幾十年來,，免疫系統(tǒng)在腫瘤進展中的作用一直受到關(guān)注討論,。許多研究表明低免疫反應可能對腫瘤的生長是有益的,，只有強烈的免疫反應才可以對付腫瘤的生長，從而抑制腫瘤進展,。
近來,，研究人員采用能捕獲癌癥干細胞和非腫瘤干細胞通過自我轉(zhuǎn)移過程中種群間動態(tài)相互作用的模型。通過這個模型研究人員模擬了免疫系統(tǒng),，觀察免疫反應對腫瘤的擴散過程的影響,。
研究人員發(fā)現(xiàn)低毒性的免疫反應能不斷地殺死癌細胞，雖然效率比較低,，但能導致空間受限的癌癥干細胞之間距離增大，推動腫瘤細胞自我轉(zhuǎn)移以及持續(xù)的腫瘤生長,。然而,，隨著免疫系統(tǒng)力量的增加，腫瘤生長達到了高峰階段,，然后腫瘤團塊最終不受限于免疫反應的影響,。這種日益增長的免疫反應與癌癥干細胞的數(shù)量和比例遞增相關(guān)，提示癌癥干細胞對免疫反應存在其他意想不到的響應,。 （生物谷：Bioon.com）
編譯自：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.
