Dendritic Cells Exposed to Triiodothyronine Deliver Pro-Inflammatory Signals and Amplify IL-17-Driven Immune Responses

ALAMINO VANINA ALEJANDRA; MONTESINOS MARÍA DEL MAR; SOLER MARÍA FLORENCIA; GIUSIANO LUCILA; GIGENA NICOLÁS; FOZZATTI LAURA; MALLER SEBASTIÁN MATÍAS; MENDEZ-HUERGO SANTIAGO PATRICIO; RABINOVICH GABRIEL ADRIÁN; PELLIZAS CLAUDIA GABRIELA

CELLULAR PHYSIOLOGY AND BIOCHEMISTRY : INTERNATIONAL JOURNAL OF EXPERIMENTAL CELLULAR PHYSIOLOGY, BIOCHEMISTRY, AND PHARMACOLOGY.

KARGER

Lugar: Basel; Año: 2019 vol. 52 p. 354 - 354

1015-8987

ackground/Aims: Although a cross-talk between immune and endocrine systems has been well established, the precise pathways by which these signals co-regulate pro- and antiinflammatory responses on antigen-presenting cells remain poorly understood. In this work we investigated the mechanisms by which triiodothyronine (T3) controls T cell activity via dendritic cell (DC) modulation. Methods: DCs from wild-type (WT) and IL-6-deficient micewere pulsed with T3. Cytokine production and programmed death protein ligands (PD-L) 1 and 2 expression were assayed by flow cytometry and ELISA. Interferon-regulatory factor-4 (IRF-4) expression was evaluated by RT-qPCR and flow cytometry. The ability of DCs to stimulate allogenic splenocytes was assessed in a mixed lymphocyte reaction and the different profile markers were analyzed by flow cytometry and ELISA. For in vivo experiments, DCs treated with ovalbumin and T3 were injected into OTII mice. Proliferation, cytokine production, frequency of FoxP3