Modulation of nuclear factor-kappa B activity can influence the susceptibility to systemic lupus erythematosus

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dc.contributor.authorKalergis, Alexis M.
dc.contributor.authorIruretagoyena, Mirentxu I.
dc.contributor.authorBarrientos, Magaly J.
dc.contributor.authorGonzalez, Pablo A.
dc.contributor.authorHerrada, Andres A.
dc.contributor.authorLeiva, Eduardo D.
dc.contributor.authorGutierrez, Miguel A.
dc.contributor.authorRiedel, Claudia A.
dc.contributor.authorBueno, Susan M.
dc.contributor.authorJacobelli, Sergio H.
dc.date.accessioned2024-01-10T12:06:44Z
dc.date.available2024-01-10T12:06:44Z
dc.date.issued2009
dc.description.abstractP>Autoimmune diseases, such as systemic lupus erythematosus (SLE), result from deficiencies in self-antigen tolerance processes, which require regulated dendritic cell (DC) function. In this study we evaluated the phenotype of DCs during the onset of SLE in a mouse model, in which deletion of the inhibitory receptor Fc gamma RIIb leads to the production of anti-nuclear antibodies and glomerulonephritis. Splenic DCs from Fc gamma RIIb-deficient mice suffering from SLE showed increased expression of co-stimulatory molecules. Furthermore, diseased mice showed an altered function of the nuclear factor-kappa B (NF-kappa B) transcription factor, which is involved in DC maturation. Compared with healthy animals, expression of the inhibitory molecule I kappa B-alpha was significantly decreased in mice suffering from SLE. Consistently, pharmacological inhibition of NF-kappa B activity in Fc gamma RIIb-deficient mice led to reduced susceptibility to SLE and prevented symptoms, such as anti-nuclear antibodies and kidney damage. Our data suggest that the occurrence of SLE is significantly influenced by alterations of NF-kappa B function, which can be considered as a new therapeutic target for this disease.
dc.description.funderFONDECYT
dc.description.funderProyecto
dc.description.funderFONDEF
dc.description.funderMillennium Nucleus on Immunology and Immunotherapy
dc.description.funderVRAID
dc.description.funderCONICYT
dc.fechaingreso.objetodigital2024-05-07
dc.format.extent9 páginas
dc.fuente.origenWOS
dc.identifier.doi10.1111/j.1365-2567.2008.02964.x
dc.identifier.issn0019-2805
dc.identifier.pubmedidMEDLINE:19016912
dc.identifier.urihttps://doi.org/10.1111/j.1365-2567.2008.02964.x
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/76201
dc.identifier.wosidWOS:000268703800015
dc.information.autorucCiencias Biológicas;Bueno SM;S/I;113541
dc.information.autorucCiencias Biológicas;González PA;S/I;15616
dc.information.autorucMedicina;Gutiérrez MA;S/I;68377
dc.information.autorucCiencias Biológicas;Herrada AA;S/I;174374
dc.information.autorucMedicina;Iacobelli SH;S/I;98345
dc.information.autorucMedicina;Iruretagoyena MI;S/I;144496
dc.information.autorucCiencias Biológicas;Kalergis AM;S/I;90610
dc.information.autorucCiencias Biológicas;Leiva ED;S/I;142382
dc.issue.numero1
dc.language.isoen
dc.nota.accesocontenido parcial
dc.publisherWILEY-BLACKWELL PUBLISHING, INC
dc.revistaIMMUNOLOGY
dc.rightsacceso restringido
dc.subjectandrographolide
dc.subjectautoimmunity
dc.subjectdendritic cells
dc.subjectnuclear factor-kappa B
dc.subjectrosiglitazone
dc.subjectsystemic lupus erythematosus
dc.subjectEXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS
dc.subjectPLASMACYTOID DENDRITIC CELLS
dc.subjectT-CELLS
dc.subjectANDROGRAPHIS-PANICULATA
dc.subjectANTIGEN PRESENTATION
dc.subjectGAMMA
dc.subjectACTIVATION
dc.subjectINHIBITION
dc.subjectDISEASE
dc.subjectALPHA
dc.subject.ods03 Good Health and Well-being
dc.subject.odspa03 Salud y bienestar
dc.titleModulation of nuclear factor-kappa B activity can influence the susceptibility to systemic lupus erythematosus
dc.typeartículo
dc.volumen128
sipa.codpersvinculados113541
sipa.codpersvinculados15616
sipa.codpersvinculados68377
sipa.codpersvinculados174374
sipa.codpersvinculados98345
sipa.codpersvinculados144496
sipa.codpersvinculados90610
sipa.codpersvinculados142382
sipa.indexWOS
sipa.indexScopus
sipa.trazabilidadCarga SIPA;09-01-2024
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