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dc.contributor.authorAmores Iniesta, Joaquín-
dc.contributor.authorBarberá Cremades, María-
dc.contributor.authorMartínez Cáceres, Carlos Manuel-
dc.contributor.authorParrilla, Pascual-
dc.contributor.authorBaroja Mazo, Alberto-
dc.contributor.authorPelegrín, Pablo-
dc.date.accessioned2025-01-20T09:46:56Z-
dc.date.available2025-01-20T09:46:56Z-
dc.date.issued2017-12-19-
dc.identifier.citationCell Reports, 2017, Vol. 21, Issue 12, pp. 3414-3426es
dc.identifier.issnPrint: 2639-1856-
dc.identifier.issnElectronic: 2211-1247-
dc.identifier.urihttp://hdl.handle.net/10201/148806-
dc.description© 2017 The Author(s). 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 Published version of a Published Work that appeared in final form in Cell Reports. To access the final edited and published work see https://doi.org/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-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.es
dc.formatapplication/pdfes
dc.format.extent14es
dc.languageenges
dc.publisherElsevieres
dc.relationJ.A.-I. is supported by a Sara Borrell postdoctoral grant from the Instituto Salud Carlos III (CD13/00059). F.D.V. is supported by the Italian Association for Cancer Research (IG 5354), Telethon (GGP06070), the ERA-NET Neuron Joint Transnational Project “Nanostroke,” the Italian Ministry of Health (RF-2011-02348435), the Italian Ministry of Education, University, and Research (RBAP11FXBC_001), and institutional funds from the University of Ferrara. P. Pelegrín and F.D.V. would like to acknowledge networking support from COST Action BM-1406. Primary funding for this study was provided by the Instituto Salud Carlos III–Fondo Europeo de Desarrollo Regional (EMER07/049, PS09/00120, and PI13/00174 to P. Pelegrín and PI12/02042 to J.A.P.), Sysmex (to P. Pelegrín), and the European Research Council (ERC-2013-CoG 614578 to P. Pelegrín).es
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.subjectAllotransplantationes
dc.subjectCaspase 1es
dc.subjectIL 18es
dc.subjectMacrophageses
dc.subjectNLRP3 inflammasomees
dc.subjectP2X7es
dc.subjectReceptores
dc.subjectSkin transplantes
dc.subjectPurinergic signalinges
dc.subjectATP releasees
dc.subjectDanger signalses
dc.titleExtracellular ATP activates the NLRP3 inflammasome and is an early danger signal of skin allograft rejectiones
dc.typeinfo:eu-repo/semantics/articlees
dc.relation.publisherversionhttps://www.sciencedirect.com/science/article/pii/S2211124717317461?via%3Dihubes
dc.identifier.doihttps://doi.org/10.1016/j.celrep.2017.11.079-
dc.contributor.departmentDepartamento de Anatomía y Anatomía Patológica Comparada-
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