PDF(Pubmed)
Abstract：
Autoimmune disorders (ADs) are chronic conditions resulting from failure or breakdown of immunological tolerance, resulting in the host immune system attacking its cells or tissues. Recent studies report shared effects, mechanisms, and evolutionary origins among ADs; however, the possible factors connecting them are unknown. This study attempts to identify gene signatures commonly shared between different autoimmune disorders and elucidate their molecular pathways linking the pathogenesis of these ADs using an integrated gene expression approach. We employed differential gene expression analysis across 19 datasets of whole blood/peripheral blood cell samples with five different autoimmune disorders (rheumatoid arthritis, multiple sclerosis, systemic lupus erythematosus, Crohn\'s disease, and type 1 diabetes) to get nine key genes-EGR1, RUNX3, SMAD7, NAMPT, S100A9, S100A8, CYBB, GATA2, and MCEMP1 that were primarily involved in cell and leukocyte activation, leukocyte mediated immunity, IL-17, AGE-RAGE signaling in diabetic complications, prion disease, and NOD-like receptor signaling confirming its role in immune-related pathways. Combined with biological interpretations such as gene ontology (GO), pathway enrichment, and protein-protein interaction (PPI) network, our current study sheds light on the in-depth research on early detection, diagnosis, and prognosis of different ADs.
摘要：
自身免疫性疾病（AD）是由于免疫耐受失败或破坏而导致的慢性疾病。导致宿主免疫系统攻击其细胞或组织。最近的研究报告了共同的影响，机制,和广告之间的进化起源；然而，连接它们的可能因素是未知的。这项研究试图鉴定通常在不同自身免疫性疾病之间共享的基因特征，并使用整合的基因表达方法阐明其分子途径，将这些AD的发病机理联系起来。我们在19个具有五种不同自身免疫性疾病（类风湿性关节炎，多发性硬化症,系统性红斑狼疮,克罗恩病,和1型糖尿病）获得9个关键基因-EGR1，RUNX3，SMAD7，NAMPT，S100A9,S100A8,CYBB,主要参与细胞和白细胞活化的GATA2和MCEMP1，白细胞介导的免疫，IL-17,AGE-RAGE信号在糖尿病并发症中,朊病毒病,和NOD样受体信号证实了其在免疫相关途径中的作用。结合基因本体论(GO)等生物学解释，途径富集，和蛋白质-蛋白质相互作用(PPI)网络，我们目前的研究为早期检测的深入研究提供了启示，诊断,和不同AD的预后。
