Ostrand-Rosenberg Suzanne
University of Maryland, Baltimore County, Department of Biological Sciences, 1000 Hilltop Circle, Baltimore, MD 21250, United States.
Curr Opin Genet Dev. 2008 Feb;18(1):11-8. doi: 10.1016/j.gde.2007.12.007. Epub 2008 Mar 4.
Precancerous and malignant cells can induce an immune response which results in the destruction of transformed and/or malignant cells, a process known as immune surveillance. However, immune surveillance is not always successful, resulting in 'edited' tumors that have escaped immune surveillance. Immunoediting is not simply because of the absence of antitumor immunity, but is because of protumor immunity that blocks antitumor adaptive and innate responses, and promotes conditions that favor tumor progression. Several immune protumor effector mechanisms are upregulated by chronic inflammation, leading to the hypothesis that inflammation promotes carcinogenesis and tumor growth by altering the balance between protumor and antitumor immunity, thereby preventing the immune system from rejecting malignant cells, and providing a tumor-friendly environment for progressive disease.
癌前细胞和恶性细胞可诱导免疫反应，导致转化细胞和/或恶性细胞被破坏，这一过程称为免疫监视。然而，免疫监视并非总能成功，从而产生逃避免疫监视的“编辑后”肿瘤。免疫编辑并非仅仅是因为缺乏抗肿瘤免疫力，而是由于促肿瘤免疫会阻断抗肿瘤适应性免疫和固有免疫反应，并促进有利于肿瘤进展的条件。慢性炎症会上调多种免疫促肿瘤效应机制，由此产生一种假说，即炎症通过改变促肿瘤免疫和抗肿瘤免疫之间的平衡来促进癌症发生和肿瘤生长，从而阻止免疫系统排斥恶性细胞，并为疾病进展提供一个有利于肿瘤生长的环境。
