ArticleJournal of immunology (Baltimore, Md. : 1950)2014
Type I IFN induces IL-10 production in an IL-27-independent manner and blocks responsiveness to IFN-γ for production of IL-12 and bacterial killing in Mycobacterium tuberculosis-infected macrophages.
Article in Journal of immunology (Baltimore, Md. : 1950), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 129 papers.
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Who cites it
129 citing papers in PubMed, 195 citations in OpenAlex.
- Trial
- Strong, sustained type I IFN signaling acts cell intrinsically to impair IFNγ responses and cause tuberculosis susceptibility.Cell host & microbe · 2026Article
- Restricted MHC-II trafficking inbioRxiv : the preprint server for biology · 2026Article
- IFN𝛾 and IFN𝛾 mimetics prevent IFN-I-mediated TB susceptibility by regulating iron metabolism and lipid peroxidation.bioRxiv : the preprint server for biology · 2026Article
- Contribution of cytotoxic CD8 T cells, neutrophils and type 1 interferon signaling to hyperinflammation in HIV-associated TB meningitis.bioRxiv : the preprint server for biology · 2026Article
- Polymorphisms in IRF3 exon 1 influence the immune response to Brucella infection in small ruminants.Mammalian genome : official journal of the International Mammalian Genome Society · 2026Article
- Comparative Transcriptomic Analysis of Human Macrophages During Mycobacterium avium Versus Mycobacterium tuberculosis Infection.Molecular microbiology · 2026Article
- Type I interferons in tuberculosis pathogenesis and prevention.Trends in microbiology · 2026Review
- Strong sustained type I IFN signaling acts cell intrinsically to impair IFNγ responses and cause tuberculosis susceptibility.bioRxiv : the preprint server for biology · 2026Article
- Exploring Host-driven Immunopathological Factors Developing Severe Tuberculosis: Insights from Comparative Mouse Models.International journal of biological sciences · 2026Article
- The Type I Interferon Axis in Systemic Autoimmune Diseases: From Molecular Pathways to Targeted Therapy.Biomolecules · 2025Review
- Interleukin-10 family cytokines: key regulators and novel therapeutic targets for respiratory diseases.Inflammopharmacology · 2025Review
- Genome-wide screen inbioRxiv : the preprint server for biology · 2025Article
- Advances in host-directed therapy for tuberculosis and HIV coinfection: enhancing immune responses.Trends in microbiology · 2025Review
- Metabolic dysfunction impairs Mycobacterium tuberculosis-specific cytokine and chemokine responses in latent tuberculosis and type 2 diabetes mellitus.Scientific reports · 2025Article
- Comparative analysis of the clinical characteristic and lung microbiota in adult and elderly patients with pulmonary tuberculosis.Scientific reports · 2025Article
- HIV-1 cell-to-cell infection of macrophages escapes type I interferon and host restriction factors, and is resistant to antiretroviral drugs.PLoS pathogens · 2025Article
- For Better or Worse: Type I Interferon Responses in Bacterial Infection.Pathogens (Basel, Switzerland) · 2025Review
- In vivo regulation of the monocyte phenotype by Mycobacterium marinum and the ESX-1 type VII secretion system.Scientific reports · 2025Article
- Investigation of the relationship between chronic hepatitis B and tuberculosis using bioinformatics and systems biology approaches.Frontiers in medicine · 2025Article
69 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
8 authors at 4 institutions in 3 countries.
Funding
Abstract
Tuberculosis, caused by the intracellular bacterium Mycobacterium tuberculosis, currently causes ∼1.4 million deaths per year, and it therefore remains a leading global health problem. The immune response during tuberculosis remains incompletely understood, particularly regarding immune factors that are harmful rather than protective to the host. Overproduction of the type I IFN family of cytokines is associated with exacerbated tuberculosis in both mouse models and in humans, although the mechanisms by which type I IFN promotes disease are not well understood. We have investigated the effect of type I IFN on M. tuberculosis-infected macrophages and found that production of host-protective cytokines such as TNF-α, IL-12, and IL-1β is inhibited by exogenous type I IFN, whereas production of immunosuppressive IL-10 is promoted in an IL-27-independent manner. Furthermore, much of the ability of type I IFN to inhibit cytokine production was mediated by IL-10. Additionally, type I IFN compromised macrophage activation by the lymphoid immune response through severely disrupting responsiveness to IFN-γ, including M. tuberculosis killing. These findings describe important mechanisms by which type I IFN inhibits the immune response during tuberculosis.
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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.