Department of Endocrinology, Indiana University School of Medicine, Indianapolis, IN, 46202, United States.
Department of Endocrinology, Indiana University School of Medicine, Indianapolis, IN, 46202, United States.
Mol Metab. 2024 Oct;88:101998. doi: 10.1016/j.molmet.2024.101998. Epub 2024 Jul 26.
Type 1 diabetes (T1D) is an autoimmune disease characterized by the specific destruction of insulin-producing beta cells in the pancreas by the immune system, including CD4 cells which orchestrate the attack and CD8 cells which directly destroy the beta cells, resulting in the loss of glucose homeostasis.
This comprehensive document delves into the complex interplay between the immune system and beta cells, aiming to shed light on the mechanisms driving their destruction in T1D. Insights into the genetic predisposition, environmental triggers, and autoimmune responses provide a foundation for understanding the autoimmune attack on beta cells. From the role of viral infections as potential triggers to the inflammatory response of beta cells, an intricate puzzle starts to unfold. This exploration highlights the importance of beta cells in breaking immune tolerance and the factors contributing to their targeted destruction. Furthermore, it examines the potential role of autophagy and the impact of cytokine signaling on beta cell function and survival.
This review collectively represents current research findings on T1D which offers valuable perspectives on novel therapeutic approaches for preserving beta cell mass, restoring immune tolerance, and ultimately preventing or halting the progression of T1D. By unraveling the complex dynamics between the immune system and beta cells, we inch closer to a comprehensive understanding of T1D pathogenesis, paving the way for more effective treatments and ultimately a cure.
1 型糖尿病(T1D)是一种自身免疫性疾病,其特征是免疫系统特异性破坏胰腺中的胰岛素产生β细胞,包括协调攻击的 CD4 细胞和直接破坏β细胞的 CD8 细胞,导致葡萄糖稳态丧失。
本文全面探讨了免疫系统和β细胞之间的复杂相互作用,旨在阐明 T1D 中导致β细胞破坏的机制。对遗传易感性、环境触发因素和自身免疫反应的深入了解为理解针对β细胞的自身免疫攻击提供了基础。从病毒感染作为潜在触发因素到β细胞的炎症反应,一个复杂的谜题开始展开。这种探索强调了β细胞在打破免疫耐受以及导致其靶向破坏的因素中的重要性。此外,还研究了自噬的潜在作用以及细胞因子信号对β细胞功能和存活的影响。
本综述综合了当前关于 T1D 的研究发现,为保护β细胞质量、恢复免疫耐受以及最终预防或阻止 T1D 进展提供了有价值的新治疗方法的观点。通过揭示免疫系统和β细胞之间的复杂动态,我们更深入地了解了 T1D 的发病机制,为更有效的治疗方法铺平了道路,并最终实现了治愈。