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Nod-Like Receptors: Key Molecular Switches in the Conundrum of Cancer

机译:点头受体:癌症难题中的关键分子开关

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摘要

It is believed the immune system can contribute to oncogenic transformation especially in settings of chronic inflammation, be activated during immunosurveillance to destroy early neoplastic cells before they undergo malignant outgrowth, and finally, can assist growth of established tumors by preventing clearance, remodeling surrounding tissue, and promoting metastatic events. These seemingly opposing roles of the immune system at the different stages of cancer development must all be mediated by innate signaling mechanisms that regulate the overall state of immune activation. Recently, the cytosolic nod-like receptor (NLR) pathway of innate immunity has gained a lot of attention in the tumor immunology field due to its known involvement in promoting inflammation and immunity, and conversely, in regulating tissue repair processes. In this review, we present all the current evidence for NLR involvement in the different stages of neoplasia to understand how a single molecular pathway can contribute to conflicting immunological interactions with cancer.
机译:据认为,免疫系统可以促进致癌转化,尤其是在慢性炎症的情况下,可以在免疫监测过程中被激活,以破坏早期的赘生性细胞,使其不受恶变的影响,最后可以通过防止清除肿瘤,重塑周围组织,并促进转移性事件。在癌症发展的不同阶段,免疫系统的这些看似相反的作用都必须由调节免疫激活总体状态的先天信号机制来介导。近来,先天免疫的胞浆点头样受体(NLR)途径由于已知参与促进炎症和免疫,并反过来参与调节组织修复过程而在肿瘤免疫学领域引起了广泛关注。在这篇综述中,我们提供了NLR参与瘤形成不同阶段的所有当前证据,以了解单个分子途径如何促成与癌症发生冲突的免疫相互作用。

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