DEXAMETHASONE COUNTERACTS THE IMMUNOSTIMULARY EFFECTS OF TRIIODOTHYRONINE (T3) ON DENDRITIC CELLS

MARÍA M. MONTESINOS1. 1 THESE AUTHORS CONTRIBUTED EQUALLY TO THIS WORK.; VANINA ALAMINO1. 1 THESE AUTHORS CONTRIBUTED EQUALLY TO THIS WORK.; IVAN MASCANFRONI; SEBASTIAN SUSPERREGUY; NICOLÁS GIGENA; ANA MASINI-REPISO; GABRIEL RABINOVICH; CLAUDIA GABRIELA PELLIZAS

STEROIDS

ELSEVIER SCIENCE INC

Lugar: Amsterdam; Año: 2012 vol. 77 p. 67 - 67

0039-128X

lucocorticoids (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-