A critical function for type I interferons in cancer immunoediting
A critical function for type I interferons in cancer immunoediting
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DOI：
10.1038/ni1213
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发表时间：
2005-07-01
影响因子：
30.5
通讯作者：
Schreiber, RD
中科院分区：
文献类型：
--
作者：
Dunn, GP;Bruce, AT;Schreiber, RD
“癌症免疫编辑”是一种过程，其中免疫系统保护宿主免受肿瘤发展并促进具有降低的免疫原性的肿瘤的生长。虽然干扰素-γ（IFN-γ）已知参与该过程，但1型干扰素（IFN-α/β）的参与尚未阐明。我们现在表明，像IFN-γ一样，内源性产生的IFN-α/β是预防原发性致癌物诱导的可移植肿瘤生长所必需的。虽然肿瘤细胞是重要的IFN-γ靶点，但它们不是1型干扰素作用的功能相关位点。相反，宿主造血细胞是保护性抗肿瘤反应发展过程中的关键IFN-α/β靶标。因此，1型干扰素是癌症免疫编辑过程的重要组成部分，其功能与IFN-γ的功能不完全重叠。
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 1 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 1 interferons. Instead, host hematopoietic cells are critical IFN-alpha/beta targets during development of protective antitumor responses. Therefore, type 1 interferons are important components of the cancer immunoediting process and function in a way that does not completely overlap the functions of IFN-gamma.