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Extracellular ATP activates the NLRP3 inflammasome and is an early danger signal of skin allograft rejection

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dc.contributor.authorAmores-Iniesta, Joaquín
dc.contributor.authorBarberá-Cremades, Maria
dc.contributor.authorPons, José A.
dc.contributor.authorRevilla-Nuín, Beatriz
dc.contributor.authorMartínez-Alarcón, Laura
dc.contributor.authorDi Virgilio, Francesco
dc.contributor.authorParrilla, Pascual
dc.contributor.authorBaroja-Mazo, Alberto
dc.contributor.authorMartínez Cáceres, Carlos Manuel
dc.contributor.authorPelegrín Vivancos, Pablo
dc.contributor.departmentBioquímica y Biología Molecular B e Inmunología
dc.date.accessioned2024-01-28T09:31:07Z
dc.date.available2024-01-28T09:31:07Z
dc.date.issued2017
dc.description©2017. This manuscript version is made available under the CC-BY-NC-ND 4.0 license http://creativecommons.org/licenses/by-nc-nd/4.0/ This document is the Accepted, version of a Published Work that appeared in final form in Cell Report. To access the final edited and published work see 10.1016/j.celrep.2017.11.079es
dc.description.abstractImmune 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-g production. Lack of IL-18 resulted in a decrease in graft- infiltrated CD8 cells, but an increase in regulatory T cells. In human liver transplant patients subjected to progressive immunosuppressive drug withdrawal, we found that patients suffering 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.es
dc.formatapplication/pdfes
dc.format.extent30es
dc.identifier.citationCell Report, volumen 21, volumen 12, año 2017, páginas 3414-3426.
dc.identifier.doi10.1016/j.celrep.2017.11.079
dc.identifier.issn2211-1247
dc.identifier.urihttp://hdl.handle.net/10201/137870
dc.languageenges
dc.publisherCell Presses
dc.relationInstituto Salud Carlos III (CD13/00059), Italian Association for Cancer Research (IG 5354), Telethon (GGP06070), ERA-NET Neuron Joint Transnational Project “Nanostroke”, Italian Ministry of Health (RF-2011-02348435), Italian Ministry of Education, University and Research (RBAP11FXBC_001), COST Action BM-1406, Instituto Salud Carlos III–Fondo Europeo de Desarrollo Regional (EMER07/049, PS09/00120, PI13/00174, PI12/02042), European Research Council (ERC-2013-CoG 614578).es
dc.relation.publisherversionhttps://www.cell.com/cell-reports/fulltext/S2211-1247(17)31746-1?_returnURL=https%3A%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2FS2211124717317461%3Fshowall%3Dtruees
dc.rightsinfo:eu-repo/semantics/openAccesses
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 Internacional*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.subjectMacrófagoses
dc.subjectCitocinases
dc.subjectInflamaciónes
dc.subjectATPes
dc.subjectTrasplantees
dc.subject.otherCDU::6 - Ciencias aplicadases
dc.titleExtracellular ATP activates the NLRP3 inflammasome and is an early danger signal of skin allograft rejectiones
dc.title.alternativeATP release in allotransplantationes
dc.typeinfo:eu-repo/semantics/articlees
dspace.entity.typePublicationes
relation.isAuthorOfPublicationa11bfbe4-fe50-4173-a96d-aa785375a6be
relation.isAuthorOfPublication547c4c2c-d906-4e1d-ae9a-0cdb40eef6d1
relation.isAuthorOfPublication.latestForDiscoverya11bfbe4-fe50-4173-a96d-aa785375a6be
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