ArticleInfection and immunity2015
Ecto-5'-Nucleotidase (CD73) Deficiency in Mycobacterium tuberculosis-Infected Mice Enhances Neutrophil Recruitment.
Article in Infection and immunity, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 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
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Who cites it
14 citing papers in PubMed, 20 citations in OpenAlex.
- Damage response signaling by the extracellular adenosine pathway: control of infection outcome during host aging.mSphere · 2025Review
- Prediction of tuberculosis treatment outcomes using biochemical makers with machine learning.BMC infectious diseases · 2025Article
- Article
- Aerobic glycolysis of bronchial epithelial cells rewiresInfection and immunity · 2024Article
- Adenosine AFrontiers in pharmacology · 2024Article
- Purinergic modulation of the immune response to infections.Purinergic signalling · 2022Review
- Anti-Inflammatory Metabolites in the Pathogenesis of Bacterial Infection.Frontiers in cellular and infection microbiology · 2022Review
- Older but Not Wiser: the Age-Driven Changes in Neutrophil Responses during Pulmonary Infections.Infection and immunity · 2021Review
- Article
- mSphere of Influence: Adenosine in Host Defense against Bacterial Pneumonia-Friend or Foe?mSphere · 2019Article
- The Ecto-5'-Nucleotidase/CD73 Inhibitor, α,β-Methylene Adenosine 5'-Diphosphate, Exacerbates Carrageenan-Induced Pleurisy in Rat.Frontiers in pharmacology · 2019Article
- Innate immunity in tuberculosis: host defense vs pathogen evasion.Cellular & molecular immunology · 2017Review
- Article
- Purinergic Signaling: A Common Path in the Macrophage Response againstFrontiers in cellular and infection microbiology · 2017Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The immune system needs safeguards that prevent collateral tissue damage mediated by the immune system while enabling an effective response against a pathogen. The purinergic pathway is one such mechanism and finely modulates inflammation by sensing nucleotides in the environment. Extracellular ATP is considered to be a danger signal leading to a proinflammatory response, whereas adenosine is immunosuppressive. CD73, also called ecto-5'-nucleotidase, occupies a strategic position in this pathway, as it is the main enzyme responsible for the generation of adenosine from ATP. Here, we explore the role of CD73 during tuberculosis, a disease characterized by an immune response that is harmful to the host and unable to eradicate Mycobacterium tuberculosis. Using CD73 knockout (KO) mice, we found that CD73 regulates the response to M. tuberculosis infection in vitro and in vivo. Mycobacterium-infected murine macrophages derived from CD73 KO mice secrete more keratinocyte chemoattractant (KC), tumor necrosis factor alpha (TNF-α), and interleukin-6 (IL-6) and release less vascular endothelial growth factor (VEGF) upon ATP stimulation than do those derived from wild-type (WT) mice. In vivo, CD73 limits the early influx of neutrophils to the lungs without affecting bacterial growth and dissemination. Collectively, our results support the view that CD73 fine-tunes antimycobacterial immune responses.
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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.