NUDT1 promotes the accumulation and longevity of CD103+ TRM cells in primary biliary cholangitis

Huang, Bingyuan; Lyu, Zhuwan; Qian, Qiwei; Chen, Yong; Zhang, Jun; Li, Bo; Li, Yikang; Liang, Jubo; Liu, Qiaoyan; Li, You; Chen, Ruiling; Lian, Min; Xiao, Xiao; Miao, Qi; Wang, Qixia; Fang, Jing‐Yuan; Lian, Zhe‐Xiong; Li, Yanmei; Helleday, Thomas; Gershwin, M. Eric; You, Zhengrui; Ma, Xiong

doi:10.1016/j.jhep.2022.06.014

Cited by 22 publications

(24 citation statements)

References 35 publications

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“…These genes included EIF3D, CYFIP2, NCBP2, DCPS, and NUDT1 . EIF3D and NUDT1 have been shown to play important regulatory roles in tumor and immune infiltration ( Huang et al, 2019 ; Huang et al, 2022 ). CYFIP2 has been shown to play vital regulatory role in the central nervous system ( Schaks et al, 2020 ).…”

Section: Discussionmentioning

confidence: 99%

Experimental verification and comprehensive analysis of m7G methylation regulators in the subcluster classification of ischemic stroke

Tian

Yu²,

Lv³

et al. 2023

Front. Genet.

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Background: Ischemic stroke (IS) is a fatal cerebrovascular disease involving several pathological mechanisms. Modification of 7-methylguanosine (m7G) has multiple regulatory functions. However, the expression pattern and mechanism of m7G in IS remain unknown. Herein, we aimed to explore the effect of m7G modification on IS.Methods: We screened significantly different m7G-regulated genes in Gene Expression Omnibus datasets, GSE58294 and GSE22255. The random forest (RF) algorithm was selected to identify key m7G-regulated genes that were subsequently validated using the middle cerebral artery occlusion (MCAO) model and quantitative polymerase chain reaction (qPCR). A risk model was subsequently generated using key m7G-regulated genes. Then, “ConsensusClusterPlus” package was used to distinguish different m7G clusters of patients with IS. Simultaneously, between two m7G clusters, differentially expressed genes (DEGs) and immune infiltration differences were also explored. Finally, we investigated functional enrichment and the mRNA–miRNA–transcription factor network of DEGs.Results: RF and qPCR confirmed that EIF3D, CYFIP2, NCBP2, DCPS, and NUDT1 were key m7G-related genes in IS that could accurately predict clinical risk (area under the curve = 0.967). NCBP2 was the most significantly associated gene with immune infiltration. Based on the expression profiles of these key m7G-related genes, the IS group could be divided into two clusters. According to the single-sample gene set enrichment analysis algorithm, four types of immune cells (immature dendritic cells, macrophages, natural killer T cells, and TH1 cells) were significantly different in the two m7G clusters. The functional enrichment of 282 DEGs between the two clusters was mainly concentrated in the “regulation of apoptotic signaling pathway,” “cellular response to DNA damage stimulus,” “adaptive immune system,” and “pyroptosis.” The miR-214–LTF–FOXJ1 axis may be a key regulatory pathway for IS.Conclusion: Our findings suggest that EIF3D, CYFIP2, NCBP2, DCPS, and NUDT1 may serve as potential diagnostic biomarkers for IS and that the m7G clusters developed by these genes provide more evidence for the regulation of m7G in IS.

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Section: Discussionmentioning

confidence: 99%

Experimental verification and comprehensive analysis of m7G methylation regulators in the subcluster classification of ischemic stroke

Tian

Yu²,

Lv³

et al. 2023

Front. Genet.

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“…Interestingly, recent work on autoreactive pyruvate dehydrogenase complex E2-specific CD8 T cells in PBC demonstrated that these cells had an intraepithelial CD103 + tissue-resident memory phenotype and were localised close to intrahepatic bile ducts. 91 A recent study on a family where 5 individuals suffered from PSC, identified a heterozygous missense mutation in SEMA4D (encoding Semaphorin-4D/CD100) in all 5 individuals, further linking T cells to PSC pathogenesis. 92 This mutation was related to T-cell functional defects on the transcriptional and functional level in murine models and patient samples, and replacement by wild-type T cells in mice carrying the same diseasecausing mutation as the sick family members attenuated cholangitis after DDC (3,5diethoxycarbonyl-1,4-dihydrocollidine) exposure.…”

Section: Adaptive Lymphocytesmentioning

confidence: 99%

Immunobiology of the biliary tract system

Björkström¹

2022

Journal of Hepatology

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“…Similar to other tissue-specific T RM cells, hepatic T RM cells downregulate the expression of tissue egression markers, like soingosine-1-phosphate 1 (S1PR1), and the homing receptors such as CD62L and CCR7 ( 43 , 44 ). Furthermore, hepatic T RM cells usually express some adhesion molecule and chemokine receptors, including CD69 ( 44 ), CD103 ( 17 , 45 ), CD49a ( 36 ), CXCR3 ( 17 , 23 ) and CXCR6 ( 46 , 47 ), which are involved in their localization and maintenance in the hepatic sinusoids and portal veins.…”

Section: Phenotype Of Liver T Rm Cellsmentioning

confidence: 99%

“…Furthermore, CD103 may define two different functional subsets of T RM cells in human liver. The CD69 + CD103 + subpopulations are antigen-specific autoreactive cytotoxic T cells in human liver, exhibiting more potent effector function than CD69 + CD103 - counterparts ( 45 , 55 , 56 ). Interestingly, there are differences between mouse and human liver T RM cells regarding CD103 expression.…”

Section: Phenotype Of Liver T Rm Cellsmentioning

confidence: 99%

Tissue-resident memory T cells in chronic liver diseases: Phenotype, development and function

You

2022

Front. Immunol.

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Tissue-resident memory (TRM) T cells are a unique subset of memory T cells that are critical for the first line of defense against pathogens or antigens in peripheral non-lymphoid tissues such as liver, gut, and skin. Generally, TRM cells are well adapted to the local environment in a tissue-specific manner and typically do not circulate but persist in tissues, distinguishing them from other memory T cell lineages. There is strong evidence that liver TRM cells provide a robust adaptive immune response to potential threats. Indeed, the potent effector function of hepatic TRM cells makes it essential for chronic liver diseases, including viral and parasite infection, autoimmune liver diseases (AILD), nonalcoholic fatty liver disease (NAFLD), hepatocellular carcinoma (HCC) and liver transplantation. Manipulation of hepatic TRM cells might provide novel promising strategies for precision immunotherapy of chronic liver diseases. Here, we provide insights into the phenotype of hepatic TRM cells through surface markers, transcriptional profiles and effector functions, discuss the development of hepatic TRM cells in terms of cellular origin and factors affecting their development, analyze the role of hepatic TRM cells in chronic liver diseases, as well as share our perspectives on the current status of hepatic TRM cell research.

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NUDT1 promotes the accumulation and longevity of CD103+ TRM cells in primary biliary cholangitis

Cited by 22 publications

References 35 publications

Experimental verification and comprehensive analysis of m7G methylation regulators in the subcluster classification of ischemic stroke

Experimental verification and comprehensive analysis of m7G methylation regulators in the subcluster classification of ischemic stroke

Immunobiology of the biliary tract system

Tissue-resident memory T cells in chronic liver diseases: Phenotype, development and function

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