Evidence map›Paper›PMID 29262323›Full record

ArticleCell reports2017

Extracellular ATP Activates the NLRP3 Inflammasome and Is an Early Danger Signal of Skin Allograft Rejection.

Joaquín Amores-Iniesta, Maria Barberà-Cremades, Carlos M Martínez, José A Pons, Beatriz Revilla-Nuin, Laura Martínez-Alarcón, Francesco Di Virgilio, Pascual Parrilla, Alberto Baroja-Mazo, Pablo Pelegrín

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 108 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
108citing papers in PubMed, 1 pooled it
10.5field-weighted citation impact, top 1% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

108 citing papers in PubMed, 1 synthesis or guideline pooled it, 175 citations in OpenAlex.

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  9. RIPK1 ubiquitination regulates its kinase-independent function in development and inflammation.Proceedings of the National Academy of Sciences of the United States of America · 2026
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48 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 2 institutions in 2 countries.

Joaquín Amores-IniestaExperimental Surgery Group, Biomedical Research Institute of Murcia (IMIB-Arrixaca), University Clinical Hospital Virgen de la Arrixaca, 30120 Murcia, Spain.
Maria Barberà-CremadesExperimental Surgery Group, Biomedical Research Institute of Murcia (IMIB-Arrixaca), University Clinical Hospital Virgen de la Arrixaca, 30120 Murcia, Spain.
Carlos M MartínezExperimental Pathology Unit, Biomedical Research Institute of Murcia (IMIB-Arrixaca), University Clinical Hospital Virgen de la Arrixaca, 30120 Murcia, Spain.
José A PonsExperimental Surgery Group, Biomedical Research Institute of Murcia (IMIB-Arrixaca), University Clinical Hospital Virgen de la Arrixaca, 30120 Murcia, Spain.
Beatriz Revilla-NuinGenomic Unit, Biomedical Research Institute of Murcia (IMIB-Arrixaca), University Clinical Hospital Virgen de la Arrixaca, 30120 Murcia, Spain.
Laura Martínez-AlarcónExperimental Surgery Group, Biomedical Research Institute of Murcia (IMIB-Arrixaca), University Clinical Hospital Virgen de la Arrixaca, 30120 Murcia, Spain.
Francesco Di VirgilioDepartment of Morphology, Surgery and Experimental Medicine, University of Ferrara, 44121 Ferrara, Italy.
Pascual ParrillaExperimental Surgery Group, Biomedical Research Institute of Murcia (IMIB-Arrixaca), University Clinical Hospital Virgen de la Arrixaca, 30120 Murcia, Spain.
Alberto Baroja-MazoExperimental Surgery Group, Biomedical Research Institute of Murcia (IMIB-Arrixaca), University Clinical Hospital Virgen de la Arrixaca, 30120 Murcia, Spain.
Pablo PelegrínExperimental Surgery Group, Biomedical Research Institute of Murcia (IMIB-Arrixaca), University Clinical Hospital Virgen de la Arrixaca, 30120 Murcia, Spain. Electronic address: pablo.pelegrin@imib.es.
Instituto Murciano de Investigación Biosanitaria · ESUniversity of Ferrara · IT

Funding

European Research Council 614578Telethon GGP06070
6 · The paper itself

Abstract

Immune cells are equipped with a number of receptors that recognize sterile injury and pathogens. We find that host immune cells release ATP as an inflammatory signal in response to allogeneic transplantation. ATP then acts via a feedback mechanism on the P2X7 channel to activate the NLRP3 inflammasome and subsequently process and release interleukin (IL)-18. This process is a necessary stage in the deleterious Th1 response against allotransplantation via interferon-γ production. Lack of IL-18 resulted in a decrease in graft-infiltrating CD8 cells but an increase in regulatory T cells. In human liver transplant patients undergoing progressive immunosuppressive drug withdrawal, we found that patients experiencing acute rejection had higher levels of the P2X7 receptor in circulating inflammatory monocytes compared to tolerant patients. These data suggest that the pharmacological inhibition of the P2X7 receptor or the NLRP3 inflammasome will aid in inducing transplant tolerance without complete immunoparalysis.

Indexed as

Signal TransductionAdenosine TriphosphateAnimalsCD8-Positive T-LymphocytesFeedback, PhysiologicalGraft RejectionHumansInflammasomesInterferon-gammaInterleukin-18MaleMiceMice, Inbred C57BLNLR Family, Pyrin Domain-Containing 3 ProteinReceptors, Purinergic P2X7SkinAdenosine TriphosphateInflammasomesInterferon-gammaInterleukin-18NLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mouseReceptors, Purinergic P2X7allotransplantationATP releasecaspase-1danger signalIL-18macrophagesNLRP3 inflammasomeP2X7 receptorpurinergic signalingskin transplant

Identifiers

PMID29262323
PMCPMC5746605
OpenAlexW2776988169

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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.