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自身炎症性疾病:家族性地中海热研究的启示。

Autoinflammation: Lessons from the study of familial Mediterranean fever.

机构信息

First Department of Internal Medicine and Laboratory of Molecular Hematology, University Hospital of Alexandroupolis, Democritus University of Thrace, Alexandroupolis, Greece.

First Department of Internal Medicine and Laboratory of Molecular Hematology, University Hospital of Alexandroupolis, Democritus University of Thrace, Alexandroupolis, Greece.

出版信息

J Autoimmun. 2019 Nov;104:102305. doi: 10.1016/j.jaut.2019.102305. Epub 2019 Jul 20.

Abstract

Autoinflammatory disorders represent a heterogeneous group of systemic inflammatory diseases caused by genetic or acquired defects in key components of the innate immunity. Familial Mediterranean fever (FMF) is the most common among the other clinical phenotypes of the rare hereditary periodic fevers (HPFs) syndromes. FMF is associated with mutations in the MEFV gene encoding pyrin and is characterized by recurrent, often stress-provoked attacks of fever and serositis, but sometimes also by chronic subclinical inflammation. FMF is prevalent in Greece and other countries of the eastern Mediterranean region. Over the last 17 years, our group has focused on FMF as a model suitable for the research on innate immunity and particularly the role of neutrophils. Therefore, the study of Greek patients with FMF has yielded lessons across several levels: the epidemiology of the disease in Greece, the spectrum of its clinical manifestations and potential overlaps with other idiopathic inflammatory conditions, the demonstration of its rather complex and heterogeneous genetic background and the suggestion of a novel mechanism involved in the crosstalk between environmental stress and inflammation. Mechanistically, during FMF attack, neutrophils release chromatin structures called neutrophil extracellular traps (NETs), which are decorated with bioactive IL-1β. REDD1 (regulated in development and DNA damage responses 1), that encodes a stress-related mTOR repressor, has been found to be the most significantly upregulated gene in neutrophils during disease attacks. Upon adrenergic stress, REDD1-induced autophagy triggers a pyrin-driven IL-1β maturation, and the release of IL-1β-bearing NETs. Consequently, not only the mode of action of IL-1β-targeting therapies is explained, but also new treatment prospects emerge with the evaluation of old or the design of new drugs targeting autophagy-induced NETosis. Information gained from FMF studies may subsequently be applied in more complex but still relevant inflammatory conditions, such as adult-onset Still's disease, gout, ulcerative colitis and Behçet's disease.

摘要

自身炎症性疾病是一组由固有免疫关键成分的遗传或获得性缺陷引起的系统性炎症性疾病,具有异质性。家族性地中海热(FMF)是罕见遗传性周期性发热(HPF)综合征的其他临床表型中最常见的一种。FMF 与编码 pyrin 的 MEFV 基因突变有关,其特征是反复发作的、常因应激引起的发热和浆膜炎,但有时也有慢性亚临床炎症。FMF 在希腊和地中海东部地区的其他国家流行。在过去的 17 年中,我们的研究小组专注于 FMF 作为研究固有免疫,特别是中性粒细胞作用的模型。因此,对希腊 FMF 患者的研究在多个层面上取得了成果:该疾病在希腊的流行病学、临床表现谱及其与其他特发性炎症性疾病的潜在重叠、其相当复杂和异质的遗传背景的证明以及涉及环境应激与炎症之间串扰的新机制的建议。从机制上讲,在 FMF 发作期间,中性粒细胞释放称为中性粒细胞胞外陷阱(NETs)的染色质结构,这些结构上装饰有生物活性的白细胞介素-1β(IL-1β)。发现 REDD1(调节发育和 DNA 损伤反应 1),其编码应激相关的 mTOR 抑制剂,是疾病发作期间中性粒细胞中上调最显著的基因。在肾上腺素能应激下,REDD1 诱导的自噬触发 pyrin 驱动的 IL-1β成熟,并释放携带 IL-1β的 NETs。因此,不仅解释了针对 IL-1β 的治疗方法的作用机制,而且还通过评估针对自噬诱导的 NETosis 的旧药物或设计新药物,出现了新的治疗前景。从 FMF 研究中获得的信息随后可应用于更复杂但仍相关的炎症性疾病,如成人Still 病、痛风、溃疡性结肠炎和 Behçet 病。

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