Department of Medicine, University of Massachusetts Medical School, Worcester, Massachusetts, USA.
Curr Opin Endocrinol Diabetes Obes. 2010 Apr;17(2):126-30. doi: 10.1097/MED.0b013e3283372819.
Type 1 diabetes (T1D) is an autoimmune disease typically believed to result from malfunctions in adaptive immune response signaling which result in activation of self-reactive T cells. However, recent research has indicated components of the innate immune response as having a key role in the initiation of the autoimmune process of T1D. This review will highlight recent studies which examined the role of innate immune response signaling and the connections to T1D pathogenesis.
Investigations indicate that components of innate immunity, including inflammation and Toll-like receptor signaling, are involved in pancreatic islet infiltration and insulitis. Recent studies examining the role of viral infections in T1D development also implicate innate immune response signaling in disease pathogenesis.
Current research indicates that components of innate immune response signaling are involved in the initiation of the autoimmune process which results in the eventual destruction of beta cells during T1D pathogenesis. Continuing efforts by researchers to uncover the molecular pathways of innate immunity linked to T1D development could potentially lead to therapeutics capable of preventing and curing the autoimmune disease.
1 型糖尿病（T1D）通常被认为是一种自身免疫性疾病，其病因是适应性免疫反应信号的功能障碍，导致自身反应性 T 细胞的激活。然而，最近的研究表明，固有免疫反应的成分在 T1D 的自身免疫过程的启动中起着关键作用。这篇综述将重点介绍最近研究固有免疫反应信号的作用及其与 T1D 发病机制的联系。
研究表明，固有免疫的组成部分，包括炎症和 Toll 样受体信号，都参与了胰岛浸润和胰岛炎。最近研究病毒感染在 T1D 发病机制中的作用也表明固有免疫反应信号在疾病发病机制中的作用。
目前的研究表明，固有免疫反应信号的组成部分参与了导致 T1D 发病过程中最终破坏β细胞的自身免疫过程的启动。研究人员继续努力揭示与 T1D 发展相关的固有免疫的分子途径，有可能开发出能够预防和治疗自身免疫性疾病的治疗方法。
