Department of Medical Science, Brain Korea 21 Project for Medical Science, Yonsei University College of Medicine, Seoul, South Korea.
Severance Biomedical Science Institute, Gangnam Severance Hospital, Yonsei University College of Medicine, Seoul, South Korea.
Front Endocrinol (Lausanne). 2021 Aug 17;12:716692. doi: 10.3389/fendo.2021.716692. eCollection 2021.
Increased incidence of type I and type II diabetes has been prevailed worldwide. Though the pathogenesis of molecular mechanisms remains still unclear, there are solid evidence that disturbed immune homeostasis leads to pancreatic β cell failure. Currently, autoimmunity and uncontrolled inflammatory signaling pathways have been considered the major factors in the pathogenesis of diabetes. Many components of immune system have been reported to implicate pancreatic β cell failure, including helper T cells, cytotoxic T cells, regulatory T cells and gut microbiota. Immune modulation of those components using small molecules and antibodies, and fecal microbiota transplantation are undergoing in many clinical trials for the treatment of type I and type II diabetes. In this review we will discuss the basis of molecular pathogenesis focusing on the disturbed immune homeostasis in type I and type II diabetes, leading to pancreatic β cell destruction. Finally, we will introduce current therapeutic strategies and clinical trials by modulation of immune system for the treatment of type I and type II diabetes patients.
全球范围内，1 型和 2 型糖尿病的发病率不断上升。尽管分子机制的发病机制仍不清楚，但有确凿的证据表明，免疫稳态的紊乱导致了胰腺β细胞的衰竭。目前，自身免疫和失控的炎症信号通路被认为是糖尿病发病机制中的主要因素。许多免疫系统的成分被报道与胰腺β细胞衰竭有关，包括辅助性 T 细胞、细胞毒性 T 细胞、调节性 T 细胞和肠道微生物群。目前正在进行许多临床试验，以使用小分子和抗体对这些成分进行免疫调节，以及粪便微生物群移植，以治疗 1 型和 2 型糖尿病。在这篇综述中，我们将讨论分子发病机制的基础，重点是 1 型和 2 型糖尿病中免疫稳态的紊乱，导致胰腺β细胞的破坏。最后，我们将介绍通过调节免疫系统治疗 1 型和 2 型糖尿病患者的当前治疗策略和临床试验。
