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

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

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.

Publication types

  • Review

MeSH terms

  • Animals
  • Carcinoma / virology
  • Carcinoma, Hepatocellular / virology
  • Hepacivirus / metabolism*
  • Herpesvirus 4, Human / metabolism*
  • Hodgkin Disease / virology
  • Homeostasis
  • Human T-lymphotropic virus 1 / metabolism*
  • Humans
  • Immunity, Innate
  • Inflammation / metabolism*
  • Leukemia, T-Cell / virology
  • Liver Neoplasms / virology
  • Lymphoma, T-Cell / virology
  • Nasopharyngeal Carcinoma
  • Nasopharyngeal Neoplasms / virology
  • Neoplasms / virology*
  • Risk Factors
  • T-Lymphocytes, Regulatory / cytology*