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Updated: Jul 14, 2026

Characterization of Thymic Settling Progenitors in the Mouse Embryo Using In Vivo and In Vitro Assays
Published on: June 9, 2015
Triiodothyronine modulates differential homing of recent thymic emigrants to peripheral lymphoid organs
M M Ribeiro-Carvalho1, S Smaniotto1, S Neves-Dos-Santos1
1Laboratory on Thymus Research, Department of Immunology, Oswaldo Cruz Institute, Oswaldo Cruz Foundation, Rio de Janeiro, BrazilDepartment of Morphology, Center for Biological Sciences, Federal University of Alagoas, Maceió, BrazilDepartment of Clinical Analyses, Faculty of Pharmacy, Federal University of Juiz de Fora, Minas Gerais, BrazilMiguelote Viana Central Laboratory, SUS, Niterói, Rio de Janeiro, BrazilDepartment of Histology and Embriology, Institute of Biomedical Sciences, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.
The functioning of the immune system partially relies on T-cell exportation from the thymus, the major site of T-cell differentiation. Although the molecular mechanisms governing this process begin to be elucidated, it is not clear if thyroid hormones can alter the homing of recent thymic emigrants (RTE) to peripheral lymphoid organs. Herein, we investigated whether triiodothyronine (T(3)) could influence the homing of thymus-derived T cells. For that we used intrathymic injection of T(3) in combination with fluorescein isothiocyanate (FITC) to trace, 16 h later, FITC(+) cells, termed RTE, in peripheral lymphoid organs. We observed that T(3) stimulated thymocyte export, increasing the frequency of CD4(+) RTE and CD8(+) RTE in the subcutaneous and mesenteric lymph nodes. By contrast, the relative numbers of CD4(+) RTE in the spleen were decreased. T(3) also changed the differential distribution pattern of CD4(+) RTE, and to a lesser extent CD8(+) RTE in the peripheral lymphoid organs. Moreover, the expression of extracellular matrix (ECM) components, such as laminin and fibronectin, which are known to be involved in T-cell migration, increased in the lymph nodes but not in the spleen following intrathymic T(3) treatment. In conclusion, our data correspond to the first demonstration that in vivo treatment with thyroid hormone stimulates thymic T-cell homing and T-cell distribution in peripheral lymphoid organs.
The functioning of the immune system partially relies on T-cell exportation from the thymus, the major site of T-cell differentiation. Although the molecular mechanisms governing this process begin to be elucidated, it is not clear if thyroid hormones can alter the homing of recent thymic emigrants (RTE) to peripheral lymphoid organs. Herein, we investigated whether triiodothyronine (T(3)) could influence the homing of thymus-derived T cells. For that we used intrathymic injection of T(3) in combination with fluorescein isothiocyanate (FITC) to trace, 16 h later, FITC(+) cells, termed RTE, in peripheral lymphoid organs. We observed that T(3) stimulated thymocyte export, increasing the frequency of CD4(+) RTE and CD8(+) RTE in the subcutaneous and mesenteric lymph nodes. By contrast, the relative numbers of CD4(+) RTE in the spleen were decreased. T(3) also changed the differential distribution pattern of CD4(+) RTE, and to a lesser extent CD8(+) RTE in the peripheral lymphoid organs. Moreover, the expression of extracellular matrix (ECM) components, such as laminin and fibronectin, which are known to be involved in T-cell migration, increased in the lymph nodes but not in the spleen following intrathymic T(3) treatment. In conclusion, our data correspond to the first demonstration that in vivo treatment with thyroid hormone stimulates thymic T-cell homing and T-cell distribution in peripheral lymphoid organs.
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