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Oncogenic transformation tunes the cross-talk between mesenchymal stem cells and T lymphocytes

机译:致癌转化可调节间充质干细胞与T淋巴细胞之间的串扰

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Stem cells from mesenchymal origin (MSC) exert a plethora of immunomodulatory effects. We created a neoplastic model based on in vitro step-wise transformation to assess whether oncogenic pathways have the capacity to mould the cross-talk of MSC and lymphocytes. Neoplastic MSC exhibit an increased inhibitory effect on T cell proliferation, either directly or mediated by myeloid derived suppressor cells. Additionally, transformation of MSC enhances T cell apoptosis without reducing either the percentage of CD25 expressing cells or the level of this protein expression. Malignant transformation drives MSC to lose dependency on nitric oxide for immunosuppression whilst increasing the constitutive production of PGE2. Our results indicate that oncogenesis tunes the interplay between MSC and immune cells, favoring cancer immune evasion.
机译:间充质来源(MSC)的干细胞发挥过多的免疫调节作用。我们基于体外逐步转化建立了一个肿瘤模型,以评估致癌途径是否具有塑造MSC和淋巴细胞串扰的能力。肿瘤性MSC直接或通过髓样来源的抑制细胞介导对T细胞增殖的抑制作用增强。另外,MSC的转化增强了T细胞凋亡,而没有降低表达CD25的细胞的百分比或该蛋白表达的水平。恶性转化驱使MSC失去对一氧化氮的免疫抑制依赖性,同时增加了PGE2的组成型产生。我们的结果表明,肿瘤发生可调节MSC与免疫细胞之间的相互作用,从而有利于癌症的免疫逃逸。

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