多发性硬化
基因
寄主(生物学)
疾病
基因表达
生物
遗传学
免疫学
医学
病理
作者
Samantha S. Soldan,Chenhe Su,Maria Chiara Monaco,Leena Yoon,Toshitha Kannan,Urvi Zankharia,R. Patel,Jayaraju Dheekollu,Olga Vladimirova,Jack W. Dowling,Simon Thebault,Natalie V. Brown,Annaliese Clauze,Frances Andrada,Andries Feder,Paul J. Planet,Andrew V. Kossenkov,Daniel E. Schäffer,Joan Ohayon,Noam Auslander,Steven Jacobson,Paul M. Lieberman
出处
期刊:Nature microbiology
日期:2024-05-28
卷期号:9 (6): 1540-1554
标识
DOI:10.1038/s41564-024-01699-6
摘要
Epstein-Barr virus (EBV) is an aetiologic risk factor for the development of multiple sclerosis (MS). However, the role of EBV-infected B cells in the immunopathology of MS is not well understood. Here we characterized spontaneous lymphoblastoid cell lines (SLCLs) isolated from MS patients and healthy controls (HC) ex vivo to study EBV and host gene expression in the context of an individual's endogenous EBV. SLCLs derived from MS patient B cells during active disease had higher EBV lytic gene expression than SLCLs from MS patients with stable disease or HCs. Host gene expression analysis revealed activation of pathways associated with hypercytokinemia and interferon signalling in MS SLCLs and upregulation of forkhead box protein 1 (FOXP1), which contributes to EBV lytic gene expression. We demonstrate that antiviral approaches targeting EBV replication decreased cytokine production and autologous CD4
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