ArticleInfection and immunity2007
Mycobacterium tuberculosis-induced gamma interferon production by natural killer cells requires cross talk with antigen-presenting cells involving Toll-like receptors 2 and 4 and the mannose receptor in tuberculous pleurisy.
Article in Infection and immunity, 2007. 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, 60 citations in OpenAlex.
- Unveiling the sensing potential of innate lymphoid cells.Communications biology · 2026Review
- TLR2 activation potentiates P-glycoprotein-mediated methotrexate efflux and enhances cytotoxicity of human NK cells against acute lymphoblastic leukemia.Frontiers in immunology · 2026Article
- CD8α marks a Mycobacterium tuberculosis-reactive human NK cell population with high activation potential.Scientific reports · 2025Article
- Impact of anti-TB drugs on modulations of T-cell-receptor-mediated signaling events in TB pleurisy patients.Frontiers in immunology · 2025Review
- IRG1/ACOD1 promotes neutrophil reverse migration and alleviates local inflammation.Journal of leukocyte biology · 2024Article
- Loss of circulating CD8αbioRxiv : the preprint server for biology · 2024Article
- Immunosuppressive Mechanisms in Brucellosis in Light of Chronic Bacterial Diseases.Microorganisms · 2022Review
- Exploring modulations in T-cell receptor-mediated T-cell signaling events in systemic circulation and at local disease site of patients with tubercular pleural effusion: An attempt to understand tuberculosis pathogenesis at the local disease site.Frontiers in medicine · 2022Article
- Pomalidomide restores immune recognition of primary effusion lymphoma through upregulation of ICAM-1 and B7-2.PLoS pathogens · 2021Article
- Sputum microbiota as a potential diagnostic marker for multidrug-resistant tuberculosis.International journal of medical sciences · 2021Observational
- Host-Directed Therapy as a Novel Treatment Strategy to Overcome Tuberculosis: Targeting Immune Modulation.Antibiotics (Basel, Switzerland) · 2020Review
- Tuberculosis Exacerbates HIV-1 Infection through IL-10/STAT3-Dependent Tunneling Nanotube Formation in Macrophages.Cell reports · 2019Article
- Pathogen recognition by NK cells amplifies the pro-inflammatory cytokine production of monocyte-derived DC via IFN-γ.BMC immunology · 2018Article
- Memory of Natural Killer Cells: A New Chance againstFrontiers in immunology · 2017Review
- Strategies to Improve Vaccine Efficacy against Tuberculosis by Targeting Innate Immunity.Frontiers in immunology · 2017Review
- Title: role of matrix metalloproteinase -9 in progression of tuberculous meningitis: a pilot study in patients at different stages of the disease.BMC infectious diseases · 2016Article
- Article
- IL-33 levels differentiate tuberculous pleurisy from malignant pleural effusions.Oncology letters · 2014Article
- Bayesian approach to model CD137 signaling in human M. tuberculosis in vitro responses.PloS one · 2013Article
- Association between elevated pleural interleukin-33 levels and tuberculous pleurisy.Annals of laboratory medicine · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tuberculous pleurisy allows the study of human cells at the site of active Mycobacterium tuberculosis infection. In this study, we found that among pleural fluid (PF) lymphocytes, natural killer (NK) cells are a major source of early gamma interferon (IFN-gamma) upon M. tuberculosis stimulation, leading us to investigate the mechanisms and molecules involved in this process. We show that the whole bacterium is the best inducer of IFN-gamma, although a high-molecular-weight fraction of culture filtrate proteins from M. tuberculosis H37Rv and the whole-cell lysate also induce its expression. The mannose receptor seems to mediate the inhibitory effect of mannosylated lipoarabinomannan, and Toll-like receptor 2 and 4 agonists activate NK cells but do not induce IFN-gamma like M. tuberculosis does. Antigen-presenting cells (APC) and NK cells bind M. tuberculosis, and although interleukin-12 is required, it is not sufficient to induce IFN-gamma expression, indicating that NK cell-APC contact takes place. Indeed, major histocompatibility complex class I, adhesion, and costimulatory molecules as well as NK receptors regulate IFN-gamma induction. The signaling pathway is partially inhibited by dexamethasone and sensitive to Ca2+ flux and cyclosporine. Inhibition of p38 and extracellular-regulated kinase mitogen-activated protein kinase pathways reduces the number of IFN-gamma+ NK cells. Phosphorylated p38 (p-p38) is detected in ex vivo PF-NK cells, and M. tuberculosis triggers p-p38 in PF-NK cells at the same time that binding between NK and M. tuberculosis reaches its maximum value. Thus, interplay between M. tuberculosis and NK cells/APC triggering IFN-gamma would be expected to play a beneficial role in tuberculous pleurisy by helping to maintain a type 1 profile.
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.