Regulatory T cells mediate immunosupression induced by experimental hypothyroidism. (P1215)
| Autor: | Eduardo Valli, Helena A Sterle, Santiago Méndez Huergo, Ivan Mascafroni, Alicia J Klecha, María L Barreiro Arcos, Gabriel A Rabinovich, Graciela A Cremaschi |
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| Rok vydání: | 2013 |
| Předmět: | |
| Zdroj: | The Journal of Immunology. 190:188.10-188.10 |
| ISSN: | 1550-6606 0022-1767 |
| Popis: | Thyroid status modulates immunity, being the circulating levels of thyroid hormones (THs) responsible for the regulation of lymphocyte activity. Formerly we observed that experimental hypothyroidism (Exp-hypo) decreases Th1 cytokine production and T cell-mediated immunity. Here we aimed to elucidate the mechanisms underlying immunosuppression triggered by Exp-hypo. Lymphocyte subsets were assessed in spleens and lymph nodes of hypothyroid (hypo-WT) and control (C) mice. Percentage of Treg (CD4+CD25+FoxP3+) cells (Tregs %) was significantly increased in the hypo-WT group without differences in CD3/CD19 or CD4/CD8 ratios. When naïve T cells were differentiated to inducible Treg cells in vitro, similar results were obtained. Treg cells overexpress galectin-1 (Gal-1), an immunoregulatory β-galactoside-binding protein, and mice lacking this lectin (Lgals1-/-) showed reduced Treg cell activity. To evaluate the role of Gal-1 in the regulation of Tregs in Exp-hypo we also analyzed lymphocyte reactivity and the percentage of Tregs % in eu- and hypothyroid Lgals1-/- mice (hypo-KO). We found an increased T cell proliferation and a reduction in the Tregs % in hypo-KO mice respect to the hypo-WT group. We conclude that modulation of immunity in the Exp-hypo with low circulating levels of THs is associated to a significant rise in the percentage of spontaneous and inducible Tregs. This increase relies on the expression of Gal-1 and may be related to a functional deficit of T cells. |
| Databáze: | OpenAIRE |
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