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Artículo

Dexamethasone counteracts the immunostimulatory effects of triiodothyronine (T3) on dendritic cells

Montesinos, Maria del MarIcon ; Alamino, Vanina AlejandraIcon ; Mascanfroni, Ivan DaríoIcon ; Susperreguy, SebastianIcon ; Gigena, NicolásIcon ; Masini, Ana María; Rabinovich, Gabriel AdriánIcon ; Pellizas, Claudia GabrielaIcon
Fecha de publicación: 01/2012
Editorial: Elsevier Science Inc
Revista: Steroids
ISSN: 0039-128X
Idioma: Inglés
Tipo de recurso: Artículo publicado
Clasificación temática:
Otras Ciencias de la Salud

Resumen

Glucocorticoids (GCs) are widely used as anti-inflammatory and immunosuppressive agents. Several studies have indicated the important role of dendritic cells (DCs), highly specialized antigen-presenting and immunomodulatory cells, in GC-mediated suppression of adaptive immune responses. Recently, we demonstrated that triiodothyronine (T3) has potent immunostimulatory effects on bone marrow-derived mouse DCs through a mechanism involving T3 binding to cytosolic thyroid hormone receptor (TR) betha 1,rapid and sustained Akt activation and IL-12 production. Here we explored the impact of GCs on T3-mediated DC maturation and function and the intracellular events underlying these effects. Dexamethasone(Dex), a synthetic GC, potently inhibited T3-induced stimulation of DCs by preventing the augmented expression of maturation markers and the enhanced IL-12 secretion through mechanisms involving the GC receptor. These effects were accompanied by increased IL-10 levels following exposure of T3-conditioned DCs to Dex. Accordingly, Dex inhibited the immunostimulatory capacity of T3-matured DCs on naive T-cell proliferation and IFN-gamma production while increased IL-10 synthesis by allogeneic T cell cultures. A mechanistic analysis revealed the ability of Dex to dampen T3 responses through modulation of Akt phosphorylation and cytoplasmic-nuclear shuttling of nuclear factor-kB (NF-kB). In addition,Dex decreased TRb1 expression in both immature and T3-maturated DCs through mechanisms involving the GC receptor. Thus GCs, which are increased during the resolution of inflammatory responses, counteract the immunostimulatory effects of T3 on DCs and their ability to polarize adaptive immune responses toward a T helper (Th)-1-type through mechanisms involving, at least in part, NF-kB- and TRb1-dependent pathways. Our data provide an alternative mechanism for the anti-inflammatory effects of GCs with critical implications in immunopathology at the cross-roads of the immune-endocrine circuits.
Palabras clave: DEXAMETHASONE , THYROID HORMONE ACTION , DENDRITIC CELLS
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info:eu-repo/semantics/openAccess Excepto donde se diga explícitamente, este item se publica bajo la siguiente descripción: Creative Commons Attribution-NonCommercial-ShareAlike 2.5 Unported (CC BY-NC-SA 2.5)
Identificadores
URI: http://hdl.handle.net/11336/84568
DOI: http://dx.doi.org/10.1016/j.steroids.2011.10.006
URL: https://www.sciencedirect.com/science/article/pii/S0039128X11003102?via%3Dihub
Colecciones
Articulos(CIBICI)
Articulos de CENTRO DE INV.EN BIOQUI.CLINICA E INMUNOLOGIA
Articulos(IBYME)
Articulos de INST.DE BIOLOGIA Y MEDICINA EXPERIMENTAL (I)
Articulos(IIBBA)
Articulos de INST.DE INVEST.BIOQUIMICAS DE BS.AS(I)
Citación
Montesinos, Maria del Mar; Alamino, Vanina Alejandra; Mascanfroni, Ivan Darío; Susperreguy, Sebastian; Gigena, Nicolás; et al.; Dexamethasone counteracts the immunostimulatory effects of triiodothyronine (T3) on dendritic cells; Elsevier Science Inc; Steroids; 77; 1-2; 1-2012; 67-76
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