Format

Send to

Choose Destination
Mediators Inflamm. 2014;2014:564296. doi: 10.1155/2014/564296. Epub 2014 Nov 30.

Control of the inflammatory response mechanisms mediated by natural and induced regulatory T-cells in HCV-, HTLV-1-, and EBV-associated cancers.

Author information

1
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.
2
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.

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.

PMID:
25525301
PMCID:
PMC4267219
DOI:
10.1155/2014/564296
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Hindawi Limited Icon for PubMed Central
Loading ...
Support Center