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Maintenance of immune tolerance by Foxp3+ regulatory T cells requires CD69 expression
dc.contributor.author | Cortés, José R. | |
dc.contributor.author | Sánchez-Díaz, Raquel | |
dc.contributor.author | Bovolenta, Elena R. | |
dc.contributor.author | Barreiro, Olga | |
dc.contributor.author | Lasarte, Sandra | |
dc.contributor.author | Matesanz-Marín, Adela | |
dc.contributor.author | Toribio, María L. | |
dc.contributor.author | Sánchez Madrid, Francisco | |
dc.contributor.author | Martín, Pilar | |
dc.contributor.other | UAM. Departamento de Medicina | es_ES |
dc.date.accessioned | 2015-05-27T10:18:03Z | |
dc.date.available | 2015-05-27T10:18:03Z | |
dc.date.issued | 2015-01-01 | |
dc.identifier.citation | Journal of Autoimmunity 55 (2014): 51-62 | en_US |
dc.identifier.issn | 0896-8411 (print) | en_US |
dc.identifier.issn | 1095-9157 (online) | en_US |
dc.identifier.uri | http://hdl.handle.net/10486/666421 | |
dc.description.abstract | Although FoxP3+ regulatory T cells are key players in the maintenance of immune tolerance and autoimmunity, the lack of specific markers constitute an obstacle to their use for immunotherapy protocols. In this study, we have investigated the role of the C-type lectin receptor CD69 in the suppressor function of Tregs and maintenance of immune tolerance towards harmless inhaled antigens. We identified a novel FoxP3+CD69+ Treg subset capable to maintain immune tolerance and protect to developing inflammation. Although CD69+ and CD69−FoxP3+ Tregs exist in homeostasis, only CD69-expressing Tregs express high levels of CTLA-4, ICOS, CD38 and GITR suppression-associated markers, secrete high amounts of TGFβ and have potent suppressor activity. This activity is regulated by STAT5 and ERK signaling pathways and is impaired by antibody-mediated down-regulation of CD69 expression. Moreover, immunotherapy with FoxP3+CD69+ Tregs restores the homeostasis in Cd69−/− mice, that fail to induce tolerance, and is also highly proficient in the prevention of inflammation. The identification of the FoxP3+CD69+ Treg subset paves the way toward the development of new therapeutic strategies to control immune homeostasis and autoimmunity | es_ES |
dc.description.sponsorship | This work was supported by funding from the Spanish Ministry of Economy and Competitiveness: SAF2011-27330 to P.M., SAF2010-15106 to M.L.T and SAF2011-25834 to F.S-M.; grant INDISNET (S2010/BMD-2332) from Comunidad de Madrid and RETICS Enfermedades Cardiovasculares (RD12/0042/0056) from Instituto de Salud Carlos III to P.M and F. S-M; and ERC-2011-AdG294340-GENTRIS to F.S-M. J.R.C. was supported by a CNIC post-doctoral fellowship, R. S-D is funded with a pre-doctoral fellowship from Comunidad de Madrid and E.R.B. and A.M-M. were supported by a FPI pre-doctoral fellowship from the Spanish Ministry of Economy and Competitiveness. The CNIC is supported by the Spanish Ministry of Economy and Competitiveness and the Pro CNIC Foundation | en_US |
dc.format.extent | 28 pag. | en |
dc.format.mimetype | application/pdf | en |
dc.language.iso | eng | en |
dc.publisher | Elsevier | en_US |
dc.relation.ispartof | Journal of Autoimmunity | en_US |
dc.rights | © 2014, Elsevier | en_US |
dc.subject.other | CD69 | es_ES |
dc.subject.other | FoxP3 | es_ES |
dc.subject.other | Immune tolerance | en_US |
dc.subject.other | Regulatory T cells | en_US |
dc.title | Maintenance of immune tolerance by Foxp3+ regulatory T cells requires CD69 expression | en_US |
dc.type | article | en |
dc.subject.eciencia | Medicina | es_ES |
dc.date.embargoend | 2015-12-01 | |
dc.identifier.publicationfirstpage | 51 | es_ES |
dc.identifier.publicationissue | 1 | es_ES |
dc.identifier.publicationlastpage | 62 | es_ES |
dc.identifier.publicationvolume | 55 | es_ES |
dc.relation.projectID | Comunidad de Madrid. S2010/BMD-2332/INDISNET | es_ES |
dc.type.version | info:eu-repo/semantics/acceptedVersion | en |
dc.rights.cc | Reconocimiento – NoComercial – SinObraDerivada | es_Es |
dc.rights.accessRights | openAccess | en |
dc.authorUAM | Sánchez Madrid, Francisco (259404) | |
dc.facultadUAM | Facultad de Medicina |