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IFNλ:平衡肺部感染中的明暗两面。

IFNλ: balancing the light and dark side in pulmonary infection.

机构信息

Division of Pulmonary Medicine, Department of Pediatrics, UPMC Children's Hospital of Pittsburgh , Pittsburgh, Pennsylvania, USA.

Department of Immunology, University of Pittsburgh , Pittsburgh, Pennsylvania, USA.

出版信息

mBio. 2023 Aug 31;14(4):e0285022. doi: 10.1128/mbio.02850-22. Epub 2023 Jun 6.

DOI:10.1128/mbio.02850-22
PMID:37278532
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10470512/
Abstract

Interferon (IFN) represents a well-known component of antiviral immunity that has been studied extensively for its mechanisms of action and therapeutic potential when antiviral treatment options are limited. Specifically in the respiratory tract, IFNs are induced directly on viral recognition to limit the spread and transmission of the virus. Recent focus has been on the IFNλ family, which has become an exciting focus in recent years for its potent antiviral and anti-inflammatory activities against viruses infecting barrier sites, including the respiratory tract. However, insights into the interplay between IFNλs and other pulmonary infections are more limited and suggest a more complex role, potentially detrimental, than what was seen during viral infections. Here, we review the role of IFNλs in pulmonary infections, including viral, bacterial, fungal, and multi-pathogen super-infections, and how this may impact future work in the field.

摘要

干扰素 (IFN) 是抗病毒免疫的一个著名组成部分,当抗病毒治疗选择有限时,其作用机制和治疗潜力已被广泛研究。具体在呼吸道中,IFNs 在病毒识别时被直接诱导,以限制病毒的传播和传播。最近的重点是 IFNλ 家族,近年来因其对感染屏障部位的病毒(包括呼吸道)具有强大的抗病毒和抗炎活性而成为一个令人兴奋的焦点。然而,对于 IFNλ 与其他肺部感染之间的相互作用的了解更为有限,并表明其作用比病毒感染时更为复杂,可能具有潜在的危害性。在这里,我们回顾了 IFNλ 在肺部感染中的作用,包括病毒、细菌、真菌和多病原体超级感染,以及这将如何影响该领域的未来工作。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d8a4/10470512/9506e4b5a399/mbio.02850-22.f002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d8a4/10470512/5f37a6fd2d35/mbio.02850-22.f001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d8a4/10470512/9506e4b5a399/mbio.02850-22.f002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d8a4/10470512/5f37a6fd2d35/mbio.02850-22.f001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d8a4/10470512/9506e4b5a399/mbio.02850-22.f002.jpg

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Nat Commun. 2022 Nov 16;13(1):6992. doi: 10.1038/s41467-022-34709-4.
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The Microbial Etiology of Community-Acquired Pneumonia in Adults: from Classical Bacteriology to Host Transcriptional Signatures.
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