1. Lack of canonical thyroid hormone receptor α signaling changes regulatory T cell phenotype in female mice
- Author
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Christina Wenzek, Devon Siemes, G. Sebastian Hönes, Eva Pastille, Nina Härting, Frank Kaiser, Lars C. Moeller, Daniel R. Engel, Astrid M. Westendorf, and Dagmar Führer
- Subjects
Molecular biology ,Immunology ,Endocrinology ,Cell biology ,Science - Abstract
Summary: The immune system has emerged as an important target of thyroid hormones (THs); however, the role of TH in T cells has so far remained elusive. In this study, we assessed the effect of TH receptor α (TRα) signaling on activation and function of T cells. Our findings show that lack of canonical TRα action not only increased the frequency of regulatory T cells (Treg) but propelled an activated and migratory Treg phenotype and nuclear factor κB (NF-κB) activation in Treg. Conversely, canonical TRα action reduced activation of the NF-κB pathway previously shown to play a pivotal role in Treg differentiation and function. Taken together, our findings demonstrate that TRα impacts T cell differentiation and phenotype. Given the well-known interaction of inflammation, immune responses, and TH axis in e.g., severe illness, altered TH-TRα signaling may have an important role in regulating T cell responses during disease.
- Published
- 2024
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