ArticleCytokine2012
Interferon-γ, tumor necrosis factor, and interleukin-18 cooperate to control growth of Mycobacterium tuberculosis in human macrophages.
Article in Cytokine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 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
30 citing papers in PubMed, 49 citations in OpenAlex.
- IL-27 neutralization with and without antibiotics as an approach to prevent and treat neonatal sepsis.JCI insight · 2026Article
- The interplay of tuberculosis and COVID-19: Insights into global health challenges.Journal of biosciences · 2025Review
- Immunopathology of PulmonaryInternational journal of molecular sciences · 2024Article
- Co-Formulation of Recombinant Porcine IL-18 Enhances the Onset of Immune Response in a NewVaccines · 2023Article
- Interleukin-27-dependent transcriptome signatures during neonatal sepsis.Frontiers in immunology · 2023Article
- Interleukin-18 Binding Protein in Immune Regulation and Autoimmune Diseases.Biomedicines · 2022Review
- Mycobacterium tuberculosis infection drives a type I IFN signature in lung lymphocytes.Cell reports · 2022Article
- Comparison of the frequency and phenotypic profile ofFrontiers in immunology · 2022Article
- Interleukin-27 in Tuberculosis: A Sheep in Wolf's Clothing?Frontiers in immunology · 2021Review
- Interleukin-27 and Its Diverse Effects on Bacterial Infections.Frontiers in immunology · 2021Review
- The Role of gp130 Cytokines in Tuberculosis.Cells · 2020Review
- Regulation of mitogen-activated protein kinase signaling pathway and proinflammatory cytokines by ursolic acid in murine macrophages infected withInfectious disease reports · 2020Article
- Elevated Levels of Interleukin-27 in Early Life Compromise Protective Immunity in a Mouse Model of Gram-Negative Neonatal Sepsis.Infection and immunity · 2020Article
- Murine myeloid-derived suppressor cells are a source of elevated levels of interleukin-27 in early life and compromise control of bacterial infection.Immunology and cell biology · 2019Article
- IL-27 amplifies cytokine responses to Gram-negative bacterial products and Salmonella typhimurium infection.Scientific reports · 2018Article
- Comparative 'omics analyses differentiate Mycobacterium tuberculosis and Mycobacterium bovis and reveal distinct macrophage responses to infection with the human and bovine tubercle bacilli.Microbial genomics · 2018Article
- The Influence ofFrontiers in microbiology · 2018Article
- Review
- Regulatory monocytes in helminth infections: insights from the modulation during human hookworm infection.BMC infectious diseases · 2017Article
- Elevated interleukin-27 levels in human neonatal macrophages regulate indoleamine dioxygenase in a STAT-1 and STAT-3-dependent manner.Immunology · 2016Article
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 2 institutions in 1 country.
Funding
Abstract
Mycobacterium tuberculosis (MTB) remains a leading infectious threat to human health. Macrophages are the cells targeted for infection by the bacterium as well as key effector cells for clearance of the pathogen. Interleukin (IL)-27 opposes macrophage-mediated control of MTB because supplying IL-12 and blocking the activity of IL-27 limits bacterial growth in primary human macrophages. The purpose of this study was to determine the immunological regulators of this macrophage mechanism to restrict MTB growth. Interferon (IFN)-γ, TNF-α, and IL-18 were all demonstrated to be important to the environment that limits bacterial growth when IL-12 is supplied and IL-27 is neutralized. We find IL-18 works in conjunction with IL-12 to achieve optimal IFN-γ production in this system. We also demonstrate novel interactions between these cytokines to influence the expression or responsiveness to one another. Quantitative assays show that IFN-γ enhances expression of the IL-18 receptor signaling chain, as well as TNF expression and secretion. In turn, TNF-α augments expression of the receptor for IFN-γ, the amount at the cell surface, and the extent of IFN-γ -induced signaling. We further define how the cytokine environment supports an enhanced state of classical macrophage activation. Collectively, these results describe novel immunological mechanisms that provide additional insights into the effects of IL-12 and IL-27 on macrophage regulation during MTB 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.