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T-Cell Dysfunction and Inhibitory Receptors in Hepatitis C Virus Infection

  • Lee, Jino (Laboratory of Immunology and Infectious Diseases, Graduate School of Medical Science and Engineering, KAIST) ;
  • Suh, William I. (Laboratory of Immunology and Infectious Diseases, Graduate School of Medical Science and Engineering, KAIST) ;
  • Shin, Eui-Cheol (Laboratory of Immunology and Infectious Diseases, Graduate School of Medical Science and Engineering, KAIST)
  • Received : 2010.08.18
  • Accepted : 2010.08.24
  • Published : 2010.08.31

Abstract

Dysfunction of the virus-specific T cells is a cardinal feature in chronic persistent viral infections such as one caused by hepatitis C virus (HCV). In chronic HCV infection, virus-specific dysfunctional CD8 T cells often overexpress various inhibitory receptors. Programmed cell death 1 (PD-1) was the first among these inhibitory receptors that were identified to be overexpressed in functionally impaired T cells. The roles of other inhibitory receptors such as cytotoxic T lymphocyte-associated antigen-4 (CTLA-4) and T cell immunoglobulin and mucin domain-containing molecule 3 (Tim-3) have also been demonstrated in T-cell dysfunctions that occur in chronic HCV patients. Blocking these inhibitory receptors in vitro restores the functions of HCV-specific CD8 T cells and allows enhanced proliferation, cytolytic activity and cytokine production. Therefore, the blockade of the inhibitory receptors is considered as a novel strategy for the treatment of chronic HCV infection.

Keywords

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