ReviewClinical & developmental immunology2011
Innate immune effectors in mycobacterial infection.
Review in Clinical & developmental immunology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 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
37 citing papers in PubMed, 91 citations in OpenAlex.
- Pathogenicity of Type I Interferons inInternational journal of molecular sciences · 2023Review
- Different modalities of host cell death and their impact onAmerican journal of physiology. Cell physiology · 2022Review
- Host-pathogen protein-nucleic acid interactions: A comprehensive review.Computational and structural biotechnology journal · 2022Review
- Macrophage Signaling Pathways in Pulmonary Nontuberculous Mycobacteria Infections.American journal of respiratory cell and molecular biology · 2020Review
- MicroRNA-106a Inhibits Autophagy Process and Antimicrobial Responses by Targeting ULK1, ATG7, and ATG16L1 During Mycobacterial Infection.Frontiers in immunology · 2020Article
- Polymorphisms in the P2X7 receptor, and differential expression of Toll-like receptor-mediated cytokines and defensins, in a Canadian Indigenous group.Scientific reports · 2019Article
- TLRs in pulmonary diseases.Life sciences · 2019Review
- Human Antimicrobial RNases Inhibit Intracellular Bacterial Growth and Induce Autophagy in Mycobacteria-Infected Macrophages.Frontiers in immunology · 2019Article
- Article
- Nanoscale Peptide Self-assemblies Boost BCG-primed Cellular Immunity Against Mycobacterium tuberculosis.Scientific reports · 2018Article
- Persistent mycobacteria evade an antibacterial program mediated by phagolysosomal TLR7/8/MyD88 in human primary macrophages.PLoS pathogens · 2017Article
- MyD88 in Mycobacterium tuberculosis infection.Medical microbiology and immunology · 2017Review
- Molecular basis of mycobacterial survival in macrophages.Cellular and molecular life sciences : CMLS · 2017Review
- Metabolic Alterations Contribute to Enhanced Inflammatory Cytokine Production in Irgm1-deficient Macrophages.The Journal of biological chemistry · 2017Article
- Bolstering Immunity through Pattern Recognition Receptors: A Unique Approach to Control Tuberculosis.Frontiers in immunology · 2017Review
- Host Antimicrobial Peptides: The Promise of New Treatment Strategies against Tuberculosis.Frontiers in immunology · 2017Review
- Roles of endoplasmic reticulum stress-mediated apoptosis in M1-polarized macrophages during mycobacterial infections.Scientific reports · 2016Article
- Single nucleotide polymorphisms in toll-like receptor genes and case-control association studies with bovine tuberculosis.Veterinary world · 2016Article
- Signaling through NOD-2 and TLR-4 Bolsters the T cell Priming Capability of Dendritic cells by Inducing Autophagy.Scientific reports · 2016Article
- The Microbiota Determines Susceptibility to Experimental Autoimmune Uveoretinitis.Journal of immunology research · 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 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tuberculosis, which is caused by infection with Mycobacterium tuberculosis (Mtb), remains one of the major bacterial infections worldwide. Host defense against Mtb is mediated by a combination of innate and adaptive immune responses. In the last 15 years, the mechanisms for activation of innate immunity have been elucidated. Toll-like receptors (TLRs) have been revealed to be critical for the recognition of pathogenic microorganisms including mycobacteria. Subsequent studies further revealed that NOD-like receptors and C-type lectin receptors are responsible for the TLR-independent recognition of mycobacteria. Several molecules, such as active vitamin D(3), secretary leukocyte protease inhibitor, and lipocalin 2, all of which are induced by TLR stimulation, have been shown to direct innate immune responses to mycobacteria. In addition, Irgm1-dependent autophagy has recently been demonstrated to eliminate intracellular mycobacteria. Thus, our understanding of the mechanisms for the innate immune response to mycobacteria is developing.
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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.