ReviewFrontiers in immunology2016
Purinergic Signaling to Terminate TLR Responses in Macrophages.
Review in Frontiers in immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 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
30 citing papers in PubMed, 39 citations in OpenAlex.
- Programmed death-ligand 1 (PD-L1) Modulates Chemokine Production Via the TLR4/TRAF6 Signaling Axis During LPS + IFN-γ-Induced Endotoxemia-mimicked Sepsis.Inflammation · 2026Article
- The authors respond to feedback onFrontiers in oncology · 2026Article
- Purinergic Receptors in Dendritic Cells.Journal of inflammation research · 2025Review
- Evidence of collective influence in innate sensing using fluidic force microscopy.Frontiers in immunology · 2024Article
- Unraveling the Intricacies of CD73/Adenosine Signaling: The Pulmonary Immune and Stromal Microenvironment in Lung Cancer.Cancers · 2023Review
- Review
- Effects of Water Extract fromAnimals : an open access journal from MDPI · 2022Article
- Purinergic modulation of the immune response to infections.Purinergic signalling · 2022Review
- Pharmacological Activities forFoods (Basel, Switzerland) · 2021Review
- Expression and Gene Regulation Network of Adenosine Receptor A2B in Lung Adenocarcinoma: A Potential Diagnostic and Prognostic Biomarker.Frontiers in molecular biosciences · 2021Article
- Microbial Colonization and Inflammation as Potential Contributors to the Lack of Therapeutic Success in Oral Squamous Cell Carcinoma.Frontiers in oral health · 2021Review
- Purinergic signalling in liver diseases: Pathological functions and therapeutic opportunities.JHEP reports : innovation in hepatology · 2020Review
- The transition of M-CSF-derived human macrophages to a growth-promoting phenotype.Blood advances · 2020Article
- Targeting CD73 to augment cancer immunotherapy.Current opinion in pharmacology · 2020Review
- Signaling Through Purinergic Receptor P2YInternational journal of molecular sciences · 2020Article
- Living in a Hostile World: Inflammation, New Drug Development, and Coronavirus.Frontiers in immunology · 2020Review
- Ectonucleotidases in Acute and Chronic Inflammation.Frontiers in pharmacology · 2020Review
- CD73: an emerging checkpoint for cancer immunotherapy.Immunotherapy · 2019Article
- Targeting the Immunomodulatory CD73/Adenosine System to Improve the Therapeutic Gain of Radiotherapy.Frontiers in immunology · 2019Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Macrophages undergo profound physiological alterations when they encounter pathogen-associated molecular patterns (PAMPs). These alterations can result in the elaboration of cytokines and mediators that promote immune responses and contribute to the clearance of pathogens. These innate immune responses by myeloid cells are transient. The termination of these secretory responses is not due to the dilution of stimuli, but rather to the active downregulation of innate responses induced by the very PAMPs that initiated them. Here, we describe a purinergic autoregulatory program whereby TLR-stimulated macrophages control their activation state. In this program, TLR-stimulated macrophages undergo metabolic alterations that result in the production of ATP and its release through membrane pannexin channels. This purine nucleotide is rapidly hydrolyzed to adenosine by ectoenzymes on the macrophage surface, CD39 and CD73. Adenosine then signals through the P1 class of seven transmembrane receptors to induce a regulatory state that is characterized by the downregulation of inflammatory cytokines and the production of anti-inflammatory cytokines and growth factors. This purinergic autoregulatory system mitigates the collateral damage that would be caused by the prolonged activation of macrophages and rather allows the macrophage to maintain homeostasis. The transient activation of macrophages can be prolonged by treating macrophages with IFN-γ. IFN-γ-treated macrophages become less sensitive to the regulatory effects of adenosine, allowing them to sustain macrophage activation for the duration of an adaptive immune response.
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.