几十年来，免疫系统在肿瘤进展中的作用一直受到关注讨论。许多研究表明低免疫反应可能对肿瘤的生长是有益的，只有强烈的免疫反应才可以对付肿瘤的生长，从而抑制肿瘤进展。
近来，研究人员采用能捕获癌症干细胞和非肿瘤干细胞通过自我转移过程中种群间动态相互作用的模型。通过这个模型研究人员模拟了免疫系统，观察免疫反应对肿瘤的扩散过程的影响。
研究人员发现低毒性的免疫反应能不断地杀死癌细胞，虽然效率比较低，但能导致空间受限的癌症干细胞之间距离增大，推动肿瘤细胞自我转移以及持续的肿瘤生长。然而，随着免疫系统力量的增加，肿瘤生长达到了高峰阶段，然后肿瘤团块最终不受限于免疫反应的影响。这种日益增长的免疫反应与癌症干细胞的数量和比例递增相关，提示癌症干细胞对免疫反应存在其他意想不到的响应。 （生物谷：Bioon.com）
编译自：Immunoediting: Evidence of the multifaceted role of the immune system in self-metastatic tumor growth
doi:10.1186/1742-4682-9-31
PMC:
PMID:
Immunoediting: Evidence of the multifaceted role of the immune system in self-metastatic tumor growth
Heiko Enderling, Lynn Hlatky and Philip Hahnfeldt
Background
The role of the immune system in tumor progression has been subject to discussion for many decades. Numerous studies suggest that a low immune response might be beneficial, if not necessary, for tumor growth, and only a strong immune response can counter tumor growth and thus inhibit progression.
Methods
We implement a cellular automaton model previously described that captures the dynamical interactions between the cancer stem and non-stem cell populations of a tumor through a process of self-metastasis. By overlaying on this model the diffusion of immune reactants into the tumor from a peripheral source to target cells, we simulate the process of immune-system-induced cell kill on tumor progression.
Results
A low cytotoxic immune reaction continuously kills cancer cells and, although at a low rate, thereby causes the liberation of space-constrained cancer stem cells to drive self-metastatic progression and continued tumor growth. With increasing immune system strength, however, tumor growth peaks, and then eventually falls below the intrinsic tumor sizes observed without an immune response. With this increasing immune response the number and proportion of cancer stem cells monotonically increases, implicating an additional unexpected consequence, that of cancer stem cell selection, to the immune response.
Conclusions
Cancer stem cells and immune cytotoxicity alone are sufficient to explain the three-step "immunoediting" concept - the modulation of tumor growth through inhibition, selection and promotion.
