Lack of canonical thyroid hormone receptor α signaling changes regulatory T cell phenotype in female mice.

Autor: Wenzek C; Department of Endocrinology, Diabetology and Metabolism, University Hospital Essen, University Duisburg-Essen, 45147 Essen, Germany., Siemes D; Institute for Experimental Immunology and Imaging, University Hospital Essen, University Duisburg-Essen, 45147 Essen, Germany., Hönes GS; Department of Endocrinology, Diabetology and Metabolism, University Hospital Essen, University Duisburg-Essen, 45147 Essen, Germany., Pastille E; Institute of Medical Microbiology, University Hospital Essen, University Duisburg-Essen, 45147 Essen, Germany., Härting N; Institute for Human Genetics, University Hospital Essen, University Duisburg-Essen, 45147 Essen, Germany., Kaiser F; Institute for Human Genetics, University Hospital Essen, University Duisburg-Essen, 45147 Essen, Germany., Moeller LC; Department of Endocrinology, Diabetology and Metabolism, University Hospital Essen, University Duisburg-Essen, 45147 Essen, Germany., Engel DR; Institute for Experimental Immunology and Imaging, University Hospital Essen, University Duisburg-Essen, 45147 Essen, Germany., Westendorf AM; Institute of Medical Microbiology, University Hospital Essen, University Duisburg-Essen, 45147 Essen, Germany., Führer D; Department of Endocrinology, Diabetology and Metabolism, University Hospital Essen, University Duisburg-Essen, 45147 Essen, Germany.
Jazyk: angličtina
Zdroj: IScience [iScience] 2024 Jul 19; Vol. 27 (8), pp. 110547. Date of Electronic Publication: 2024 Jul 19 (Print Publication: 2024).
DOI: 10.1016/j.isci.2024.110547
Abstrakt: 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.
Competing Interests: The authors declare no competing interests.
(© 2024 The Author(s).)
Databáze: MEDLINE