免疫系统
先天免疫系统
免疫学
生物
免疫失调
败血症
获得性免疫系统
重编程
免疫抑制
核糖核酸
转录组
细胞
基因表达
基因
遗传学
作者
Hongyan Chen,Xiaoting Zhang,Hao Su,Judeng Zeng,Hung Chan,Qing Li,Xiaodong Liu,Lin Zhang,William Ka Kei Wu,Matthew T.V. Chan,Huarong Chen
摘要
Abstract Sepsis is defined as life‐threatening organ dysfunction caused by the host immune dysregulation to infection. It is a highly heterogeneous syndrome with complex pathophysiological mechanisms. The host immune response to sepsis can be divided into hyper‐inflammatory and immune‐suppressive phases which could exist simultaneously. In the initial stage, systemic immune response is activated after exposure to pathogens. Both innate and adaptive immune cells undergo epigenomic, transcriptomic, and functional reprogramming, resulting in systemic and persistent inflammatory responses. Following the hyper‐inflammatory phase, the body is in a state of continuous immunosuppression, which is related to immune cell apoptosis, metabolic failure, and epigenetic reprogramming. Immunosuppression leads to increased susceptibility to secondary infections in patients with sepsis. RNA N6‐Methyladenosine (m6A) has been recognized as an indispensable epitranscriptomic modification involved in both physiological and pathological processes. Recent studies suggest that m6A could reprogram both innate and adaptive immune cells through posttranscriptional regulation of RNA metabolism. Dysregulated m6A modifications contribute to the pathogenesis of immune‐related diseases. In this review, we summarize immune cell changes and the potential role of m6A modification in sepsis. This article is categorized under: RNA in Disease and Development > RNA in Disease RNA Processing > RNA Editing and Modification
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