Gilz-Activin A as a Novel Signaling Axis Orchestrating Mesenchymal Stem Cell and Th17 Cell Interplay

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dc.contributor.authorLuz-Crawford, Patricia
dc.contributor.authorEspinosa-Carrasco, Gabriel
dc.contributor.authorIpseiz, Natacha
dc.contributor.authorContreras, Rafael
dc.contributor.authorTejedor, Gautier
dc.contributor.authorMedina, Daniel A.
dc.contributor.authorVega-Letter, Ana-Maria
dc.contributor.authorNgo, Devi
dc.contributor.authorMorand, Eric F.
dc.contributor.authorPene, Jerome
dc.contributor.authorHernandez, Javier
dc.contributor.authorJorgensen, Christian
dc.contributor.authorDjouad, Farida
dc.date.accessioned2025-01-23T21:22:37Z
dc.date.available2025-01-23T21:22:37Z
dc.date.issued2018
dc.description.abstractMesenchymal stem cells (MSC) are highly immunosuppressive cells able to reduce chronic inflammation through the active release of mediators. Recently, we showed that glucocorticoid-induced leucine zipper (Gilz) expression by MSC is involved in their therapeutic effect by promoting the generation of regulatory T cells. However, the mechanisms underlying this pivotal role of Gilz remain elusive.
dc.description.abstractMethods and Results In this study, we have uncovered evidence that Gilz modulates the phenotype and function of Th1 and Th17 cells likely by upregulating the level of Activin A and NO2 secreted by MSC. Adoptive transfer experiments sustained this Gilz-dependent suppressive effect of MSC on Th1 and Th17 cell functions. In immunoregulatory MSC, obtained by priming with IFN-gamma and TNF-alpha, Gilz was translocated to the nucleus and bound to the promoters of inos and Activin beta A to induce their expression. The increased expression of Activin A directly impacted on Th17 cells fate by repressing their differentiation program through the activation of Smad3/2 and enhancing IL-10 production.
dc.description.abstractConclusion Our results reveal how Gilz controls inos and Activin beta A gene expression to ultimately assign immunoregulatory status to MSC able to repress the pathogenic Th17 cell differentiation program and uncover Activin A as a novel mediator of MSC in this process.
dc.fuente.origenWOS
dc.identifier.doi10.7150/thno.21793
dc.identifier.issn1838-7640
dc.identifier.urihttps://doi.org/10.7150/thno.21793
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/101259
dc.identifier.wosidWOS:000435598500010
dc.issue.numero3
dc.language.isoen
dc.pagina.final859
dc.pagina.inicio846
dc.revistaTheranostics
dc.rightsacceso restringido
dc.subjectMesenchymal Stem Cells
dc.subjectGilz
dc.subjectActivin A
dc.subjectTh17 cells
dc.subjectImmunosuppression
dc.subject.ods03 Good Health and Well-being
dc.subject.odspa03 Salud y bienestar
dc.titleGilz-Activin A as a Novel Signaling Axis Orchestrating Mesenchymal Stem Cell and Th17 Cell Interplay
dc.typeartículo
dc.volumen8
sipa.indexWOS
sipa.trazabilidadWOS;2025-01-12
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