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首页> 外文期刊>Molecular Immunology >TLR1/TLR2 signaling blocks the suppression of monocytic myeloid-derived suppressor cell by promoting its differentiation into Ml-type macrophage
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TLR1/TLR2 signaling blocks the suppression of monocytic myeloid-derived suppressor cell by promoting its differentiation into Ml-type macrophage

机译:TLR1 / TLR2信号传导通过促进其分化为ML型巨噬细胞来阻断单核细胞骨髓衍生的抑制细胞的抑制

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摘要

Myeloid derived suppressor cells (MDSCs) play a key role in tumor immunosuppressive microenvironment, which helps tumors avoid immune destruction. Blocking the suppressive activities of MDSCs could be a promising strategy to enhance the effect of anti-tumor immunotherapies. In this study, we found that TLR1/TLR2 expression predicted favorable prognosis of lung cancer patients, In the related mice tumor model, TLR1/TLR2 activation by synthetic bacterial lipoprotein (BLP), a TLR1/2 agonist, greatly inhibited tumor growth and selectively decreased monocytic MDSCs (M-MDSCs). Furthermore, BLP treatment redirected M-MDSC differentiation towards Ml macrophage through JNK pathway, and thus blocked the suppressive activity of M-MDSCs in a TLR2-dependent manner. Therefore, our data demonstrated that TLR2 could be a promising biomarker and a potential immunotherapeutic target for lung cancer.
机译:骨髓衍生的抑制细胞(MDSC)在肿瘤免疫抑制微环境中起关键作用,这有助于肿瘤避免免疫破坏。 阻断MDSCS的抑制活性可能是提高抗肿瘤免疫治疗的影响的有希望的策略。 在这项研究中,我们发现TLR1 / TLR2表达预测肺癌患者的良好预后,在相关小鼠肿瘤模型中,通过合成细菌脂蛋白(BLP)的TLR1 / TLR2活化,TLR1 / 2激动剂,极大地抑制肿瘤生长和选择性 减少单核细胞MDSC(MSCS)。 此外,通过JNK途径将BLP处理重定向于ML巨噬细胞的M-MDSC分化,从而阻止了以TLR2依赖性方式抑制M-MDSC的抑制活性。 因此,我们的数据表明TLR2可以是有希望的生物标志物和肺癌的潜在免疫治疗靶标。

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