Aldosterone Promotes Autoimmune Damage by Enhancing Th17-Mediated Immunity

dc.contributor.authorHerrada, Andres A.
dc.contributor.authorContreras, Francisco J.
dc.contributor.authorMarini, Natacha P.
dc.contributor.authorAmador, Cristian A.
dc.contributor.authorGonzalez, Pablo A.
dc.contributor.authorCortes, Claudia M.
dc.contributor.authorRiedel, Claudia A.
dc.contributor.authorCarvajal, Cristian A.
dc.contributor.authorFigueroa, Fernando
dc.contributor.authorMichea, Luis F.
dc.contributor.authorFardella, Carlos E.
dc.contributor.authorKalergis, Alexis M.
dc.date.accessioned2024-01-10T13:45:42Z
dc.date.available2024-01-10T13:45:42Z
dc.date.issued2010
dc.description.abstractExcessive production of aldosterone leads to the development of hypertension and cardiovascular disease by generating an inflammatory state that can be promoted by T cell immunity. Because nature and intensity of T cell responses is controlled by dendritic cells (DCs), it is important to evaluate whether the function of these cells can be modulated by aldosterone. In this study we show that aldosterone augmented the activation of CD8(+) T cells in a DC-dependent fashion. Consistently, the mineralocorticoid receptor was expressed by DCs, which showed activation of MAPK pathway and secreted IL-6 and TGF-beta in response to aldosterone. In addition, DCs stimulated with aldosterone impose a Th17 phenotype to CD4(+) T cells, which have recently been associated with the promotion of inflammatory and autoimmune diseases. Accordingly, we observed that aldosterone enhances the progression of experimental autoimmune encephalomyelitis, an autoimmune disease promoted by Th17 cells. In addition, blockade of the mineralocorticoid receptor prevented all aldosterone effects on DCs and attenuated experimental autoimmune encephalomyelitis development in aldosterone-treated mice. Our data suggest that modulation of DC function by aldosterone enhances CD8(+) T cell activation and promotes Th17-polarized immune responses, which might contribute to the inflammatory damage leading to hypertension and cardiovascular disease. The Journal of Immunology, 2010, 184: 191-202.
dc.description.funderFondo Nacional de Desarrollo Cientifico y Tecnologico
dc.description.funderFondo de Fomento al Desarrollo Cientifico y Tecnologico
dc.description.funderMillennium Nucleus on Immunology and Immunotherapy
dc.fechaingreso.objetodigital2024-05-30
dc.format.extent12 páginas
dc.fuente.origenWOS
dc.identifier.doi10.4049/jimmunol.0802886
dc.identifier.eissn1550-6606
dc.identifier.issn0022-1767
dc.identifier.pubmedidMEDLINE:19949098
dc.identifier.urihttps://doi.org/10.4049/jimmunol.0802886
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/79069
dc.identifier.wosidWOS:000272985300024
dc.information.autorucMedicina;Carvajal CA;S/I;8586
dc.information.autorucCiencias Biológicas;Contreras FJ;S/I;95101
dc.information.autorucMedicina;Fardella CE;S/I;66235
dc.information.autorucCiencias Biológicas;González PA;S/I;15616
dc.information.autorucCiencias Biológicas;Herrada AA;S/I;174374
dc.information.autorucCiencias Biológicas;Kalergis AM;S/I;90610
dc.information.autorucCiencias Biológicas;Marini NP;S/I;149695
dc.information.autorucCiencias Biológicas;Riedel CA;S/I;88772
dc.issue.numero1
dc.language.isoen
dc.nota.accesoContenido parcial
dc.pagina.final202
dc.pagina.inicio191
dc.publisherAMER ASSOC IMMUNOLOGISTS
dc.revistaJOURNAL OF IMMUNOLOGY
dc.rightsacceso restringido
dc.subjectT-CELL-ACTIVATION
dc.subjectFC-GAMMA RECEPTORS
dc.subjectDENDRITIC CELLS
dc.subjectMINERALOCORTICOID RECEPTOR
dc.subjectANTIGEN PRESENTATION
dc.subjectHYPERTENSIVE-RATS
dc.subjectOXIDATIVE STRESS
dc.subjectANGIOTENSIN-II
dc.subjectTH17 CELLS
dc.subjectENCEPHALOMYELITIS
dc.subject.ods03 Good Health and Well-being
dc.subject.odspa03 Salud y bienestar
dc.titleAldosterone Promotes Autoimmune Damage by Enhancing Th17-Mediated Immunity
dc.typeartículo
dc.volumen184
sipa.codpersvinculados8586
sipa.codpersvinculados95101
sipa.codpersvinculados66235
sipa.codpersvinculados15616
sipa.codpersvinculados174374
sipa.codpersvinculados90610
sipa.codpersvinculados149695
sipa.codpersvinculados88772
sipa.indexWOS
sipa.indexScopus
sipa.trazabilidadCarga SIPA;09-01-2024
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