Department of Endocrinology, Lequn Branch, The First Hospital of Jilin University, Changchun, Jilin 130021, P.R. China.
Department of Cardiology, Lequn Branch, The First Hospital of Jilin University, Changchun, Jilin 130021, P.R. China.
J Clin Endocrinol Metab. 2023 Aug 18;108(9):2176-2183. doi: 10.1210/clinem/dgad165.
Type 1 diabetes (T1D) is usually caused by immune-mediated destruction of islet β cells, and genetic and environmental factors are thought to trigger autoimmunity. Convincing evidence indicates that viruses are associated with T1D development and progression. During the COVID-19 pandemic, cases of hyperglycemia, diabetic ketoacidosis, and new diabetes increased, suggesting that SARS-CoV-2 may be a trigger for or unmask T1D. Possible mechanisms of β-cell damage include virus-triggered cell death, immune-mediated loss of pancreatic β cells, and damage to β cells because of infection of surrounding cells. This article examines the potential pathways by which SARS-CoV-2 affects islet β cells in these 3 aspects. Specifically, we emphasize that T1D can be triggered by SARS-CoV-2 through several autoimmune mechanisms, including epitope spread, molecular mimicry, and bystander activation. Given that the development of T1D is often a chronic, long-term process, it is difficult to currently draw firm conclusions as to whether SARS-CoV-2 causes T1D. This area needs to be focused on in terms of the long-term outcomes. More in-depth and comprehensive studies with larger cohorts of patients and long-term clinical follow-ups are required.
1 型糖尿病（T1D）通常由胰岛β细胞的免疫介导破坏引起，遗传和环境因素被认为是触发自身免疫的原因。令人信服的证据表明，病毒与 T1D 的发生和发展有关。在 COVID-19 大流行期间，高血糖症、糖尿病酮症酸中毒和新发糖尿病的病例增加，这表明 SARS-CoV-2 可能是 T1D 的触发因素或使其显现。β细胞损伤的可能机制包括病毒触发的细胞死亡、免疫介导的胰腺β细胞丧失以及周围细胞感染导致的β细胞损伤。本文从这 3 个方面探讨了 SARS-CoV-2 影响胰岛β细胞的潜在途径。具体而言，我们强调 SARS-CoV-2 通过几种自身免疫机制引发 T1D，包括表位扩展、分子模拟和旁观者激活。鉴于 T1D 的发生通常是一个慢性、长期的过程，目前很难确定 SARS-CoV-2 是否会导致 T1D。这方面需要关注长期结果。需要对更多患者的更大队列进行更深入和全面的研究，并进行长期的临床随访。
