ArticleCell communication and signaling : CCS2014
CD39 is a negative regulator of P2X7-mediated inflammatory cell death in mast cells.
Article in Cell communication and signaling : CCS, 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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Who cites it
20 citing papers in PubMed, 31 citations in OpenAlex.
- Impact of cryopreservation on immune cell subset frequencies in human peripheral blood mononuclear cells following assessment of monoclonal antibodies to CD39 and P2X7.Purinergic signalling · 2026Article
- The P2X7 receptor: insights from the murine monoclonal antibody clone L4.Purinergic signalling · 2026Review
- Article
- Clostridioides difficile meets the adenosine system: the art of manipulating host homeostasis.Journal of biomedical science · 2025Review
- ATP/IL-33-Co-Sensing by Mast Cells (MCs) Requires Activated c-Kit to Ensure Effective Cytokine Responses.Cells · 2023Article
- Pyroptosis in neutrophils: Multimodal integration of inflammasome and regulated cell death signaling pathways.Immunological reviews · 2023Review
- Efficient recovery of potent tumour-infiltrating lymphocytes through quantitative immunomagnetic cell sorting.Nature biomedical engineering · 2022Article
- Targeting CD39 in cancer.Nature reviews. Immunology · 2020Review
- On the mechanism of anti-CD39 immune checkpoint therapy.Journal for immunotherapy of cancer · 2020Review
- Article
- Toll-Like Receptor-Mediated Activation of CD39 Internalization in BMDCs Leads to Extracellular ATP Accumulation and Facilitates P2X7 Receptor Activation.Frontiers in immunology · 2019Article
- ATP as a Pathophysiologic Mediator of Bacteria-Host Crosstalk in the Gastrointestinal Tract.International journal of molecular sciences · 2018Review
- Article
- Blockade of Pannexin-1 Channels and Purinergic P2X7 Receptors Shows Protective Effects Against Cytokines-Induced Colitis of Human Colonic Mucosa.Frontiers in pharmacology · 2018Article
- Tissue-resident memory features are linked to the magnitude of cytotoxic T cell responses in human lung cancer.Nature immunology · 2017Article
- Purinergic Signaling in Gut Inflammation: The Role of Connexins and Pannexins.Frontiers in neuroscience · 2016Review
- Inflammasomes in pancreatic physiology and disease.American journal of physiology. Gastrointestinal and liver physiology · 2015Review
- P2X7 on Mouse T Cells: One Channel, Many Functions.Frontiers in immunology · 2015Review
- ATP-Induced IL-1β Specific Secretion: True Under Stringent Conditions.Frontiers in immunology · 2015Article
- E-NTPDase1/CD39 modulates renin release from heart mast cells during ischemia/reperfusion: a novel cardioprotective role.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2015Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMast cells (MCs) are major contributors to an inflammatory milieu. One of the most potent drivers of inflammation is the cytokine IL-1β, which is produced in the cytoplasm in response to danger signals like LPS. Several controlling mechanisms have been reported which limit the release of IL-1β. Central to this regulation is the NLRP3 inflammasome, activation of which requires a second danger signal with the capacity to subvert the homeostasis of lysosomes and mitochondria. High concentrations of extracellular ATP have the capability to perturb the plasma membrane by activation of P2X7 channels and serve as such a danger signal. In this study we investigate the role of P2X7 channels and the ecto-5'-nucleotidase CD39 in ATP-triggered release of IL-1β from LPS-treated mast cells.
resultsWe report that in MCs CD39 sets an activation threshold for the P2X7-dependent inflammatory cell death and concomitant IL-1β release. Knock-out of CD39 or stimulation with non-hydrolysable ATP led to a lower activation threshold for P2X7-dependent responses. We found that stimulation of LPS-primed MCs with high doses of ATP readily induced inflammatory cell death. Yet, cell death-dependent release of IL-1β yielded only minute amounts of IL-1β. Intriguingly, stimulation with low ATP concentrations augmented the production of IL-1β in LPS-primed MCs in a P2X7-independent but caspase-1-dependent manner.
conclusionOur study demonstrates that the fine-tuned interplay between ATP and different surface molecules recognizing or modifying ATP can control inflammatory and cell death decisions.
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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.