Nuclear factor NF- kappa B-dependent thyroid hormone receptor beta 1-expression controls dendritic cell function via AKT signaling

MASCANFRONI ID; MONTESINOS, MM; ALAMINO VA; SUSPERREGUY S; NICOLA JP; ILARREGUI JM; MASINI-REPISO AM; RABINOVICH GA; PELLIZAS CG

American Society for Biochenmistry and Molecular Biology

Año: 2010 vol. 285 p. 9569 - 9569

p class="MsoNormal" style="MARGIN: 0cm 0cm 0pt; TEXT-ALIGN: justify">In spite of considerable progress in our understanding of the interplay between immune and endocrine systems, the role of thyroid hormones and their receptors in the control of adaptive immunity is still uncertain. Here we investigated the role of thyroid hormone receptor (TR)â1 signaling in modulating dendritic cell (DC) physiology and the intracellular mechanisms underlying these immunoregulatory effects. Exposure of DCs to triiodothyronine (T3) resulted in rapid and sustained increase in Akt phosphorylation independently of PI3K activation, which was essential for supporting T3-induced DC maturation and IL-12 production. This effect was dependent on intact TRbeta1 signaling as siRNA-mediated silencing of TRbeta1 expression prevented T3-induced DC maturation and IL-12 secretion as well as Akt activation and IKB deg