ArticlePloS one2012
Improved control of tuberculosis and activation of macrophages in mice lacking protein kinase R.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 26 papers.
What it found
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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
26 citing papers in PubMed, 41 citations in OpenAlex.
- Host-directed therapy to combat mycobacterial infections.Immunological reviews · 2021Review
- Protein Kinase R in Bacterial Infections: Friend or Foe?Frontiers in immunology · 2021Review
- New insights into the evasion of host innate immunity by Mycobacterium tuberculosis.Cellular & molecular immunology · 2020Review
- Protein Kinase R Restricts the Intracellular Survival ofFrontiers in microbiology · 2020Article
- Cytoplasmic RNA Sensor Pathways and Nitazoxanide Broadly Inhibit Intracellular Mycobacterium tuberculosis Growth.iScience · 2019Article
- Emerging therapeutic targets for treatment of leishmaniasis.Expert opinion on therapeutic targets · 2018Review
- Evidence for dispensability of protein kinase R in host control of tuberculosis.European journal of immunology · 2018Article
- Correction: Improved Control of Tuberculosis and Activation of Macrophages in Mice Lacking Protein Kinase R.PloS one · 2018Article
- A potential target gene for the host-directed therapy of mycobacterial infection in murine macrophages.International journal of molecular medicine · 2016Article
- Leishmania Infection Engages Non-Receptor Protein Kinases Differentially to Persist in Infected Hosts.Frontiers in immunology · 2016Review
- Host-Directed Therapies for Tuberculosis.Cold Spring Harbor perspectives in medicine · 2015Review
- The immune response and antibacterial therapy.Medical microbiology and immunology · 2015Review
- Advancing host-directed therapy for tuberculosis.Nature reviews. Immunology · 2015Review
- New insights into TB physiology suggest untapped therapeutic opportunities.Immunological reviews · 2015Review
- Differential transcriptional response in macrophages infected with cell wall deficient versus normal Mycobacterium Tuberculosis.International journal of biological sciences · 2015Article
- Macrophage polarization drives granuloma outcome during Mycobacterium tuberculosis infection.Infection and immunity · 2015Article
- Cell death and autophagy in tuberculosis.Seminars in immunology · 2014Review
- Interaction of Mycobacterium tuberculosis with host cell death pathways.Cold Spring Harbor perspectives in medicine · 2014Review
- Increased severity of tuberculosis in Guinea pigs with type 2 diabetes: a model of diabetes-tuberculosis comorbidity.The American journal of pathology · 2014Article
- Are reactive oxygen species always detrimental to pathogens?Antioxidants & redox signaling · 2014Review
Corrections and comments
- Erratum issued
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Host factors that microbial pathogens exploit for their propagation are potential targets for therapeuic countermeasures. No host enzyme has been identified whose genetic absence benefits the intact mammalian host in vivo during infection with Mycobacterium tuberculosis (Mtb), the leading cause of death from bacterial infection. Here, we report that the dsRNA-dependent protein kinase (PKR) is such an enzyme. PKR-deficient mice contained fewer viable Mtb and showed less pulmonary pathology than wild type mice. We identified two potential mechanisms for the protective effect of PKR deficiency: increased apoptosis of macrophages in response to Mtb and enhanced activation of macrophages in response to IFN-gamma. The restraining effect of PKR on macrophage activation was explained by its mediation of a previously unrecognized ability of IFN-gamma to induce low levels of the macrophage deactivating factor interleukin 10 (IL10). These observations suggest that PKR inhibitors may prove useful as an adjunctive treatment for tuberculosis.
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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.