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首页> 外文期刊>Cell cycle >Fas ligand promotes tumor immune evasion of colon cancer in vivo.
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Fas ligand promotes tumor immune evasion of colon cancer in vivo.

机译：Fas配体在体内促进结肠癌的肿瘤免疫逃避。

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The study of the role of Fas ligand (FasL/CD95L) in tumor immune evasion has been complicated by the discovery that FasL may trigger cytokine secretion and induce inflammation. Antisense suppression of FasL expression by colon tumor cells was used to investigate if a reduction in endogenously expressed FasL in tumors resulted in reduced tumor development and improved anti-tumor immune challenge in vivo. Downregulation of FasL expression had no effect on tumor growth in vitro but significantly reduced tumor development in syngeneic immune-competent mice in vivo. Tumor size was also significantly decreased. Reduced FasL expression by tumor cells was associated with increased lymphocyte infiltration. Moreover, constitutively expressed FasL was not pro-inflammatory. This study indicates that upregulation of FasL expression by colon tumor cells results in an improved anti-tumor immune challenge in vivo, providing functional evidence in favor of the 'Fas counterattack' as a mechanism of tumor immune evasion.
机译：FasL（FasL / CD95L）在肿瘤免疫逃逸中的作用的研究由于发现FasL可能触发细胞因子分泌并诱导炎症而变得复杂。结肠肿瘤细胞对FasL表达的反义抑制被用于研究肿瘤中内源性表达FasL的减少是否导致肿瘤的发展减少和体内抗肿瘤免疫攻击的改善。 FasL表达的下调在体外对肿瘤的生长没有影响，但是在体内具有同种免疫能力的小鼠体内显着降低了肿瘤的生长。肿瘤大小也明显减少。肿瘤细胞FasL表达减少与淋巴细胞浸润增加有关。此外，组成型表达的FasL不是促炎的。这项研究表明，结肠肿瘤细胞对FasL表达的上调导致体内抗肿瘤免疫攻击的改善，提供了支持“ Fas反攻”作为肿瘤免疫逃逸机制的功能证据。

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