Direct effects of type I interferons on cells of the immune system

Clin Cancer Res. 2011 May 1;17(9):2619-27. doi: 10.1158/1078-0432.CCR-10-1114. Epub 2011 Mar 3.

Abstract

Type I interferons (IFN-I) are well-known inducers of tumor cell apoptosis and antiangiogenesis via signaling through a common receptor interferon alpha receptor (IFNAR). IFNAR induces the Janus activated kinase-signal transducer and activation of transcription (JAK-STAT) pathway in most cells, along with other biochemical pathways that may differentially operate, depending on the responding cell subset, and jointly control a large collection of genes. IFNs-I were found to systemically activate natural killer (NK) cell activity. Recently, mouse experiments have shown that IFNs-I directly activate other cells of the immune system, such as antigen-presenting dendritic cells (DC) and CD4 and CD8 T cells. Signaling through the IFNAR in T cells is critical for the acquisition of effector functions. Cross-talk between IFNAR and the pathways turned on by other surface lymphocyte receptors has been described. Importantly, IFNs-I also increase antigen presentation of the tumor cells to be recognized by T lymphocytes. These IFN-driven immunostimulatory pathways offer opportunities to devise combinatorial immunotherapy strategies.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Antigen-Presenting Cells / drug effects
  • Antigen-Presenting Cells / immunology
  • Cells / drug effects*
  • Cells / immunology
  • Humans
  • Immune System / drug effects*
  • Interferon Type I / pharmacology*
  • Mice
  • Models, Biological
  • Signal Transduction / drug effects
  • Signal Transduction / physiology
  • T-Lymphocytes / drug effects
  • T-Lymphocytes / immunology

Substances

  • Interferon Type I