TY - JOUR
T1 - A critical function for type I interferons in cancer immunoediting
AU - Dunn, Gavin P.
AU - Bruce, Allen T.
AU - Sheehan, Kathleen C.F.
AU - Shankaran, Vijay
AU - Uppaluri, Ravindra
AU - Bui, Jack D.
AU - Diamond, Mark S.
AU - Koebel, Catherine M.
AU - Arthur, Cora
AU - White, J. Michael
AU - Schreiber, Robert D.
N1 - Funding Information:
We thank L. Old of the Ludwig Institute for Cancer Research; members of the Schreiber laboratory for discussions throughout this work; W. Yokoyama and M. Orihuela and the Speed Congenics Core facility of the Rheumatic Diseases Core Center at Washington University for genetic marker analyses; and D. Kreamalmeyer, K. Kooi and T. Irwin for assistance with animal work. Supported by the National Cancer Institute (CA43059 and CA107527), Ludwig Institute for Cancer Research and Cancer Research Institute.
PY - 2005
Y1 - 2005
N2 - 'Cancer immunoediting' is a process wherein the immune system protects hosts against tumor development and facilitates outgrowth of tumors with reduced immunogenicity. Although interferon-γ (IFN-γ) is known to be involved in this process, the involvement of type I interferons (IFN-α/β) has not been elucidated. We now show that, like IFN-γ, endogenously produced IFN-α/β was required for the prevention of the growth of primary carcinogen-induced and transplantable tumors. Although tumor cells are important IFN-γ targets, they are not functionally relevant sites of the actions of the type I interferons. Instead, host hematopoietic cells are critical IFN-α/β 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-γ.
AB - 'Cancer immunoediting' is a process wherein the immune system protects hosts against tumor development and facilitates outgrowth of tumors with reduced immunogenicity. Although interferon-γ (IFN-γ) is known to be involved in this process, the involvement of type I interferons (IFN-α/β) has not been elucidated. We now show that, like IFN-γ, endogenously produced IFN-α/β was required for the prevention of the growth of primary carcinogen-induced and transplantable tumors. Although tumor cells are important IFN-γ targets, they are not functionally relevant sites of the actions of the type I interferons. Instead, host hematopoietic cells are critical IFN-α/β 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-γ.
UR - http://www.scopus.com/inward/record.url?scp=22144465860&partnerID=8YFLogxK
U2 - 10.1038/ni1213
DO - 10.1038/ni1213
M3 - Article
C2 - 15951814
AN - SCOPUS:22144465860
SN - 1529-2908
VL - 6
SP - 722
EP - 729
JO - Nature immunology
JF - Nature immunology
IS - 7
ER -