Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, Missouri, United States of America.
PLoS One. 2013;8(3):e59701. doi: 10.1371/journal.pone.0059701. Epub 2013 Mar 26.
Our ability to successfully intervene in disease processes is dependent on definitive diagnosis. In the case of autoimmune disease, this is particularly challenging because progression of disease is lengthy and multifactorial. Here we show the first chronological compendium of transcriptional and cellular signatures of diabetes in the non-obese diabetic mouse. Our data relates the immunological environment of the islets of Langerhans with the transcriptional profile at discrete times. Based on these data, we have parsed diabetes into several discrete phases. First, there is a type I interferon signature that precedes T cell activation. Second, there is synchronous infiltration of all immunological cellular subsets and a period of control. Finally, there is the killing phase of the diabetogenic process that is correlated with an NF-kB signature. Our data provides a framework for future examination of autoimmune diabetes and its disease progression markers.
我们成功干预疾病进程的能力取决于明确的诊断。在自身免疫性疾病的情况下，这尤其具有挑战性，因为疾病的进展是漫长的且多因素的。在这里，我们展示了非肥胖型糖尿病小鼠中糖尿病的转录和细胞特征的第一个时间顺序概要。我们的数据将胰岛的免疫学环境与离散时间的转录谱相关联。基于这些数据，我们将糖尿病分为几个离散阶段。首先，存在一个先于 T 细胞激活的 I 型干扰素特征。其次，所有免疫细胞亚群同步浸润，并经历一个控制期。最后，是导致糖尿病的过程的杀伤阶段，与 NF-kB 特征相关。我们的数据为未来研究自身免疫性糖尿病及其疾病进展标志物提供了一个框架。
