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dc.contributor.authorSchmidt-Weber, C.B.-
dc.contributor.authorLetarte, Michelle-
dc.contributor.authorKunzmann, D.-
dc.contributor.authorRuckert, B.-
dc.contributor.authorBernabéu, Carmelo-
dc.contributor.authorBlaser, K.-
dc.date.accessioned2012-05-21T07:08:31Z-
dc.date.available2012-05-21T07:08:31Z-
dc.date.issued2005-07-01-
dc.identifier.citationInternational Immunology 17 921-930 (2005)es_ES
dc.identifier.issn0953-8178-
dc.identifier.urihttp://hdl.handle.net/10261/49868-
dc.description10 páginas, 6 figuras -- PAGS nros. 921-930es_ES
dc.description.abstractTransforming growth factor beta (TGF-β) inhibits T cell activation and alters differentiation of naive T cells into effector cells. Although four main cell-surface proteins can interact with TGF-β, only the signaling receptors type I (TGF-βR type I) and type II (TGF-βR type II) have so far been described on T cells. The aim of the present study was to investigate the expression of the ancillary receptor endoglin (CD105) by T cells and its role in TGF-β-mediated signal transduction and function. CD105 expression was analyzed on resting and activated human CD4+ T cells by flow cytometry, western blot, immunoprecipitation, proliferation and SMAD-responsive reporter gene assays. CD4+ T cells constitutively expressed CD105 in memory T cells and partially also in naive T cells; however, surface expression is regulated and is increased following TCR engagement, which induced serine/threonine phosphorylation of CD105. In contrast to the suppressive signal mediated by the TGF-β, cross-linking of CD105 substantially enhanced T cell proliferation, indicating that CD105 by itself mediates signal transduction. Furthermore, CD105 cross-linking induced SMAD-independent signaling via ERK kinase phosphorylation. The present study demonstrates that CD105 is expressed on the surface by activated CD4+ T cells and CD3 regulated by post-translational means. Furthermore, CD105 acts as a regulatory receptor, counteracting TGF-β-mediated suppressiones_ES
dc.description.sponsorshipThis work was supported by the Swiss National Foundation Grant no. 31.52986.97, no. 31-65436.01 and no. 3100A0-100164; the Roche Research Foundation (Mkl/stm 115-2001); Saurer Foundation, Zurich; EMDO Foundation, Zurich; OPO Foundation, Zurich and the Canadian Institute of Health Research (M.L.). S.K. was fellow of the Deutsche Forschungsgemeinschaft (KU 1403/1-1)es_ES
dc.language.isoenges_ES
dc.publisherOxford University Presses_ES
dc.rightsclosedAccesses_ES
dc.subjectcytokine receptores_ES
dc.subjectTlymphocyteses_ES
dc.subjecttolerance/suppression/anergyes_ES
dc.titleTGF-beta signaling of human T cells is modulated by the ancillary TGF-beta receptor endoglines_ES
dc.typeArtículoes_ES
dc.identifier.doi10.1093/intimm/dxh272-
dc.description.peerreviewedPeer reviewedes_ES
dc.relation.publisherversionhttp://dx.doi.org/ 0.1093/intimm/dxh272es_ES
dc.identifier.e-issn1460-2377-
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