ArticleThe Journal of experimental medicine2010
The adaptor molecule CARD9 is essential for tuberculosis control.
Article in The Journal of experimental medicine, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 117 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
117 citing papers in PubMed, 196 citations in OpenAlex.
- Diverse infection models demonstrate robust resistance ofbioRxiv : the preprint server for biology · 2026Article
- Spatial and temporal immune landscapes of non-necrotic granulomas in two murine tuberculosis models with divergent disease outcomes.Frontiers in immunology · 2026Article
- Mycobacterium avium-complex infection mimicking lymphoma in a miniature schnauzer.BMC veterinary research · 2025Article
- Genome-wide screen inbioRxiv : the preprint server for biology · 2025Article
- Tuberculosis susceptibility in genetically diverse mice reveals functional diversity of neutrophils.eLife · 2025Article
- Unravelling the transcriptome of the human tuberculosis lesion and its clinical implications.Nature communications · 2025Article
- The C-Type Lectin Receptors.Advances in experimental medicine and biology · 2025Review
- Type I IFN-mediated NET release promotes Mycobacterium tuberculosis replication and is associated with granuloma caseation.Cell host & microbe · 2024Article
- Increased susceptibility to Mycobacterium avium complex infection in miniature Schnauzer dogs caused by a codon deletion in CARD9.Scientific reports · 2024Article
- Role of CARD9 in Cell- and Organ-Specific Immune Responses in Various Infections.International journal of molecular sciences · 2024Review
- Card9/neutrophil signalling axis promotes IL-17A-mediated ankylosing spondylitis.Annals of the rheumatic diseases · 2024Article
- Granulocytes subsets and their divergent functions in host resistance to Mycobacterium tuberculosis - a 'tipping-point' model of disease exacerbation.Current opinion in immunology · 2023Review
- Article
- Animal models for COVID-19 and tuberculosis.Frontiers in immunology · 2023Review
- Card9 protects sepsis by regulating Ripk2-mediated activation of NLRP3 inflammasome in macrophages.Cell death & disease · 2022Article
- An In Vivo Model of SeparateInternational journal of molecular sciences · 2022Article
- Exploring the Role of Low-Density Neutrophils DuringFrontiers in cellular and infection microbiology · 2022Review
- The role and mechanism of CARD9 gene polymorphism in diseases.Biomedical journal · 2021Review
- Neutrophils in Tuberculosis: Cell Biology, Cellular Networking and Multitasking in Host Defense.International journal of molecular sciences · 2021Review
- TREM2 is a receptor for non-glycosylated mycolic acids of mycobacteria that limits anti-mycobacterial macrophage activation.Nature communications · 2021Article
57 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
10 authors at 3 institutions in 1 country.
Funding
Abstract
The cross talk between host and pathogen starts with recognition of bacterial signatures through pattern recognition receptors (PRRs), which mobilize downstream signaling cascades. We investigated the role of the cytosolic adaptor caspase recruitment domain family, member 9 (CARD9) in tuberculosis. This adaptor was critical for full activation of innate immunity by converging signals downstream of multiple PRRs. Card9(-/-) mice succumbed early after aerosol infection, with higher mycobacterial burden, pyogranulomatous pneumonia, accelerated granulocyte recruitment, and higher abundance of proinflammatory cytokines and granulocyte colony-stimulating factor (G-CSF) in serum and lung. Neutralization of G-CSF and neutrophil depletion significantly prolonged survival, indicating that an exacerbated systemic inflammatory disease triggered lethality of Card9(-/-) mice. CARD9 deficiency had no apparent effect on T cell responses, but a marked impact on the hematopoietic compartment. Card9(-/-) granulocytes failed to produce IL-10 after Mycobacterium tuberculosis infection, suggesting that an absent antiinflammatory feedback loop accounted for granulocyte-dominated pathology, uncontrolled bacterial replication, and, ultimately, death of infected Card9(-/-) mice. Our data provide evidence that deregulated innate responses trigger excessive lung inflammation and demonstrate a pivotal role of CARD9 signaling in autonomous innate host defense against tuberculosis.
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.