{"title":"Tuberculosis as an unconventional interferonopathy","authors":"Russell E Vance","doi":"10.1016/j.coi.2024.102508","DOIUrl":null,"url":null,"abstract":"<div><div>Tuberculosis is caused by <em>Mycobacterium tuberculosis</em>, a bacterium that accounts for more human mortality than any other. Evidence is accumulating for the view that tuberculosis is an interferonopathy — a disease driven by type I interferons. However, how type I interferons exacerbate tuberculosis remains poorly understood. As an infection, tuberculosis is distinct from conventional interferonopathies, which are autoinflammatory diseases. Here I consider the hypothesis that type I interferons promote bacterial replication by impairing key antibacterial immune responses, including those orchestrated by interleukin-1 and interferon γ. Paradoxically, during tuberculosis, the underlying state of impaired antibacterial immunity co-exists with overt (but ineffective) inflammation. Conceiving of tuberculosis as an unconventional interferonopathy may suggest fruitful avenues for therapeutic intervention.</div></div>","PeriodicalId":11361,"journal":{"name":"Current Opinion in Immunology","volume":"92 ","pages":"Article 102508"},"PeriodicalIF":5.8000,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Current Opinion in Immunology","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0952791524000980","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"IMMUNOLOGY","Score":null,"Total":0}
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Abstract
Tuberculosis is caused by Mycobacterium tuberculosis, a bacterium that accounts for more human mortality than any other. Evidence is accumulating for the view that tuberculosis is an interferonopathy — a disease driven by type I interferons. However, how type I interferons exacerbate tuberculosis remains poorly understood. As an infection, tuberculosis is distinct from conventional interferonopathies, which are autoinflammatory diseases. Here I consider the hypothesis that type I interferons promote bacterial replication by impairing key antibacterial immune responses, including those orchestrated by interleukin-1 and interferon γ. Paradoxically, during tuberculosis, the underlying state of impaired antibacterial immunity co-exists with overt (but ineffective) inflammation. Conceiving of tuberculosis as an unconventional interferonopathy may suggest fruitful avenues for therapeutic intervention.
期刊介绍：
Current Opinion in Immunology aims to stimulate scientifically grounded, interdisciplinary, multi-scale debate and exchange of ideas. It contains polished, concise and timely reviews and opinions, with particular emphasis on those articles published in the past two years. In addition to describing recent trends, the authors are encouraged to give their subjective opinion of the topics discussed.
In Current Opinion in Immunology we help the reader by providing in a systematic manner: 1. The views of experts on current advances in their field in a clear and readable form. 2. Evaluations of the most interesting papers, annotated by experts, from the great wealth of original publications.
Current Opinion in Immunology will serve as an invaluable source of information for researchers, lecturers, teachers, professionals, policy makers and students.
Current Opinion in Immunology builds on Elsevier''s reputation for excellence in scientific publishing and long-standing commitment to communicating reproducible biomedical research targeted at improving human health. It is a companion to the new Gold Open Access journal Current Research in Immunology and is part of the Current Opinion and Research(CO+RE) suite of journals. All CO+RE journals leverage the Current Opinion legacy-of editorial excellence, high-impact, and global reach-to ensure they are a widely read resource that is integral to scientists'' workflow.
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