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Endocrine Abstracts (2016) 41 GP210 | DOI: 10.1530/endoabs.41.GP210

1Department of Endocrinology, Hospital Universitario de la Princesa, Instituto de Investigación Sanitaria Princesa, Universidad Autónoma de Madrid, Madrid, Spain; 2Department of Immunology, School of Medicine, UASLP, San Luis Potosí, Mexico; 3Section of Endocrinology & Internal Medicine, Department of Medical Sciences, University of Ferrara, Ferrara, Italy.


Introduction: Signalling lymphocytic activation molecule SLAMF1 (CD150) is a modulatory receptor expressed in most immune cells. Different data indicate that CD150 is involved in T cell cytokine production, NK cell and CD8 T cell mediated cytotoxicity, and T regulatory (Treg) cell activity. Patients with autoimmune thyroid disease (AITD) show defects in their immune-regulatory mechanisms. Herein we assessed the expression and function CD150 in lymphocytes subpopulations from patients with AITD.

Patients and methods: Peripheral blood samples from 17 patients with Graves’ disease (GD), 11 Hashimoto’s thyroiditis (HT), and 21 healthy subjects were studied. Thyroid tissue samples were also analysed in five patients and expression of CD150 was assessed by flow cytometry and immunohistochemistry. In addition, the functional role of CD150 in CD4+CD25+Treg cells was assessed by a carboxyfluorescein proliferative assay.

Results: An increased expression of SLAMF1 by peripheral blood CD4+T cells and Th17 cells was found in AITD patients compared to controls. In contrast, a decreased expression of SLAMF1 was observed in Treg cells from these patients. The SLAMF1 expression was diminished in thyroid mononuclear cells from AITD patients in comparison with peripheral blood CD4+T cells. Finally, in vitro functional assays showed that exogenous SLAMF1 agonist increased activity in Treg cells from healthy controls but not in AITD patients.

Conclusion: The altered pattern of expression and the functional alteration of SLAMF1 found in patients with AITD suggests that SLAMF1 could be involved in the pathogenesis of AITD.

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