It is incredible how many non-endocrinology sectors are looking at T3...
Cancer Res. 2015 Feb 11. pii: canres.1875.2014. [Epub ahead of print]
Antitumor responses stimulated by dendritic cells are improved by triiodothyronine binding to the thyroid hormone receptor β
Alamino VA1, Mascanfroni ID2, Montesinos MM1, Gigena N1, Donadio AC1, Blidner AG3, Milotich SI4, Cheng SY5, Masini-Repiso AM6, Rabinovich GA7, Pellizas CG8.
Author information
1Dpto. Bioquímica Clínica, Facultad de Ciencias Químicas, Universidad Nacional de Córdoba, Centro de Investigaciones en Bioquímica Clínica e Inmunología (CIBICI-CONICET).
2Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Institutes of Medicine.
3Laboratorio de Inmunopatología, Instituto de Biología y Medicina Experimental (IBYME-CONICET).
4Sanatorio Allende, Hospital Materno-Neonatal Ramón Carrillo.
5Molecular Biology, NCI.
6Universidad Nacional de Córdoba, CIBICI-CONICET. Departamento de Bioquímica Clínica. Facultad de Ciencias Químicas.
7Departamento de Quimica Biologica, Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires.
8Dpto. Bioquímica Clínica, Facultad de Ciencias Químicas, Universidad Nacional de Córdoba, Centro de Investigaciones en Bioquímica Clínica e Inmunología (CIBICI-CONICET) claudia@fcq.unc.edu.ar.
Abstract
Bi-directional crosstalk between the neuroendocrine and immune systems orchestrates immune responses in both physiologic and pathologic settings. In this study, we provide in vivo evidence of a critical role for the thyroid hormone triiodothyronine (T3) in controlling the maturation and antitumor functions of dendritic cells (DC). We used a thyroid hormone receptor (TR) β mutant mouse (TRβPV) to establish the relevance of the T3-TRβ system in vivo. In this model, TRβ signaling endowed DC with the ability to stimulate antigen-specific cytotoxic T-cell responses during tumor development. T3 binding to TRβ increased DC viability and augmented DC migration to lymph nodes. Moreover, T3 stimulated the ability of DC to cross-present antigens and to stimulate cytotoxic T cell responses. In a B16-OVA mouse model of melanoma, vaccination with T3-stimulated DC inhibited tumor growth and prolonged host survival, in part by promoting the generation of IFN-γ-producing CD8+ T cells. Overall, our results establish an adjuvant effect of T3-TRβ signaling in DC, suggesting an immediately translatable method to empower DC vaccination approaches for cancer immunotherapy.
Copyright © 2015, American Association for Cancer Research.
PMID: 25672979
ncbi.nlm.nih.gov/pubmed/256...
Rod