Walker Sophie L, Leete Pia, Boldison Joanne
Department of Clinical and Biomedical Sciences, University of Exeter, RILD Building (Level 4), Barrack Road, Exeter EX2 5DW, UK.
Biomolecules. 2025 Mar 19;15(3):441. doi: 10.3390/biom15030441.
Type 1 diabetes (T1D) is an organ-specific autoimmune disease that results in the selective loss of pancreatic beta cells and an eventual deficit in insulin production to maintain glucose homeostasis. It is now increasingly accepted that this dynamic disease process is multifactorial; involves a variety of immune cells which contribute to an inflamed pancreatic microenvironment; and that the condition is heterogenous, resulting in variable rates of subsequent beta cell damage. In this review, we will explore the current understanding of the cellular interactions between both resident and infiltrating immune cells within the pancreatic environment, highlighting key mechanisms which may promote the beta cell destruction and islet damage associated with T1D.
1型糖尿病(T1D)是一种器官特异性自身免疫性疾病,会导致胰腺β细胞选择性丧失,最终胰岛素分泌不足,无法维持葡萄糖稳态。现在越来越多的人认识到,这种动态的疾病过程是多因素的;涉及多种免疫细胞,这些细胞会导致胰腺微环境炎症;而且这种疾病是异质性的,导致后续β细胞损伤的速率各不相同。在这篇综述中,我们将探讨目前对胰腺环境中驻留免疫细胞和浸润免疫细胞之间细胞相互作用的理解,重点介绍可能促进与T1D相关的β细胞破坏和胰岛损伤的关键机制。