Myeloid cells interact with a subset of thyrocytes to promote their migration and follicle formation through NF-κB

Rui-Meng Yang, Shi-Yang Song, Feng-Yao Wu, Rui-Feng Yang, Yan-Ting Shen, Ping-Hui Tu, Zheng Wang, Jun-Xiu Zhang, Feng Cheng, Guan-Qi Gao, Jun Liang, Miao-Miao Guo, Liu Yang, Yi Zhou, Shuang-Xia Zhao (), Ming Zhan () and Huai-Dong Song ()
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Rui-Meng Yang: Shanghai Jiao Tong University School of Medicine
Shi-Yang Song: Shanghai Jiao Tong University School of Medicine
Feng-Yao Wu: Shanghai Jiao Tong University School of Medicine
Rui-Feng Yang: Shanghai Medical College, Fudan University
Yan-Ting Shen: Shanghai Jiao Tong University School of Medicine
Ping-Hui Tu: Shanghai Jiao Tong University School of Medicine
Zheng Wang: Shanghai Jiao Tong University School of Medicine
Jun-Xiu Zhang: Maternal and Child Health Institute of Bozhou
Feng Cheng: Fujian Medical University
Guan-Qi Gao: The Linyi People’s Hospital
Jun Liang: The Central Hospital of Xuzhou Affiliated to Xuzhou Medical College
Miao-Miao Guo: Shanghai Jiao Tong University School of Medicine
Liu Yang: Shanghai Jiao Tong University School of Medicine
Yi Zhou: Boston Children’s Hospital and Harvard Stem Cell Institute
Shuang-Xia Zhao: Shanghai Jiao Tong University School of Medicine
Ming Zhan: Shanghai Jiao Tong University School of Medicine
Huai-Dong Song: Shanghai Jiao Tong University School of Medicine

Nature Communications, 2023, vol. 14, issue 1, 1-16

Abstract: Abstract The pathogenesis of thyroid dysgenesis (TD) is not well understood. Here, using a combination of single-cell RNA and spatial transcriptome sequencing, we identify a subgroup of NF-κB-activated thyrocytes located at the center of thyroid tissues in postnatal mice, which maintained a partially mesenchymal phenotype. These cells actively protruded out of the thyroid primordium and generated new follicles in zebrafish embryos through continuous tracing. Suppressing NF-κB signaling affected thyrocyte migration and follicle formation, leading to a TD-like phenotype in both mice and zebrafish. Interestingly, during thyroid folliculogenesis, myeloid cells played a crucial role in promoting thyrocyte migration by maintaining close contact and secreting TNF-α. We found that cebpa mutant zebrafish, in which all myeloid cells were depleted, exhibited thyrocyte migration defects. Taken together, our results suggest that myeloid-derived TNF-α-induced NF-κB activation plays a critical role in promoting the migration of vertebrate thyrocytes for follicle generation.

Date: 2023
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DOI: 10.1038/s41467-023-43895-8

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