ArticlePloS one2014
Methylthioadenosine reprograms macrophage activation through adenosine receptor stimulation.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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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.
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Who cites it
20 citing papers in PubMed.
- Human genetic and metabolite variation reveals that methylthioadenosine is a prognostic biomarker and an inflammatory regulator in sepsis.Science advances · 2017Trial
- Discovery of non-invasive biomarkers for accurate detection of membranous nephropathy.Scientific reports · 2025Article
- The glioma microenvironment and its impact on antitumor immunity.Neuro-oncology advances · 2025Review
- Inhibition of methylthioadenosine phosphorylase protects from experimental acute kidney injury.American journal of physiology. Renal physiology · 2025Article
- Adenosine receptors on the immuno-oncology expressway: TIME, perspectives, and translation.Frontiers in immunology · 2025Review
- Fluorogenic Probes of the Mycobacterial Membrane as Reporters of Antibiotic Action.Journal of the American Chemical Society · 2024Article
- Article
- Enzyme-mediated depletion of methylthioadenosine restores T cell function in MTAP-deficient tumors and reverses immunotherapy resistance.Cancer cell · 2023Article
- Patch repair protects cells from the small pore-forming toxin aerolysin.Journal of cell science · 2023Article
- Epigenetic regulation of macrophage polarization in wound healing.Burns & trauma · 2023Review
- Article
- MTAP loss correlates with an immunosuppressive profile in GBM and its substrate MTA stimulates alternative macrophage polarization.Scientific reports · 2022Article
- The role of polyamine metabolism in remodeling immune responses and blocking therapy within the tumor immune microenvironment.Frontiers in immunology · 2022Review
- 9p21 loss confers a cold tumor immune microenvironment and primary resistance to immune checkpoint therapy.Nature communications · 2021Article
- The Oncometabolite 5'-Deoxy-5'-Methylthioadenosine Blocks Multiple Signaling Pathways of NK Cell Activation.Frontiers in immunology · 2020Article
- Primed mesenchymal stem cells package exosomes with metabolites associated with immunomodulation.Biochemical and biophysical research communications · 2019Article
- Methylthioadenosine Suppresses Salmonella Virulence.Infection and immunity · 2018Article
- Cholesterol-dependent cytolysins impair pro-inflammatory macrophage responses.Scientific reports · 2018Article
- Epigenetic control of macrophage polarization: implications for targeting tumor-associated macrophages.Oncotarget · 2018Review
- Dnase1L3 Regulates Inflammasome-Dependent Cytokine Secretion.Frontiers in immunology · 2017Article
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
Regulation of inflammation is necessary to balance sufficient pathogen clearance with excessive tissue damage. Central to regulating inflammation is the switch from a pro-inflammatory pathway to an anti-inflammatory pathway. Macrophages are well-positioned to initiate this switch, and as such are the target of multiple therapeutics. One such potential therapeutic is methylthioadenosine (MTA), which inhibits TNFα production following LPS stimulation. We found that MTA could block TNFα production by multiple TLR ligands. Further, it prevented surface expression of CD69 and CD86 and reduced NF-KB signaling. We then determined that the mechanism of this action by MTA is signaling through adenosine A2 receptors. A2 receptors and TLR receptors synergized to promote an anti-inflammatory phenotype, as MTA enhanced LPS tolerance. In contrast, IL-1β production and processing was not affected by MTA exposure. Taken together, these data demonstrate that MTA reprograms TLR activation pathways via adenosine receptors to promote resolution of inflammation.
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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.