RNF43 p.G659fs 通过 PI3K/AKT/mTOR 信号通路和 HLA-E 上调导致 MSI-high 结直肠癌中 NK 细胞功能障碍
RNF43 p.G659fs leads to natural killer cell dysfunction in MSI-high colorectal cancer through PI3K/AKT/mTOR signaling and HLA-E up-regulation.
CELL INTELLIGENCE · 肿瘤细胞治疗研究
肿瘤细胞治疗研究
英文原题:Mathematical modeling of tumor-immune system interactions: the effect of rituximab on breast cancer immune response.
Mathematical modeling of tumor-immune system interactions: the effect of rituximab on breast cancer immune response.
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tBregs 是新发现的 B 调节细胞亚类,由乳腺癌产生,导致 Tregs 增加,从而导致 NK 细胞死亡。在本研究中,我们使用数学和计算方法来研究上述细胞以及 CD8 + T 细胞、CD4 + T 细胞和 B 细胞之间复杂的相互作用。此外,我们使用数据拟合来证明 NK 细胞裂解乳腺癌细胞的功能反应具有比率依赖形式。另外,我们在模型中纳入了 rituximab 的浓度——一种已被建议作为潜在乳腺癌治疗的单克隆抗体——并测试其在给予标准剂量以及实验剂量时的效果。
tBregs are a newly discovered subcategory of B regulatory cells, which are generated by breast cancer, resulting in the increase of Tregs and therefore in the death of NK cells. In this study, we use a mathematical and computational approach to investigate the complex interactions between the aforementioned cells as well as CD8 + T cells, CD4 + T cells and B cells.
Furthermore, we use data fitting to prove that the functional response regarding the lysis of breast cancer cells by NK cells has a ratio-dependent form.
Additionally, we include in our model the concentration of rituximab - a monoclonal antibody that has been suggested as a potential breast cancer therapy - and test its effect, when the standard, as well as experimental dosages, are administered.
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