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Role of Toll-like receptors in gastrointestinal malignancies

机译：Toll样受体在胃肠道恶性肿瘤中的作用

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Mounting evidence supports the tenet that innate immune responses to luminal microbes participate in the development of gastrointestinal malignancies. The gastrointestinal tract is relatively unique in that it has evolved in the presence of diverse enteric microflora. Intestinal flora is required to develop a normal adaptive immune response in the periphery. With the characterization of the innate immune system, we have begun to understand the adaptations the intestine has made to the microbiota. The interaction between the microbiota and the intestinal mucosa through Toll-like receptors (TLRs) is required to maintain intestinal homeostasis. In particular, intestinal epithelial cells and lamina propria mononuclear cells such as antigen-presenting cells and T cells must respond to breaches in the mucosal barrier by activating TLR-dependent pathways that result in increased epithelial proliferation, wound healing and recruitment of acute inflammatory cells. In the setting of chronic inflammation such as Helicobacter pylori (H. pylori) infection in the stomach or idiopathic inflammatory bowel disease, the process of repair may eventually result in carcinogenesis. The following review highlights human and animal data that support a role for innate immune responses and TLRs specifically in promoting gastrointestinal malignancies. Candidate pathways linking TLRs to gastrointestinal malignancies include activation of nuclear factor-κB and cyclooxygenase-2. Studying the link between innate immune signaling and gastrointestinal malignancies offers the possibility to identify novel ways to both prevent and treat gastrointestinal cancer.
机译：越来越多的证据支持这样的信条，即对腔内微生物的先天免疫反应参与胃肠道恶性肿瘤的发展。胃肠道是相对独特的，因为它已在多种肠道菌群的存在下进化。需要肠道菌群以在外周产生正常的适应性免疫反应。通过先天免疫系统的表征，我们已经开始了解肠道对微生物群的适应性。通过Toll样受体（TLR），微生物群与肠粘膜之间的相互作用是维持肠内稳态所必需的。特别是，肠上皮细胞和固有层单核细胞（如抗原呈递细胞和T细胞）必须通过激活TLR依赖性途径来响应粘膜屏障的破坏，从而导致上皮增殖，伤口愈合和急性炎症细胞募集增加。在诸如胃中的幽门螺杆菌（H. pylori）感染之类的慢性炎症或特发性炎症性肠病的情况下，修复过程最终可能导致癌变。以下评论重点介绍了人类和动物数据，这些数据支持先天性免疫应答和TLR在促进胃肠道恶性肿瘤中的作用。连接TLR与胃肠道恶性肿瘤的候选途径包括核因子-κB和环氧合酶2的激活。研究先天性免疫信号传导与胃肠道恶性肿瘤之间的联系提供了识别预防和治疗胃肠道癌症的新方法的可能性。

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