A state of chronic inflammation is common in organs affected by autoimmune disorders,
such as autoimmune thyroid diseases (AITD). Epithelial cells, such as thyroid follicular cells (TFCs),
can experience a total or partial transition to a mesenchymal phenotype under these conditions. One
of the major cytokines involved in this phenomenon is transforming growth factor beta (TGF-β),
which, at the initial stages of autoimmune disorders, plays an immunosuppressive role. However, at
chronic stages, TGF- β contributes to fibrosis and/or transition to mesenchymal phenotypes. The
importance of primary cilia (PC) has grown in recent decades as they have been shown to play a key
role in cell signaling and maintaining cell structure and function as mechanoreceptors. Deficiencies
of PC can trigger epithelial–mesenchymal transition (EMT) and exacerbate autoimmune diseases. A
set of EMT markers (E-cadherin, vimentin, α-SMA, and fibronectin) were evaluated in thyroid tissues
from AITD patients and controls through RT-qPCR, immunohistochemistry (IHC), and western blot
(WB). We established an in vitro TGF-β–stimulation assay in a human thyroid cell line to assess EMT
and PC disruption. EMT markers were evaluated in this model using RT-qPCR and WB, and PC
was evaluated with a time-course immunofluorescence assay. We found an increased expression of
the mesenchymal markers α-SMA and fibronectin in TFCs in the thyroid glands of AITD patients.
Furthermore, E-cadherin expression was maintained in these patients compared to the controls.
The TGF-β-stimulation assay showed an increase in EMT markers, including vimentin, α-SMA,
and fibronectin in thyroid cells, as well as a disruption of PC. The TFCs from the AITD patients
experienced a partial transition to a mesenchymal phenotype, preserving epithelial characteristics
associated with a disruption in PC, which might contribute to AITD pathogenesisThis work was supported by the following grants: Proyectos de Investigación en Salud (PI) PI19-00584 and PI22/01404, and Proyectos de investigación de Medicina Personalizada de Precisión (PMP) PMP22/00021 (funded by Instituto de Salud Carlos III); iTIRONET P2022/BMD7379 (funded by Comunidad de Madrid); FEDER funds to M.M and R.M.-H. (cofinanced); predoctoral fellowship funded by Instituto de Salud Carlos III and FSE+ funds (FI20/00035) to P.S.-G; and predoctoral fellowships funded by Comunidad de Madrid (PEJ-2020-AI_BMD-18292) to N.S.d.l.B.C. The funders had no role in the study design, data collection, data analysis, interpretation, or writing of the repor
