Nuclear factor NF-kB-dependent thyroid hormone receptor B1-expression controls dendritic cell function via AKT signaling

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

AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC

Año: 2010 vol. 285 p. 9569 - 9569

span lang="en" style="FONT-SIZE: 10pt; FONT-FAMILY: "Arial Narrow","sans-serif"; mso-bidi-font-size: 12.0pt; mso-fareast-font-family: ´Times New Roman´; mso-bidi-font-family: Arial; mso-ansi-language: ES; mso-fareast-language: ES; mso-bidi-language: AR-SA"> 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)B1 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 e