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Immune landscape in NOD.H-2h4 mouse model thyroid revealed by single-cell RNA sequencing.
Bochuan Wang1, Linye He2, Huandi Qiu3
1State Key Laboratory of Biotherapy, Sichuan University, Chengdu, Sichuan, China.
Biochemical and Biophysical Research Communications
|February 24, 2026
Summary
This study reveals that thyrocyte plasticity and regulatory T cell (Treg) dysfunction drive Hashimoto's thyroiditis progression. Understanding these cellular mechanisms offers new insights into autoimmune thyroid disease.
Area of Science:
- Immunology
- Endocrinology
- Genomics
Background:
- Hashimoto's thyroiditis is an autoimmune disorder causing hypothyroidism and increasing thyroid cancer risk.
- The precise roles of thyroid cells in immune dysregulation during Hashimoto's thyroiditis are not fully understood.
Purpose of the Study:
- To investigate the cellular and molecular mechanisms underlying Hashimoto's thyroiditis.
- To characterize the transcriptomic profiles of thyroid cells and immune infiltrates in a mouse model.
Main Methods:
- Single-cell RNA sequencing was performed on thyroid tissues from NOD.H-2h4 mice at 4, 8, and 16 weeks.
- 38,461 cells were analyzed to identify distinct cell populations and their transcriptomic profiles.
Main Results:
- A downregulation of Nkx2-1 suggests thyrocyte identity and function loss.
- Intercellular communication analysis indicated potential interactions between thyrocytes, stromal cells, and immune cells via the App-Cd74 axis.
- Regulatory T cells (Tregs) showed signs of dysfunction, and thyrocytes exhibited inflammatory and antigen-presenting phenotypes, potentially due to chronic stress.
Conclusions:
- A single-cell transcriptomic atlas of the NOD.H-2h4 mouse model was created.
- Thyrocyte plasticity and Treg dysfunction are identified as key drivers of Hashimoto's thyroiditis progression.
- This dataset facilitates further research into the cellular mechanisms of Hashimoto's thyroiditis.
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