The RNA polymerase III-RIG-I axis in antiviral immunity and inflammation

被引:8
|
作者
Naesens, Leslie [1 ,2 ]
Haerynck, Filomeen [1 ,2 ]
Gack, Michaela U. [3 ]
机构
[1] Univ Ghent, Dept Internal Med & Pediat, Ghent, Belgium
[2] Ghent Univ Hosp, Ctr Primary Immunodeficiency, Jeffrey Modell Diag & Res Ctr, Primary Immunodeficiency Res Lab, Ghent, Belgium
[3] Cleveland Clin, Florida Res & Innovat Ctr, Port St Lucie, FL 34987 USA
基金
美国国家卫生研究院;
关键词
5S RIBOSOMAL-RNA; DOUBLE-STRANDED-RNA; STRUCTURAL BASIS; INTERFERON RESPONSE; UBIQUITIN LIGASE; NONCODING RNA; TRANSCRIPTION; RECOGNITION; DNA; ACTIVATION;
D O I
10.1016/j.it.2023.04.002
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Nucleic acid sensors survey subcellular compartments for atypical or mislocalized RNA or DNA, ultimately triggering innate immune responses. Retinoic acid-inducible gene-I (RIG-I) is part of the family of cytoplasmic RNA receptors that can detect viruses. A growing literature demonstrates that mammalian into immunostimulatory RIG-I ligands, which elicits antiviral or inflammatory responses. Dysregulation of the Pol III-RIG-I sensing axis can lead to human diseases including severe viral infection outcomes, autoimmunity, and tumor progression. Here, we summarize the newly emerging role of viral and hostderived Pol III transcripts in immunity and also highlight recent advances in understanding how mammalian cells prevent unwanted immune activation by these RNAs to maintain homeostasis.
引用
收藏
页码:435 / 449
页数:15
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