ArticleJournal of immunology (Baltimore, Md. : 1950)2011
Mycobacterium tuberculosis triggers host type I IFN signaling to regulate IL-1β production in human macrophages.
Article in Journal of immunology (Baltimore, Md. : 1950), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 160 papers.
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Who cites it
160 citing papers in PubMed, 246 citations in OpenAlex.
- Trial
- EsxN drives ISG15-mediated dsDNA release to activate cGAS-STING signaling and promote mycobacterial survival.Microbiology spectrum · 2026Article
- Comparative Transcriptomic Analysis of Human Macrophages During Mycobacterium avium Versus Mycobacterium tuberculosis Infection.Molecular microbiology · 2026Article
- Type I interferon signaling promotes early innate control ofbioRxiv : the preprint server for biology · 2026Article
- Pericentromeric Transcription of Novel Pathogen-Related Human GPS Genes in Cancers is Regulated by C19MC miRNAs, CEBPB, IFN-γ, and IFN-β.Research square · 2026Article
- Pharmacological inhibition of USP18 improves antibacterial responses and the intracellular control ofFrontiers in immunology · 2026Article
- Article
- The Type I Interferon Axis in Systemic Autoimmune Diseases: From Molecular Pathways to Targeted Therapy.Biomolecules · 2025Review
- The dual role of type I interferons in bacterial infections: from immune defense to pathogenesis.mBio · 2025Review
- Cytokine profiles dynamics in COVID-19 patients: a longitudinal analysis of disease severity and outcomes.Scientific reports · 2025Article
- Deconvoluting the interplay of innate and adaptive immunity in BCG-induced nonspecific and TB-specific host resistance.The Journal of experimental medicine · 2025Review
- For Better or Worse: Type I Interferon Responses in Bacterial Infection.Pathogens (Basel, Switzerland) · 2025Review
- Comparison the impact of IFN-β alone or in combination with vitamin D on critical pathways involved in AML progression.PloS one · 2025Article
- Type I interferons in bacterial diseases: myeloid cells at the crossroads of protection and pathology.Frontiers in immunology · 2025Review
- Differential Host Gene Expression in Response to Infection by DifferentMicroorganisms · 2024Article
- Cytosolic serpins act in a cytoprotective feedback loop that limits ESX-1-dependent death ofmBio · 2024Article
- Unmasking the hidden impact of viruses on tuberculosis risk.Trends in immunology · 2024Review
- GATA2 promotes castration-resistant prostate cancer development by suppressing IFN-β axis-mediated antitumor immunity.Oncogene · 2024Article
- Human Alveolar and Monocyte-Derived Human Macrophage Responses to Mycobacterium tuberculosis.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
- Role of Type I Interferons duringBiomolecules · 2024Review
100 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
11 authors at 6 institutions in 1 country.
Funding
Abstract
Mycobacterium tuberculosis is a virulent intracellular pathogen that survives in macrophages even in the presence of an intact adaptive immune response. Type I IFNs have been shown to exacerbate tuberculosis in mice and to be associated with disease progression in infected humans. Nevertheless, the mechanisms by which type I IFNs regulate the host response to M. tuberculosis infection are poorly understood. In this study, we show that M. tuberculosis induces an IFN-related gene expression signature in infected primary human macrophages, which is dependent on host type I IFN signaling as well as the mycobacterial virulence factor, region of difference-1. We further demonstrate that type I IFNs selectively limit the production of IL-1β, a critical mediator of immunity to M. tuberculosis. This regulation occurs at the level of IL1B mRNA expression, rather than caspase-1 activation or autocrine IL-1 amplification and appears to be preferentially used by virulent mycobacteria since avirulent M. bovis bacillus Calmette-Guérin (BCG) fails to trigger significant expression of type I IFNs or release of mature IL-1β protein. The latter property is associated with decreased caspase-1-dependent IL-1β maturation in the BCG-infected macrophages. Interestingly, human monocytes in contrast to macrophages produce comparable levels of IL-1β in response to either M. tuberculosis or BCG. Taken together, these findings demonstrate that virulent and avirulent mycobacteria employ distinct pathways for regulating IL-1β production in human macrophages and reveal that in the case of M. tuberculosis infection the induction of type I IFNs is a major mechanism used for this purpose.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.