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 细胞攻击并破坏胰岛中产生胰岛素的 β 细胞。遗传和环境因素通过损害免疫稳态来增加 T1D 风险。尽管胰岛素的发现和使用改变了 T1D 治疗，但胰岛素治疗并没有改变潜在的疾病或完全预防并发症。在过去的二十年里，研究已经确定了多种免疫细胞类型和破坏产生胰岛素的 β 细胞的可溶性因子。这些对疾病发病机制的见解使得能够开发预防和改善 T1D 的疗法。在这篇综述中，我们重点介绍了在 1 型糖尿病中引发和维持胰岛炎症的关键事件、免疫疗法的现状以及它们在 1 型糖尿病治疗中的优势。