Interferon-γ and cancer immunoediting
Interferon-γ and cancer immunoediting
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DOI：
10.1385/ir:32:1-3:231
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发表时间：
2005-01-01
影响因子：
4.4
通讯作者：
Schreiber, RD
中科院分区：
文献类型：
--
作者：
Dunn, GP;Ikeda, H;Schreiber, RD
在过去的12年里，我们已经证明了干扰素-伽马和淋巴细胞合作来调节小鼠的肿瘤发展。具体地说，我们发现免疫系统不仅防止原发(致癌物诱导的和自发的)和移植肿瘤的生长，而且还塑造了形成的肿瘤的免疫原性。这些观察使我们将Burnet和Thomas的旧的和有争议的“癌症免疫监控”假说改进为我们称之为癌症免疫编辑的假说，该假说更好地强调了免疫在肿瘤发展中自相矛盾的宿主保护和肿瘤生长作用。我们目前的工作重点是定义癌症免疫编辑的分子机制，并探索这一过程对癌症免疫治疗的影响。
Over the last 12 yr, we have shown that interferon-gamma and lymphocytes collaborate to regulate tumor development in mice. Specifically, we found that the immune system not only prevents the growth of primary (carcinogen-induced and spontaneous) and transplanted tumors but also sculpts the immunogenicity of tumors that form. These observations led us to refine the old and controversial "cancer immunosurveillance" hypothesis of Burnet and Thomas into one that we termed cancer immunoediting that better emphasizes the paradoxical host-protective and tumor-sculpting roles of immunity on developing tumors. Our current work focuses on defining the molecular mechanisms that underlie cancer immunoediting and exploring the implications of this process for cancer immunotherapy.