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本文引用的文献

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Patient ancestry significantly contributes to molecular heterogeneity of systemic lupus erythematosus.患者的遗传背景显著影响系统性红斑狼疮的分子异质性。
JCI Insight. 2020 Aug 6;5(15):140380. doi: 10.1172/jci.insight.140380.
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Distinct and Orchestrated Functions of RNA Sensors in Innate Immunity.RNA 传感器在先天免疫中的独特和协调功能。
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The Bacterial Ro60 Protein and Its Noncoding Y RNA Regulators.细菌 Ro60 蛋白及其非编码 Y RNA 调控因子。
Annu Rev Microbiol. 2020 Sep 8;74:387-407. doi: 10.1146/annurev-micro-020620-062812. Epub 2020 Jul 13.
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Noncoding Y RNAs regulate the levels, subcellular distribution and protein interactions of their Ro60 autoantigen partner.非编码 Y RNA 调节其 Ro60 自身抗原伴侣的水平、亚细胞分布和蛋白相互作用。
Nucleic Acids Res. 2020 Jul 9;48(12):6919-6930. doi: 10.1093/nar/gkaa414.
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2020 American College of Rheumatology Guideline for the Management of Reproductive Health in Rheumatic and Musculoskeletal Diseases.2020 年美国风湿病学会风湿病和肌肉骨骼疾病生殖健康管理指南。
Arthritis Rheumatol. 2020 Apr;72(4):529-556. doi: 10.1002/art.41191. Epub 2020 Feb 23.
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Lymphoma Driver Mutations in the Pathogenic Evolution of an Iconic Human Autoantibody.淋巴瘤驱动突变在标志性人类自身抗体的致病进化中的作用。
Cell. 2020 Mar 5;180(5):878-894.e19. doi: 10.1016/j.cell.2020.01.029. Epub 2020 Feb 13.
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Mechanisms of action of hydroxychloroquine and chloroquine: implications for rheumatology.羟氯喹和氯喹的作用机制:对风湿病学的影响。
Nat Rev Rheumatol. 2020 Mar;16(3):155-166. doi: 10.1038/s41584-020-0372-x. Epub 2020 Feb 7.
8
Rare copy number variants in over 100,000 European ancestry subjects reveal multiple disease associations.在超过 10 万欧洲血统个体中罕见的拷贝数变异揭示了多种疾病的关联。
Nat Commun. 2020 Jan 14;11(1):255. doi: 10.1038/s41467-019-13624-1.
9
Population-based estimates of humoral autoimmunity from the U.S. National Health and Nutrition Examination Surveys, 1960-2014.基于美国国家健康和营养调查(1960-2014 年)的人群体液自身免疫估计。
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10
Identification of U11snRNA as an endogenous agonist of TLR7-mediated immune pathogenesis.鉴定 U11snRNA 为 TLR7 介导的免疫发病机制的内源性激动剂。
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自身抗原谱与微生物 RNA 世界。

The Autoantigen Repertoire and the Microbial RNP World.

机构信息

National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), National Institutes of Health (NIH), Bethesda, MD, USA; RNA Biology Laboratory, Center for Cancer Research, National Cancer Institute (NCI), NIH, Frederick, MD 21702, USA.

RNA Biology Laboratory, Center for Cancer Research, National Cancer Institute (NCI), NIH, Frederick, MD 21702, USA.

出版信息

Trends Mol Med. 2021 May;27(5):422-435. doi: 10.1016/j.molmed.2021.02.003. Epub 2021 Mar 12.

DOI:10.1016/j.molmed.2021.02.003
PMID:33722441
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9004447/
Abstract

Although autoimmunity and autoimmune disease (AID) are relatively common, the repertoire of autoantigens is paradoxically very limited. Highly enriched in this autoantigen repertoire are nucleic acids and their binding proteins, which together form large macromolecular structures. Most of these complexes are of ancient evolutionary origin, with homologs throughout multiple kingdoms of life. Why and if these nucleic acid-protein particles drive the development of autoimmunity remains unresolved. Recent advances in our understanding of the microbiome may provide clues about the origins of autoimmunity - and the particular puzzle of why the autoantigen repertoire is so particularly enriched in ribonucleoprotein particles (RNPs). We discuss the possibility that autoimmunity to some RNPs may arise from molecular mimicry to microbial orthologs.

摘要

虽然自身免疫和自身免疫性疾病(AID)相对常见,但自身抗原的范围实际上非常有限。在自身抗原谱中高度富集的是核酸及其结合蛋白,它们共同形成大型大分子结构。这些复合物大多数具有古老的进化起源,在生命的多个王国中都有同源物。为什么以及是否这些核酸-蛋白质颗粒会引发自身免疫仍然没有解决。我们对微生物组的理解的最新进展可能为自身免疫的起源提供线索-以及为什么自身抗原谱特别富含核糖核蛋白颗粒(RNP)的特殊难题。我们讨论了某些 RNP 的自身免疫可能源于与微生物同源物的分子模拟的可能性。