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细胞溶质核酸传感器在炎症和自身免疫性疾病中的作用。

Cytosolic Nucleic Acid Sensors in Inflammatory and Autoimmune Disorders.

机构信息

Department of Pathology, UT Southwestern Medical Center, Dallas, TX, United States.

Department of Pathology, UT Southwestern Medical Center, Dallas, TX, United States.

出版信息

Int Rev Cell Mol Biol. 2019;344:215-253. doi: 10.1016/bs.ircmb.2018.10.002. Epub 2018 Dec 3.

Abstract

Innate immunity employs germline-encoded pattern recognition receptors (PRRs) to sense microbial pattern molecules. Recognition of pathogen-associated molecular patterns (PAMPs) by various PPRs located on the cell membrane or in the cytosol leads to the activation of cell signaling pathways and production of inflammatory mediators. Nucleic acids including DNA, RNA, and their derivatives are potent PAMPs which can be recognized by multiple PRRs to induce inflammatory responses. While nucleic acid sensors can also sense endogenous nucleic acids, they are capable of discriminating self from non-self. However, defects in nucleic acid sensing PRRs or dysregulation of nucleic acid sensing signaling pathways may cause excessive activation of the immune system resulting in the development of inflammatory and autoimmune diseases. This review will discuss the major pathways for sensing intracellular nucleic acids and how defects in these nucleic acid sensing are associated with different kinds of autoimmune and inflammatory disorders.

摘要

先天免疫利用种系编码的模式识别受体 (PRR) 来感知微生物模式分子。位于细胞膜或细胞质中的各种 PRR 识别病原体相关分子模式 (PAMP) 会导致细胞信号通路的激活和炎症介质的产生。包括 DNA、RNA 及其衍生物在内的核酸是有效的 PAMP,可以被多种 PRR 识别,从而引发炎症反应。虽然核酸传感器也可以感知内源性核酸,但它们能够区分自我和非自我。然而,核酸感应 PRR 的缺陷或核酸感应信号通路的失调可能导致免疫系统过度激活,从而导致炎症和自身免疫性疾病的发生。本综述将讨论细胞内核酸感应的主要途径,以及这些核酸感应的缺陷如何与不同类型的自身免疫和炎症性疾病相关。

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