A critical function for type I interferons in cancer immunoediting

Nat Immunol. 2005 Jul;6(7):722-9. doi: 10.1038/ni1213. Epub 2005 Jun 12.


'Cancer immunoediting' is a process wherein the immune system protects hosts against tumor development and facilitates outgrowth of tumors with reduced immunogenicity. Although interferon-gamma (IFN-gamma) is known to be involved in this process, the involvement of type I interferons (IFN-alpha/beta) has not been elucidated. We now show that, like IFN-gamma, endogenously produced IFN-alpha/beta was required for the prevention of the growth of primary carcinogen-induced and transplantable tumors. Although tumor cells are important IFN-gamma targets, they are not functionally relevant sites of the actions of the type I interferons. Instead, host hematopoietic cells are critical IFN-alpha/beta targets during development of protective antitumor responses. Therefore, type I interferons are important components of the cancer immunoediting process and function in a way that does not completely overlap the functions of IFN-gamma.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • DNA-Binding Proteins / immunology
  • Hematopoiesis / immunology
  • Interferon-alpha / immunology*
  • Membrane Proteins / immunology*
  • Methylcholanthrene
  • Mice
  • Mice, Knockout
  • Neoplasms, Experimental / immunology*
  • Radiation Chimera
  • Receptor, Interferon alpha-beta
  • Receptors, Interferon / immunology*
  • Sarcoma / immunology*
  • Tumor Escape / immunology*


  • DNA-Binding Proteins
  • Interferon-alpha
  • Membrane Proteins
  • Rag2 protein, mouse
  • Receptors, Interferon
  • V(D)J recombination activating protein 2
  • Receptor, Interferon alpha-beta
  • Methylcholanthrene