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Por favor, use este identificador para citar o enlazar a este item: http://hdl.handle.net/10261/49870
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dc.contributor.authorIglesias, Marcos-
dc.contributor.authorGenre, Fernanda-
dc.contributor.authorMerino, Jesús-
dc.contributor.authorMerino, Ramón-
dc.date.accessioned2012-05-21T07:23:45Z-
dc.date.available2012-05-21T07:23:45Z-
dc.date.issued2010-
dc.identifierdoi: 10.1016/j.jaut.2010.07.002-
dc.identifierissn: 0896-8411-
dc.identifier.citationJournal of Autoimmunity 35(4): 316-324 (2010)-
dc.identifier.urihttp://hdl.handle.net/10261/49870-
dc.descriptionEl pdf del artículo es la versión pre-print.-- et al.-
dc.description.abstractGenetic abnormalities predisposing to autoimmunity generally act in a cooperative manner affecting one or several mechanisms regulating immunological tolerance. In addition, many of these genetic abnormalities are also involved in the development of lymphoproliferative diseases. In the present study, we have determined the possible cooperation between deficiencies in members of the Cip/Kip family of cell cycle regulators (p21WAF1/Cip1 or p27kip1) and the overexpression of human Bcl-2 in B lymphocytes in the induction of autoimmune and lymphoproliferative diseases in non-autoimmune C57BL/6 (B6) mice. Unlike single mutant mice, B6.p21-/- mice transgenic for human Bcl-2 in B cells developed a lethal autoimmune syndrome characterized by the production of autoantibodies, the prominent expansion of memory B and CD4+ T cells and the development of severe glomerular lesions resembling IgA nephropathy. Furthermore, these mice presented a high incidence of B-cell lymphoproliferative disorders. Such genetic cooperation in the induction of autoimmunity was not observed in B6.p27-/- mice transgenic for human Bcl-2 in B cells. Altogether, what we have demonstrated here is the existence of preferential interactions among particular regulators of the G1/S transition of the cell cycle and B-cell survival in the induction of systemic autoimmune and lymphoproliferative diseases. © 2010 Elsevier Ltd.-
dc.description.sponsorshipThis work was supported by grants from the Ministerio de Educación y Ciencia, Spain to RM (SAF2008-02042) and JM (BFU2009-07206), by grants REDINREN RD06/0016 from the Instituto de Salud Carlos III and from Fundación Eugenio Rodríguez Pascual, Spain to RM, from the Fundación Marqués de Valdecilla, Spain to JM (API-07/02), by a grant from the Swiss National Foundation for Scientific Research to SI. FG is supported by a pre-doctoral fellowship from the Instituto Danone, Spain.-
dc.language.isoeng-
dc.publisherElsevier-
dc.rightsopenAccess-
dc.titleB-cell overexpression of Bcl-2 cooperates with p21 deficiency for the induction of autoimmunity and lymphomas-
dc.typeartículo-
dc.identifier.doi10.1016/j.jaut.2010.07.002-
dc.relation.publisherversionhttp://dx.doi.org/10.1016/j.jaut.2010.07.002-
dc.date.updated2012-05-21T07:23:45Z-
dc.description.versionPeer Reviewed-
dc.type.coarhttp://purl.org/coar/resource_type/c_6501es_ES
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.fulltextWith Fulltext-
item.cerifentitytypePublications-
item.openairetypeartículo-
item.languageiso639-1en-
item.grantfulltextopen-
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