UCSF Diabetes Center, University of California San Francisco, San Francisco, CA 94143, USA.
Center for Translational Immunology, Benaroya Research Institute (BRI) at Virginia Mason, Seattle, WA, USA.
Science. 2021 Jul 30;373(6554):510-516. doi: 10.1126/science.abh1654. Epub 2021 Jul 29.
Type 1 diabetes (T1D) is an autoimmune disease in which T cells attack and destroy the insulin-producing β cells in the pancreatic islets. Genetic and environmental factors increase T1D risk by compromising immune homeostasis. Although the discovery and use of insulin have transformed T1D treatment, insulin therapy does not change the underlying disease or fully prevent complications. Over the past two decades, research has identified multiple immune cell types and soluble factors that destroy insulin-producing β cells. These insights into disease pathogenesis have enabled the development of therapies to prevent and modify T1D. In this review, we highlight the key events that initiate and sustain pancreatic islet inflammation in T1D, the current state of the immunological therapies, and their advantages for the treatment of T1D.
1 型糖尿病（T1D）是一种自身免疫性疾病，其中 T 细胞攻击并破坏胰腺胰岛中的胰岛素产生β细胞。遗传和环境因素通过破坏免疫稳态增加 T1D 的风险。尽管胰岛素的发现和使用改变了 T1D 的治疗方法，但胰岛素治疗并不能改变潜在疾病或完全预防并发症。在过去的二十年中，研究已经确定了多种免疫细胞类型和可溶性因子，这些因子会破坏产生胰岛素的β细胞。这些对疾病发病机制的认识使预防和改变 T1D 的治疗方法得以发展。在这篇综述中，我们强调了在 T1D 中引发和维持胰腺胰岛炎症的关键事件、免疫治疗的现状以及它们在 T1D 治疗中的优势。
