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Nat Immunol ; 6(7): 722-9, 2005 Jul.
Article in English | MEDLINE | ID: mdl-15951814

ABSTRACT

'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.


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