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Updated: Mar 12, 2026
04:39
Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model
Published on: March 17, 2023
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Exploring the molecular mechanisms underlying the inflammation-cancer transformation in Hashimoto thyroiditis using
Mengsha Zou1, Shang Shi1, Huihui Li1
1Thyroid Department, The Affiliated Lihuili Hospital of Ningbo University, Ningbo City, Zhejiang Province, P. R. China.
Autoimmunity
|March 11, 2026
Summary
Hashimoto thyroiditis (HT) inflammation drives papillary thyroid carcinoma (PTC) via IL1B-negative follicular epithelial cells recruiting mast cells. Mast cell IL-8 then activates the PI3K/AKT pathway, promoting cancer development.
Area of Science:
- Oncology
- Immunology
- Cell Biology
Background:
- Hashimoto thyroiditis (HT) is linked to papillary thyroid carcinoma (PTC) development.
- The tumor immune microenvironment and inflammation-to-cancer mechanisms in HT-PTC are not well understood.
Purpose of the Study:
- To investigate the molecular mechanisms driving the inflammation-to-cancer transition in HT-PTC coexistence.
- To identify key cell-cell interactions and signaling pathways involved.
Main Methods:
- Single-cell RNA sequencing (scRNA-seq) of HT and PTC tissues.
- Copy number variation (CNV) analysis to identify malignant cells.
- Cell-cell communication analysis and in vitro validation using Transwell co-culture models.
Main Results:
- Identified 11 cell subtypes, with IL1B upregulated in malignant follicular epithelial cells (FECs).
- IL1B-negative FECs communicate with mast cells via the FN1/CD44 axis.
- Mast cells secrete IL-8, activating the PI3K/AKT pathway and promoting malignant phenotypes under inflammation.
Conclusions:
- IL1B-negative FECs recruit mast cells through the FN1/CD44 axis.
- Mast cell-derived IL-8 activates the PI3K/AKT pathway, driving the HT to PTC transition.
- Provides novel insights into the inflammation-to-cancer mechanism in HT-PTC.
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