| First Author | Wenzek C | Year | 2024 |
| Journal | iScience | Volume | 27 |
| Issue | 8 | Pages | 110547 |
| PubMed ID | 39175769 | Mgi Jnum | J:353819 |
| Mgi Id | MGI:7714159 | Doi | 10.1016/j.isci.2024.110547 |
| Citation | Wenzek C, et al. (2024) Lack of canonical thyroid hormone receptor alpha signaling changes regulatory T cell phenotype in female mice. iScience 27(8):110547 |
| abstractText | 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 alpha (TRalpha) signaling on activation and function of T cells. Our findings show that lack of canonical TRalpha action not only increased the frequency of regulatory T cells (Treg) but propelled an activated and migratory Treg phenotype and nuclear factor kappaB (NF-kappaB) activation in Treg. Conversely, canonical TRalpha action reduced activation of the NF-kappaB pathway previously shown to play a pivotal role in Treg differentiation and function. Taken together, our findings demonstrate that TRalpha 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-TRalpha signaling may have an important role in regulating T cell responses during disease. |
