Dendritic cells exposed to triiodothyronine deliver pro-inflammatory signals and amplify IL-17-driven immune responses

ALAMINO VA; MONTESINOS MM; SOLER MF; GIUSIANO L; GIGENA N; FOZZATTI L; MALLER SM; MENDEZ-HUERGO SP; RABINOVICH GA; PELLIZAS CG

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 beenwell established, the precise pathways by which these signals co-regulate pro- and antiinflammatoryresponses on antigen-presenting cells remain poorly understood. In this workwe investigated the mechanisms by which triiodothyronine (T3) controls T cell activity viadendritic 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 and2 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 stimulateallogenic splenocytes was assessed in a mixed lymphocyte reaction and the different profilemarkers were analyzed by flow cytometry and ELISA. For in vivo experiments, DCs treated withovalbumin and T3 were injected into OTII mice. Proliferation, cytokine production, frequencyof FoxP3+ regulat