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oai:repisalud.isciii.es:20.500.12105/54092024-09-27T09:17:10Zcom_20.500.12105_19604com_20.500.12105_2051col_20.500.12105_19605

00925njm 22002777a 4500 dc Leskela, Susanna author Serrano, Ana author de la Fuente, Hortensia author Rodriguez-Munoz, Ana author Ramos-Levi, Ana author Sampedro-Nuñez, Miguel author Sanchez-Madrid, Francisco author Gonzalez-Amaro, Roberto author Marazuela, Monica author 2015 Introduction Patients with autoimmune thyroid disease (AITD) show defects in their immune-regulatory mechanisms. Herein we assessed the expression and function of galectin-1 and galectin-9 (Gal-1, Gal-9) in dendritic cells (DCs) from patients with AITD. Materials and Methods Peripheral blood samples from 25 patients with Graves' disease (GD), 11 Hashimoto's thyroiditis (HT), and 24 healthy subjects were studied. Thyroid tissue samples from 44 patients with AITD and 22 patients with goiter were also analyzed. Expression and function of Gal-1 and Gal-9 was assessed by quantitative RT-PCR, immunofluorescence and flow cytometry. Results A diminished expression of Gal-9, but not of Gal-1, by peripheral blood DCs was observed in GD patients, mainly in those with Graves ` ophthalmopathy, and a significant negative association between disease severity and Gal-9 expression was detected. In addition, the mRNA levels of Gal-9 and its ligand TIM-3 were increased in thyroid tissue from AITD patients and its expression was associated with the levels of Th1/Th12/Th17 cytokines. Immunofluorescence studies proved that intrathyroidal Gal-9 expression was confined to DCs and macrophages. Finally, in vitro functional assays showed that exogenous Gal-9 had a suppressive effect on the release of Th1/Th2/Th17 cytokines by DC/lymphocyte autologous co-cultures from both AITD patients and healthy controls. Conclusions The altered pattern of expression of Gal-9 in peripheral blood DCs from GD patients, its correlation with disease severity as well as its ability to suppress cytokine release suggest that Gal-9 could be involved in the pathogenesis of AITD. PLoS One. 2015; 10(4):e0123938 10.1371/journal.pone.0123938 1932-6203 PLoS One 25880730 http://hdl.handle.net/20.500.12105/5409 AUTOIMMUNE THYROID-DISEASE T-CELLS OPHTHALMOPATHY PROLIFERATION GLYCOSYLATION INFLAMMATION LYMPHOCYTES SUPPRESSES ACTIVATION INDUCTION Graves' Disease Is Associated with a Defective Expression of the Immune Regulatory Molecule Galectin-9 in Antigen-Presenting Dendritic Cells