564296, 15 pages
Review Article

Control of the Inflammatory Response Mechanisms Mediated by Natural and Induced Regulatory T-Cells in HCV-, HTLV-1-, and EBV-Associated Cancers

1CNRS UMR 8161, Institut de Biologie de Lille, Universit Lille-Nord de France, SIRIC ONCOLille, Institut Pasteur de Lille, IFR142, 1 rue du Professeur Calmette, 59021 Lille Cedex, France
2UFR de Biologie, Université de Lille 1, Cité Scientifique, Bâtiment SN3, 59655 Villeneuve d’Ascq Cedex, France

Received 14 March 2014; Revised 18 June 2014; Accepted 30 July 2014; Published 30 November 2014

Academic Editor: Constantino López-Macías

Copyright © 2014 Laurissa Ouaguia et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Virus infections are involved in chronic inflammation and, in some cases, cancer development. Although a viral infection activates the immune system’s response that eradicates the pathogen mainly through inflammatory mechanisms, it is now recognized that this inflammatory condition is also favorable to the development of tumors. Indeed, it is well described that viruses, such as hepatitis C virus (HCV), Epstein Barr virus (EBV), human papillomavirus (HPV) or human T-cell lymphotropic virus type-1 (HTLV-1), are important risk factors for tumor malignancies. The inflammatory response is a fundamental immune mechanism which involves several molecular and cellular components consisting of cytokines and chemokines that are released by various proinflammatory cells. In parallel to this process, some endogenous recruited components release anti-inflammatory mediators to restore homeostasis. The development of tools and strategies using viruses to hijack the immune response is mostly linked to the presence of regulatory T-cells (Treg) that can inhibit inflammation and antiviral responses of other effector cells. In this review, we will focus on current understanding of the role of natural and induced Treg in the control and the resolution of inflammatory response in HCV-, HTLV-1-, and EBV-associated cancers.