ObjectiveThe multisystem involvement and high heterogeneity of systemic lupus erythematosus (SLE) lead to great challenges in its diagnosis and treatment. The purpose of this study was to find new lncRNAs in peripheral blood mononuclear cells of SLE patients by transcriptome sequencing and explore their potential as biomarkers and their correlation with clinical features.Materials and MethodsTranscriptome sequencing was used to screen differentially expressed lncRNAs (DELs) and mRNAs (DEMs). The expression of these selected lncRNAs and mRNAs in SLE patients and healthy controls was verified by qPCR. DAVID and WebGestalt were used to perform enrichment analysis. Cytoscape was used to construct a protein–protein network, a coexpression network, and a competitive endogenous RNA network to reveal the regulatory mechanisms of lncRNAs at the transcriptome level.ResultsA total of 1737 DELs and 4078 DEMs were identified between SLE patients and healthy controls. Ten lncRNAs and eight genes were verified by qPCR in a larger sample set. The lncRNA NONHSAT101022.2 was significantly downregulated in SLE patients and was also significantly related to the activity and severity of disease. The upregulated genes were enriched in defense and the immune response, while the downregulated genes were mainly enriched in SLE-related pathways. Topology network analysis revealed that the lncRNAs were involved in regulation at the transcriptome level, including acting directly on mRNA or indirectly affecting gene expression by acting on miRNA.ConclusionIn this work, we identified many mRNAs and novel lncRNAs by transcriptome sequencing. The functions and regulatory mechanisms of these lncRNAs were analyzed by bioinformatic methods. The novel lncRNA NONHSAT101022.2 is significantly downregulated in SLE patients and is significantly related to the activity and severity of disease. Additionally, we propose that NONHSAT101022.2 may enhance the signal transduction of β2-AR by cis regulating LMBRD2, inducing NK cells to produce high levels of IFN-γ and thereby exacerbating SLE.

Background Primary Sjögren’s syndrome (pSS) is a chronic autoimmune disease characterized by abnormal immune cell activation. This study aimed to investigate differentially expressed long non-coding RNA (lncRNA) in peripheral blood mononuclear cells (PBMCs) in patients with pSS to identify lncRNAs that affect pSS pathogenesis. Methods Total RNA was extrated from PBMCs of 30 patients with pSS and 15 healthy persons. Transcriptome sequencing was used to screen differentially expressed lncRNAs and mRNAs in 8 RNA samples from the discovery cohort. The differentially expressed mRNAs underwent functional enrichment analysis. A protein interaction relationship (PPI) and competitive endogenous RNA (ceRNA) network was constructed. Real-time PCR was used to validate screened lncRNAs in all 45 RNA samples.. Results 1180 lncRNAs and 640 mRNAs were differentially expressed in pSS patients (fold change > 2 in healthy persons). The PPI network was constructed with 640 mRNAs and a ceRNA network with four key lncRNAs (GABPB1-AS1, PSMA3-AS1, LINC00847 and SNHG1). Real-time PCR revealed that GABPB1-AS1 and PSMA3-AS1 were significantly up-regulated 3.0- and 1.4-fold in the pSS group, respectively. The GABPB1-AS1 expression level was positively correlated with the percentage of B cells and IgG levels. Conclusions GABPB1-AS1 was significently up-regulated in pSS patients, and its expression level is positively correlated with the percentage of B cells and IgG levels. GABPB1-AS1 may be involved in the pathogenesis of pSS and may be a promising biological marker.

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The objectives of this study are to evaluate whether tapering or stopping strategies of pharmacologic therapies are efficacious for maintaining remission in patients with axial spondyloarthritis (axSPA) and to analyze the risk factors of disease relapse. Patients diagnosed as axSPA with ankylosing spondylitis disease activity score based on C reactive protein (ASDAS-CRP) ≤2.0 for at least 3 months were randomized into three groups: continuing non-steroidal anti-inflammatory drugs (NSAIDs) and disease-modifying antirheumatic drugs (DMARDs) (group 1), tapering NSAIDs and DMARDs by 50% (group 2), or discontinuing NSAIDs and DMARDs (group3) after 6 months of tapering. The primary endpoint of observation was disease relapse or sustained remission till 12 months. One hundred and eight patients were analyzed in this study. All patients fulfilled ASDAS remission criteria at baseline. Other than NSAIDs therapy, 63.0% of the patients received sulfasalazine, 33.3% biological DMARDs, and 19.4% other DMARDs. Overall, 87 patients (80.6%) remained in remission for 12 months, whereas 21 patients (19.4%) relapsed at the end of the study. There were significant differences of relapse rates among three different study groups (group 1, 5.4%; group 2, 13.2%; group 3, 42.7%; p<0.001), while no significant difference was found between group 1 and group 2 (p=0.430). Multivariate logistic regression identified high ASDAS-CRP at baseline (p=0.001) and drug discontinuation (p<0.001) as predictors for relapse. This randomized controlled study demonstrated that tapering NSAIDs and DMARDs by 50% in patients with axSPA in sustained remission is a feasible treatment strategy. Besides, disease relapse may be related with ASDAS-CRP before treatment tapering.