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Article
Nature Immunology  6, 722 - 729 (2005)
Published online: 12 June 2005; Corrected online: 24 June 2005 | doi:10.1038/ni1213


There is a Corrigendum (August 2005) associated with this Article.

A critical function for type I interferons in cancer immunoediting

Gavin P Dunn1, 2, Allen T Bruce1, 2, Kathleen C F Sheehan1, Vijay Shankaran1, Ravindra Uppaluri1, Jack D Bui1, Mark S Diamond1, Catherine M Koebel1, Cora Arthur1, J Michael White1 & Robert D Schreiber1

1  Department of Pathology and Immunology, Center for Immunology, Washington University School of Medicine, St. Louis, Missouri 63110, USA.

2  These authors contributed equally to this work.

Correspondence should be addressed to Robert D Schreiber schreiber@immunology.wustl.edu
'Cancer immunoediting' is a process wherein the immune system protects hosts against tumor development and facilitates outgrowth of tumors with reduced immunogenicity. Although interferon-bold gamma (IFN-bold 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-bold 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-bold 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-bold gamma.

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Nature Immunology
ISSN: 1529-2908
EISSN: 1529-2916
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