4.8 Article

Proteomics and Organoid Culture Reveal the Underlying Pathogenesis of Hashimoto's Thyroiditis

Journal

FRONTIERS IN IMMUNOLOGY
Volume 12, Issue -, Pages -

Publisher

FRONTIERS MEDIA SA
DOI: 10.3389/fimmu.2021.784975

Keywords

Hashimoto's thyroiditis; autoimmune diseases; proteomics; organoid; pathogenesis

Categories

Funding

  1. National Key R&D Program of China [2019YFA0801900, 2018YFA0800300, 2020YFA0803800]
  2. National Natural Science Foundation of China [31971074]
  3. Innovation Team and Talents Cultivation Program of National Administration of Traditional Chinese Medicine [ZYYCXTD-D-202001]
  4. Shanghai Municipal Science and Technology Major Project [2017SHZDZX01]
  5. Shanghai Frontiers Science Research Base of Exercise and Metabolic Health, the National Natural Science Foundation of China [31971097]
  6. Construction Project of High-Level Local Universities in Shanghai, China, Shanghai Municipal Science and Technology Committee of Shanghai outstanding academic leaders plan [21XD1403200]
  7. fundamental research Fund of heilongjiang province [2020KYYWF-FC1]
  8. China Postdoctoral Science Foundation [2021M690680]

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The study used mass spectrometric analysis of thyroid tissue from HT patients and healthy individuals, identifying 44 differentially expressed proteins and providing an in-depth understanding of the pathogenesis of HT. Patient-derived HT and PTC organoids were developed as a new preclinical model to validate potential markers.
Hashimoto's thyroiditis (HT) is an autoimmune disease, and its incidence continues to rise. Although scientists have studied this disease for many years and discovered the potential effects of various proteins in it, the specific pathogenesis is still not fully comprehended. To understand HT and translate this knowledge to clinical applications, we took the mass spectrometric analysis on thyroid tissue fine-needle puncture from HT patients and healthy people in an attempt to make a further understanding of the pathogenesis of HT. A total of 44 proteins with differential expression were identified in HT patients, and these proteins play vital roles in cell adhesion, cell metabolism, and thyroxine synthesis. Combining patient clinical trial sample information, we further compared the transient changes of gene expression regulation in HT and papillary thyroid carcinoma (PTC) samples. More importantly, we developed patient-derived HT and PTC organoids as a promising new preclinical model to verify these potential markers. Our data revealed a marked characteristic of HT organoid in upregulating chemokines that include C-C motif chemokine ligand (CCL) 2 and CCL3, which play a key role in the pathogenesis of HT. Overall, our research has enriched everyone's understanding of the pathogenesis of HT and provides a certain reference for the treatment of the disease.

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