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Identification of novel genes associated with dysregulation of B cells in patients with primary Sjogren's syndrome.

ABSTRACT: BACKGROUND:The aim of this study was to identify the molecular mechanism of dysregulation of B cell subpopulations of primary Sjögren's syndrome (pSS) at the transcriptome level. METHODS:We enrolled patients with pSS (n?=?6) and healthy controls (HCs) (n?=?6) in the discovery cohort using microarray and pSS (n?=?14) and HCs (n?=?12) in the validation cohort using quantitative PCR (qPCR). Peripheral B cells acquired from these subjects were separated by cell sorting into four subsets: CD38-IgD+ (Bm1), CD38+IgD+ (naive B cells), CD38highIgD+ (pre-germinal centre B cells) and CD38±IgD- (memory B cells). We performed differentially expressed gene (DEG) analysis and weighted gene co-expression network analysis (WGCNA). RESULTS:Expression of the long non-coding RNA LINC00487 was significantly upregulated in all B cell subsets, as was that of HLA and interferon (IFN) signature genes. Moreover, the normalized intensity value of LINC00487 significantly correlated with the disease activity score of all pSS B cell subsets. Studies of human B cell lines revealed that the expression of LINC00487 was strongly induced by IFN?. WGCNA revealed six gene clusters associated with the B cell subpopulation of pSS. Further, SOX4 was identified as an inter-module hub gene. CONCLUSION:Our transcriptome analysis revealed key genes involved in the dysregulation of B cell subpopulations associated with pSS. TRIAL REGISTRATION:Not required.


PROVIDER: S-EPMC7310138 | BioStudies | 2020-01-01

REPOSITORIES: biostudies

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