Antitumor responses stimulated by dendritic cells are improved by triiodothyronine binding to the thyroid hormone receptor β

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

4 Replies

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  • Rod, it gives me hope that someday endocrinology will actually look more at it. PR

  • Just remind me again what an Endo does-ah yes study the hormones like thyroid ones! I'm beginning to think all medics should be forced to have study leave and give feedback on their findings. Trouble is the topics like endocrinology and neurology would be ignored as 'complicated' but at least the specialists would have to pick their own subject! We need greater understanding now.

  • Very interesting Rod.

    3 years ago I had marker for myeloma in my blood.I have to have blood tested every year for the marker and it has gone.I started on T3 and was then switched to NDT. Co-incidence or just a blip as Gp reckons.I know what I think!!

    Jill

  • Silverfox7

    Last time I saw my "Endo " I noticed it had Diabetologist on the board.

    Nuff said !!!

    Mary

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