ArticleJCI insight2019
Blocking IL-10 receptor signaling ameliorates Mycobacterium tuberculosis infection during influenza-induced exacerbation.
Article in JCI insight, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
22 citing papers in PubMed, 38 citations in OpenAlex.
- Tissue-resident-like CD4+ T cells secreting IL-17 control Mycobacterium tuberculosis in the human lung.The Journal of clinical investigation · 2021Trial
- Review
- Mechanisms ofBreathe (Sheffield, England) · 2026Review
- The impact of cytomegalovirus coinfection on tuberculosis in the mouse model.BMC infectious diseases · 2026Article
- Exploring Host-driven Immunopathological Factors Developing Severe Tuberculosis: Insights from Comparative Mouse Models.International journal of biological sciences · 2026Article
- Interleukin-1 receptor antagonist is a conserved early factor for exacerbating tuberculosis susceptibility.bioRxiv : the preprint server for biology · 2025Article
- Coinfections in Tuberculosis in Low- and Middle-Income Countries: Epidemiology, Clinical Implications, Diagnostic Challenges, and Management Strategies-A Narrative Review.Journal of clinical medicine · 2025Review
- Sex-specific impact of B cell-derived IL-10 on tuberculosis resistance.Frontiers in immunology · 2025Article
- Article
- Mycobacterium tuberculosis growth inhibition by peripheral blood mononuclear cells from household contacts is not affected by previous SARS-CoV-2 infection.Gates open research · 2025Article
- Unmasking the hidden impact of viruses on tuberculosis risk.Trends in immunology · 2024Review
- A Tale of Two Cytokines: IL-10 Blocks IFN-γ in Influenza A Virus-American journal of respiratory cell and molecular biology · 2024Article
- Article
- RKIP suppresses the influenza A virus‑induced airway inflammatory response via the ERK/MAPK pathway.International journal of molecular medicine · 2023Article
- Co-infection of mice with SARS-CoV-2 andFrontiers in immunology · 2023Article
- Microbial (co)infections: Powerful immune influencers.PLoS pathogens · 2022Review
- Immunopathogenesis in SARS-CoV-2 andFrontiers in pharmacology · 2022Article
- IL-10 Overexpression After BCG Vaccination Does Not Impair Control ofFrontiers in immunology · 2022Article
- Lung Protection vs. Infection Resolution: Interleukin 10 Suspected of Double-Dealing in COVID-19.Frontiers in immunology · 2021Review
- High burden of viral respiratory co-infections in a cohort of children with suspected pulmonary tuberculosis.BMC infectious diseases · 2020Observational
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epidemiological findings indicate that coinfection with influenza viruses is associated with an increased risk of death in patients suffering from tuberculosis but the underlying pathomechanisms are not well understood. In this study, we demonstrate that influenza A virus (IAV) coinfection rapidly impairs control of Mycobacterium tuberculosis (Mtb) in C57BL/6 mice. IAV coinfection was associated with significantly increased bacterial loads, reduced survival and a substantial modulation of innate and adaptive immune defenses including an impaired onset and development of Mtb-specific CD4+ T cell responses and the accumulation of macrophages with increased arginase-1 production in the lungs. Our findings strongly indicate that IAV coinfection compromises the host's ability to control Mtb infection via the production of IL-10 which was rapidly induced upon viral infection. The blockade of IL-10 receptor signaling reduced the bacterial load in coinfected mice to a level comparable with that in Mtb-only-infected animals. Taken together, our data suggest that IL-10 signaling constitutes a major pathway that enhances susceptibility to Mtb during concurrent IAV infection.
Indexed as
Identifiers
What OpenQuestion holds
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.