title: Control of the inflammatory response mechanisms mediated by natural and induced regulatory T-cells in HCV-, HTLV-1-, and EBV-associated cancers.
abstract: 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.
authors.affiliation: CNRS 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.
authors.forename: Laurissa
authors.identifier: 0000-0002-3216-3950
authors.initials: L
authors.lastname: Ouaguia
authors.affiliation: CNRS 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.
authors.forename: Dhafer
authors.identifier: 0000-0003-1767-3300
authors.initials: D
authors.lastname: Mrizak
authors.affiliation: CNRS 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.
authors.forename: Sarah
authors.identifier: 0000-0002-7595-754X
authors.initials: S
authors.lastname: Renaud
authors.affiliation: CNRS 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.
authors.forename: Olivier
authors.initials: O
authors.lastname: Moralès
authors.affiliation: CNRS 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 ; UFR de Biologie, Université de Lille 1, Cité Scientifique, Bâtiment SN3, 59655 Villeneuve d'Ascq Cedex, France.
authors.forename: Nadira
authors.initials: N
authors.lastname: Delhem
mesh_terms: D000818:Animals; D002277:Carcinoma / Q000821:virology; D006528:Carcinoma, Hepatocellular / Q000821:virology; D016174:Hepacivirus / Q000378:metabolism*; D004854:Herpesvirus 4, Human / Q000378:metabolism*; D006689:Hodgkin Disease / Q000821:virology; D006706:Homeostasis; D015368:Human T-lymphotropic virus 1 / Q000378:metabolism*; D006801:Humans; D007113:Immunity, Innate; D007249:Inflammation / Q000378:metabolism*; D015458:Leukemia, T-Cell / Q000821:virology; D008113:Liver Neoplasms / Q000821:virology; D016399:Lymphoma, T-Cell / Q000821:virology; D000077274:Nasopharyngeal Carcinoma; D009303:Nasopharyngeal Neoplasms / Q000821:virology; D009369:Neoplasms / Q000821:virology*; D012307:Risk Factors; D050378:T-Lymphocytes, Regulatory / Q000166:cytology*