IFIT3 mediates TBK1 phosphorylation to promote activation of pDCs and exacerbate systemic sclerosis in mice

Xiangyang Huang; Yi Liu; Xia Rong; Yiheng Zhao; Dan Feng; Jun Wang; Wanhong Xing

doi:10.1002/ctm2.1800

Clinical and Translational Medicine ›› 2024, Vol. 14 ›› Issue (9) : e1800 DOI: 10.1002/ctm2.1800

RESEARCH ARTICLE

IFIT3 mediates TBK1 phosphorylation to promote activation of pDCs and exacerbate systemic sclerosis in mice

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Abstract

	•This study elucidates the pivotal role of plasmacytoid dendritic cells (pDCs) in systemic sclerosis (SSc).
	•This study identified the key regulatory gene involved in systemic sclerosis (SSc) as IFIT3.
	•This study has found that IFIT3 functions as an upstream regulatory factor, activating TBK1.
	•This study provides Evidence of the regulatory effects of the IFIT3/TBK1 pathway on plasmacytoid dendritic cells (pDCs).
	•This study validated the therapeutic potential using the IFIT3^-/- mouse model.

Keywords

CRISPR/Cas9 / fibrosis / IFIT3/TBK1 signalling pathway / pDCs activation / scRNA-seq / systemic sclerosis

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Xiangyang Huang, Yi Liu, Xia Rong, Yiheng Zhao, Dan Feng, Jun Wang, Wanhong Xing. IFIT3 mediates TBK1 phosphorylation to promote activation of pDCs and exacerbate systemic sclerosis in mice. Clinical and Translational Medicine, 2024, 14(9): e1800 DOI:10.1002/ctm2.1800

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2024 The Author(s). Clinical and Translational Medicine published by John Wiley & Sons Australia, Ltd on behalf of Shanghai Institute of Clinical Bioinformatics.