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Type I interferon signaling facilitates resolution of acute liver injury by priming macrophage polarization 被引量:1

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摘要 Due to their broad functional plasticity,myeloid cells contribute to both liver injury and recovery during acetaminophen overdose-induced acute liver injury(APAP-ALI).A comprehensive understanding of cellular diversity and intercellular crosstalk is essential to elucidate the mechanisms and to develop therapeutic strategies for APAP-ALI treatment.Here,we identified the function of IFN-I in the myeloid compartment during APAP-ALI.Utilizing single-cell RNA sequencing,we characterized the cellular atlas and dynamic progression of liver CD11b+cells post APAP-ALI in WT and STAT2 T403A mice,which was further validated by immunofluorescence staining,bulk RNA-seq,and functional experiments in vitro and in vivo.We identified IFN-I-dependent transcriptional programs in a three-way communication pathway that involved IFN-I synthesis in intermediate restorative macrophages,leading to CSF-1 production in aging neutrophils that ultimately enabled Trem2+restorative macrophage maturation,contributing to efficient liver repair.Overall,we uncovered the heterogeneity of hepatic myeloid cells in APAP-ALI at single-cell resolution and the therapeutic potential of IFN-I in the treatment of APAP-ALI.
出处 《Cellular & Molecular Immunology》 SCIE CAS CSCD 2023年第2期143-157,共15页 中国免疫学杂志(英文版)
基金 supported by the Key R&D Program of Shandong Province(2020CXGC010503) Shandong Provincial Key Laboratory Platform Project(2021ZDSYS11) Major Program of National Natural Science Foundation of China(81991525).
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