Children's Hospital, University of Helsinki and Helsinki University Central Hospital, Helsinki, Finland; Folkhälsan Research Center, FI-00290 Helsinki, Finland.
Cold Spring Harb Perspect Med. 2012 Jul;2(7):a007690. doi: 10.1101/cshperspect.a007690.
Type 1 diabetes (T1D) is perceived as a progressive immune-mediated disease, the clinical diagnosis of which is preceded by an asymptomatic preclinical period of highly variable duration. It has long been postulated that the disease process leading to overt T1D is triggered by an infectious agent, the strongest candidate being a diabetogenic enterovirus. The initiation and progression of the disorder likely requires, in addition to genetic T1D susceptibility, a trigger, an exogenous antigen capable of driving the development of this disease. This may be a dietary antigen similar to gluten in celiac disease. Recent data further suggests that the initiation of autoimmunity is preceded by inflammation reflected by a proinflammatory metabolic serum profile. The cause of the inflammation remains open, but given that the intestinal microbiome appears to differ between individuals who progress to clinical T1D and nonprogressors, one may speculate that changes in the gut microflora might contribute to the inflammatory process.
1 型糖尿病(T1D)被认为是一种进行性免疫介导的疾病,其临床诊断之前有一段无症状的、持续时间高度可变的临床前期。长期以来,人们一直假设导致显性 T1D 的疾病过程是由感染因子引发的,而候选因子中最强的是致糖尿病肠病毒。除了遗传易感性 T1D 之外,该疾病的发生和进展可能还需要一个触发因素,即一种能够导致这种疾病发展的外源性抗原。这个抗原可能类似于乳糜泻中的谷胶。最近的数据进一步表明,自身免疫的启动之前是炎症反应,表现为促炎代谢血清特征。炎症的原因尚不清楚,但鉴于肠道微生物组似乎在进展为临床 T1D 的个体和非进展者之间存在差异,人们可能会推测肠道微生物群的变化可能会导致炎症过程。