Kent Andrew, Blander J Magarian
Immunology Institute, Department of Medicine, Graduate School of Biological Sciences , New York, NY , USA.
Immunology Institute, Department of Medicine, Graduate School of Biological Sciences , New York, NY , USA ; Tisch Cancer Institute, Icahn School of Medicine at Mount Sinai , New York, NY , USA.
Front Immunol. 2014 Apr 23;5:185. doi: 10.3389/fimmu.2014.00185. eCollection 2014.
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.
人们认为,免疫系统可促成致癌转化,尤其是在慢性炎症环境中,在免疫监视期间被激活,以在早期肿瘤细胞发生恶性生长之前将其摧毁,最后,可通过阻止清除、重塑周围组织以及促进转移事件来协助已形成肿瘤的生长。免疫系统在癌症发展不同阶段的这些看似相互矛盾的作用,必定都由调节免疫激活整体状态的固有信号传导机制介导。最近,固有免疫的胞质内NOD样受体(NLR)途径在肿瘤免疫学领域备受关注,因为已知其参与促进炎症和免疫,反之,也参与调节组织修复过程。在本综述中,我们展示了NLR参与肿瘤形成不同阶段的所有现有证据,以了解单一分子途径如何导致与癌症相互矛盾的免疫相互作用。