Identificador persistente para citar o vincular este elemento: http://hdl.handle.net/10553/50004
Campo DC Valoridioma
dc.contributor.authorRincón, Mercedesen_US
dc.contributor.authorTugores, Antonioen_US
dc.contributor.authorLópez‐Rivas, Abelardoen_US
dc.contributor.authorSilva, Augustoen_US
dc.contributor.authorAlonso, Miguelen_US
dc.contributor.authorDe Landázuri, Manuel O.en_US
dc.contributor.authorLópez‐Botet, Miguelen_US
dc.date.accessioned2018-11-24T12:29:06Z-
dc.date.available2018-11-24T12:29:06Z-
dc.date.issued1988en_US
dc.identifier.issn0014-2980en_US
dc.identifier.urihttp://hdl.handle.net/10553/50004-
dc.description.abstractWe have analyzed the effect mediated by prostaglandin E2 (PGE2) and different reagents that increase intracellular cAMP on the expression of the p55 subunit (CD25) of interleukin 2 receptors (IL2R), on the levels of CD25-specific mRNA and on the expression of high affinity IL 2R. In purified T cells, activated either by an anti-CD3 monoclonal antibody or phytohemagglutinin, the addition of PGE2 (10−6 M), forskolin (5 × 10−5 M), cholera toxin (0.2 μg/ml) or dibutyryl cAMP (dBcAMP) (10−4 M) decreased the cell surface expression of IL 2R by reducing (40%-78% inhibition) the proportions of CD25+ cells as well as the expression of high affinity IL2R, detectable after 24 h. Furthermore, it was observed that PGE2 reduced the concentration of IL2R-specific mRNA after a 6-h period of activation, indicating that its regulatory activity takes place at a pretranslational level. The addition of exogenous recombinant IL2 only partially reversed the inhibition, thus suggesting that PGE2 and increased intracellular concentration of cAMP directly interfered with CD25 expression and that their effect could not be merely attributed to a lack of IL2 dependent positive feedback. Cells cultured under the same conditions in the presence of phorbol myristate acetate, that activates protein kinase C, were refractory to the CAMP-mediated regulation. Finally, we demonstrate that both PGE2 and dBcAMP inhibit the generation of inositol metabolites after T cell activation, thus indicating that these reagents interfere with early signal transduction mechanisms which precede the synthesis of IL2R.en_US
dc.languageengen_US
dc.relation.ispartofEuropean Journal of Immunologyen_US
dc.sourceEuropean Journal of Immunology[ISSN 0014-2980],v. 18(11), p. 1791-1796 (Noviembre 1988)en_US
dc.subject32 Ciencias médicasen_US
dc.subject3205 Medicina internaen_US
dc.subject.otherProstaglandinen_US
dc.subject.othercAMPen_US
dc.subject.otherInterleukinen_US
dc.subject.otherHuman T cellsen_US
dc.titleProstaglandin E2 and the increase of intracellular cAMP inhibit the expression of interleukin 2 receptors in human T cellsen_US
dc.typeinfo:eu-repo/semantics/articleen_US
dc.typeArticleen_US
dc.identifier.doi10.1002/eji.1830181121en_US
dc.identifier.scopus0024165481-
dc.contributor.authorscopusid7005951573-
dc.contributor.authorscopusid6701671839-
dc.contributor.authorscopusid7006074182-
dc.contributor.authorscopusid7403221693-
dc.contributor.authorscopusid7401661849-
dc.contributor.authorscopusid7006816026-
dc.contributor.authorscopusid7004993664-
dc.description.lastpage1796en_US
dc.description.firstpage1791en_US
dc.relation.volume18en_US
dc.investigacionCiencias de la Saluden_US
dc.type2Artículoen_US
dc.description.numberofpages6en_US
dc.utils.revisionen_US
dc.date.coverdateNoviembre 1988en_US
dc.identifier.ulpgcen_US
dc.contributor.buulpgcBU-MEDen_US
dc.description.scieSCIE-
item.fulltextSin texto completo-
item.grantfulltextnone-
crisitem.author.deptGIR IUIBS: Diabetes y endocrinología aplicada-
crisitem.author.deptIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.orcid0000-0002-1849-9239-
crisitem.author.parentorgIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.fullNameTugores Céster,Antonio-
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