ArticleJournal of immunology (Baltimore, Md. : 1950)2012
Dynamic roles of type I and type II IFNs in early infection with Mycobacterium tuberculosis.
Article in Journal of immunology (Baltimore, Md. : 1950), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 112 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
112 citing papers in PubMed, 168 citations in OpenAlex.
- A Clinical Multicenter Trial of Recombinant Human Interferon Gamma in Tuberculosis (GAM2022): Experience with the Use of Human Recombinant Interferon Gamma in TB Practice.Infectious disorders drug targets · 2025Trial
- Host-pathogen interactions in tuberculosis: from immunological mechanisms to translational applications.Cell insight · 2026Review
- IFN𝛾 and IFN𝛾 mimetics prevent IFN-I-mediated TB susceptibility by regulating iron metabolism and lipid peroxidation.bioRxiv : the preprint server for biology · 2026Article
- CCR6 is essential for effective immunity againstInfection and immunity · 2026Article
- Type I interferons in tuberculosis pathogenesis and prevention.Trends in microbiology · 2026Review
- 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
- The virulence regulator Rv3425 mediates stress adaptation and promotes intracellular survival of Mycobacterium tuberculosis avirulent strain.Archives of microbiology · 2026Article
- Host-directed broad-spectrum immunotherapeutic strategy for respiratory infections: Heat-killed Caulobacter crescentus (HKCC) as an innate-immune based biotherapeutic/postbiotic.PLoS pathogens · 2026Article
- Type I IFN drives neutrophil swarming, impeding lung T cell-macrophage interactions and TB control.The Journal of experimental medicine · 2025Article
- Alveolar macrophage transcriptional signatures associated with resistance to TST/IGRA conversion following Mycobacterium tuberculosis exposure.BMC genomics · 2025Article
- Genome-wide screen inbioRxiv : the preprint server for biology · 2025Article
- Tuberculosis susceptibility in genetically diverse mice reveals functional diversity of neutrophils.eLife · 2025Article
- Cathepsin Z is a conserved susceptibility factor underlying tuberculosis severity.PLoS biology · 2025Article
- The Role of Type I Interferons in Tuberculosis and in Tuberculosis-Risk-Associated Comorbidities.Infectious disease reports · 2025Review
- Protein Kinase C δ: a critical hub regulating macrophage immunomodulatory functions duringbioRxiv : the preprint server for biology · 2025Article
- Exposure to Urban Air Pollution Particulate Matter Modifies Th1/Th2American journal of respiratory cell and molecular biology · 2025Article
- Type I interferons in bacterial diseases: myeloid cells at the crossroads of protection and pathology.Frontiers in immunology · 2025Review
- Role of Type I Interferons duringBiomolecules · 2024Review
- Mycobacterium tuberculosis resides in lysosome-poor monocyte-derived lung cells during chronic infection.PLoS pathogens · 2024Article
- A protective role for type I interferon signaling following infection with Mycobacterium tuberculosis carrying the rifampicin drug resistance-conferring RpoB mutation H445Y.PLoS pathogens · 2024Article
52 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Although the protective role of type II IFN, or IFN-γ, against Mycobacterium tuberculosis has been established, the effects of type I IFNs are still unclear. One potential confounding factor is the overlap of function between the two signaling pathways. We used mice carrying null mutations in the type I IFNR, type II IFNR, or both and compared their immune responses to those of wild-type mice following aerosol infection with M. tuberculosis. We discovered that, in the absence of a response to IFN-γ, type I IFNs play a nonredundant protective role against tuberculosis. Mice unable to respond to both types of IFNs had more severe lung histopathology for similar bacterial loads and died significantly earlier than did mice with impaired IFN-γ signaling alone. We excluded a role for type I IFN in T cell recruitment, which was IFN-γ dependent, whereas both types of IFNs were required for optimal NK cell recruitment to the lungs. Type I IFN had a time-dependent influence on the composition of lung myeloid cell populations, in particular by limiting the abundance of M. tuberculosis-infected recruited macrophages after the onset of adaptive immunity. We confirmed that response to IFN-γ was essential to control intracellular mycobacterial growth, without any additional effect of type I IFN. Together, our results imply a model in which type I IFN limit the number of target cells that M. tuberculosis can infect in the lungs, whereas IFN-γ enhances their ability to restrict bacterial growth.
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