Paun Alexandra, Yau Christopher, Danska Jayne S
Program in Genetics and Genome Biology, The Hospital for Sick Children, Toronto, Ontario M5G 0A4, Canada.
Department of Immunology, University of Toronto, Toronto, Ontario M5S 1A8, Canada; and.
J Immunol. 2017 Jan 15;198(2):590-595. doi: 10.4049/jimmunol.1601519.
Type 1 diabetes (T1D) is characterized by the autoimmune destruction of pancreatic β cells. The rapid rise in T1D incidence during the past 50 y suggests environmental factors contribute to the disease. The trillion symbiotic microorganisms inhabiting the mammalian gastrointestinal tract (i.e., the microbiota) influence numerous aspects of host physiology. In this study we review the evidence linking perturbations of the gut microbiome to pancreatic autoimmunity. We discuss data from rodent models demonstrating the essential role of the gut microbiota on the development and function of the host's mucosal and systemic immune systems. Furthermore, we review findings from human longitudinal cohort studies examining the influence of environmental and lifestyle factors on microbiota composition and pancreatic autoimmunity. Taken together, these data underscore the requirement for mechanistic studies to identify bacterial components and metabolites interacting with the innate and adaptive immune system, which would set the basis for preventative or therapeutic strategies in T1D.
1型糖尿病(T1D)的特征是胰腺β细胞发生自身免疫性破坏。在过去50年里,T1D发病率迅速上升,这表明环境因素与该疾病有关。栖息在哺乳动物胃肠道中的数万亿共生微生物(即微生物群)会影响宿主生理学的诸多方面。在本研究中,我们回顾了将肠道微生物组紊乱与胰腺自身免疫联系起来的证据。我们讨论了来自啮齿动物模型的数据,这些数据证明了肠道微生物群对宿主黏膜和全身免疫系统的发育及功能的重要作用。此外,我们还回顾了人类纵向队列研究的结果,这些研究考察了环境和生活方式因素对微生物群组成及胰腺自身免疫的影响。综合来看,这些数据强调了进行机制研究以确定与先天性和适应性免疫系统相互作用的细菌成分及代谢产物的必要性,这将为T1D的预防或治疗策略奠定基础。