1 Department of Infectious Diseases and Pathology, University of Florida , Gainesville, Florida.
J Interferon Cytokine Res. 2013 Nov;33(11):619-31. doi: 10.1089/jir.2013.0046. Epub 2013 Aug 20.
Current data support a role for gut colonization in maintaining balanced mucosal and systemic immune responses and have suggested aberrant innate immune recognition of enteric bacteria as an initiator of the adaptive immune damage associated with inflammatory bowel disease (Crohn's disease and ulcerative colitis). In fact, data from human studies and experimental mouse models have implicated transformation of the gut microbiota from a beneficial symbiotic state to one of imbalance or "dysbiosis" in the pathogenesis of several autoinflammatory diseases, including allergic skin and respiratory disorders, rheumatoid arthritis, type I diabetes, and colorectal cancer. The host has evolved to co-exist and maintain a mutualistic relationship with the commensal microbes of the gut, and it is the function of the host innate immune system to initiate and maintain this homeostasis, while retaining the ability to respond appropriately to pathogenic organisms. In this review, we discuss the molecular and cellular interactions of the mucosal immune system that decide this delicate balance of mutualism. Furthermore, we will highlight the role of dendritic cells in preserving this precarious balance and how gene products of commensal microbes may play an integral role in re-establishing this balance once it has gone awry.
目前的数据支持肠道定植在维持黏膜和全身免疫平衡反应中的作用，并提示固有免疫对肠道细菌的异常识别可能是与炎症性肠病（克罗恩病和溃疡性结肠炎）相关的适应性免疫损伤的启动因素。事实上，来自人类研究和实验性小鼠模型的数据表明，肠道微生物群从有益的共生状态向失衡或“生态失调”的转变，与几种自身炎症性疾病的发病机制有关，包括过敏性皮肤和呼吸道疾病、类风湿关节炎、I 型糖尿病和结直肠癌。宿主已经进化到与肠道共生微生物共存并维持共生关系，宿主固有免疫系统的功能是启动和维持这种体内平衡，同时保持对病原体的适当反应能力。在这篇综述中，我们讨论了决定这种共生微妙平衡的黏膜免疫系统的分子和细胞相互作用。此外，我们将强调树突状细胞在维持这种脆弱平衡中的作用，以及共生微生物的基因产物如何在这种平衡出现异常时发挥重要作用，重新建立这种平衡。
