ETA2023 Poster Presentations Thyroid hormone receptors basic (9 abstracts)
Local thyroid hormone action in T cells - shaping T cell immunity
Christina Wenzek 1 , Devon Siemes 2 , Anita Boelen 3 , Astrid M. Westendorf 4 , Daniel Engel 2 , Lars Christian Möller 5 & Dagmar Führer 6
1University Hospital Essen, Department of Endocrinology, Essen, Germany; 2University Hospital Essen, Department of Immunodynamics, Essen, Germany; 3Amsterdam Umc, Laboratory of Endocrinology, Location Amc | K2-283, Amsterdam, Netherlands; 4Institute of Medical Microbiology, University Hospital Essen, University Duisburg-Essen, Essen, Germany; 5University Hospital Essen, University Hospital Essen, Department of Endocrinology, Diabetes and Metabolism, Essen, Germany; 6Universitätsklinikum Essen, University Hospital Essen, Klinik für Endokrinologie und Stoffwechselerkrankungen, Essen, Germany
The systemic function of thyroid hormones (TH) is highly dependent on their local action in distinct cell populations. A major target of TH are immune cells, yet knowledge on the effect of TH on immune responses is still incomplete. Within this study we aimed to determine the impact of TH on T cells, key players of immune responses, in more detail. To this end, we analyzed the activation and function of T cells from mice lacking TRα (TRα0/0) or expressing a TRα mutant unable to bind to DNA (TRαGS/GS). Initial phenotypic analysis of naïve mice by flow cytometry revealed an increase in circulating CD4+ T cells in TRαGS/GS compared with WT mice. Moreover, CD4+ T cells in the spleen of TRαGS/GS mice displayed a migratory and activated phenotype. Interestingly, the frequency of regulatory T cells (Treg), an important anti-inflammatory subpopulation of CD4+ T cells, was also elevated within TRαGS/GS mice. This was accompanied by an increase in thymus-derived natural Tregs while TRαGS/GS CD4+ T cells also showed an enhanced differentiation into induced Treg during in vitro polarization. RNA sequencing analysis of isolated regulatory T cells from naïve mice indicated an activated phenotype of TRαGS/GS Treg. Moreover, we could detect an enhanced activation of the NFκB pathway in TRαGS/GS CD4+ T cells based on RNA sequencing as well as protein analysis. Taken together, we show an altered T cell phenotype in TRαGS/GS mice, characterized by an augmented Treg immunity, which might be associated with increase activation of the NFκB signaling. These results might provide a better understanding of local TH action in T cells as a prerequisite to further elucidate the role of TH imbalance for immune responses during infectious and non-infectious diseases.
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Endocrine Abstracts
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