Unraveling the molecular architecture of autoimmune thyroid diseases at spatial resolution

Rebeca Martínez-Hernández (), Nuria Sánchez de la Blanca, Pablo Sacristán-Gómez, Ana Serrano-Somavilla, José Luis Muñoz De Nova, Fátima Sánchez Cabo, Holger Heyn, Miguel Sampedro-Núñez and Mónica Marazuela ()
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Rebeca Martínez-Hernández: Universidad Autónoma de Madrid, and Centro de Investigación Biomédica en Red de Enfermedades Raras (CIBERER GCV14/ER/12)
Nuria Sánchez de la Blanca: Universidad Autónoma de Madrid, and Centro de Investigación Biomédica en Red de Enfermedades Raras (CIBERER GCV14/ER/12)
Pablo Sacristán-Gómez: Universidad Autónoma de Madrid, and Centro de Investigación Biomédica en Red de Enfermedades Raras (CIBERER GCV14/ER/12)
Ana Serrano-Somavilla: Universidad Autónoma de Madrid, and Centro de Investigación Biomédica en Red de Enfermedades Raras (CIBERER GCV14/ER/12)
José Luis Muñoz De Nova: Hospital Universitario de la Princesa, Instituto de Investigación Sanitaria Princesa, Universidad Autónoma de Madrid
Fátima Sánchez Cabo: Centro Nacional de Investigaciones Cardiovasculares (CNIC)
Holger Heyn: Centro Nacional de Análisis Genómico (CNAG)
Miguel Sampedro-Núñez: Universidad Autónoma de Madrid, and Centro de Investigación Biomédica en Red de Enfermedades Raras (CIBERER GCV14/ER/12)
Mónica Marazuela: Universidad Autónoma de Madrid, and Centro de Investigación Biomédica en Red de Enfermedades Raras (CIBERER GCV14/ER/12)

Nature Communications, 2024, vol. 15, issue 1, 1-19

Abstract: Abstract Autoimmune thyroid diseases (AITD) such as Graves’ disease (GD) or Hashimoto’s thyroiditis (HT) are organ-specific diseases that involve complex interactions between distinct components of thyroid tissue. Here, we use spatial transcriptomics to explore the molecular architecture, heterogeneity and location of different cells present in the thyroid tissue, including thyroid follicular cells (TFCs), stromal cells such as fibroblasts, endothelial cells, and thyroid infiltrating lymphocytes. We identify damaged antigen-presenting TFCs with upregulated CD74 and MIF expression in thyroid samples from AITD patients. Furthermore, we discern two main fibroblast subpopulations in the connective tissue including ADIRF+ myofibroblasts, mainly enriched in GD, and inflammatory fibroblasts, enriched in HT patients. We also demonstrate an increase of fenestrated PLVAP+ vessels in AITD, especially in GD. Our data unveil stromal and thyroid epithelial cell subpopulations that could play a role in the pathogenesis of AITD.

Date: 2024
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DOI: 10.1038/s41467-024-50192-5

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