ArticleImmunity, inflammation and disease2023
PRMT5 participates in B cell overactivation in patients with primary Sjogren's syndrome (pSS) through RSAD2-mediated NF-κB signaling.
Article in Immunity, inflammation and disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 4 papers, 1 of them a synthesis that pooled it.
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Who cites it
4 citing papers in PubMed, 1 synthesis or guideline pooled it, 5 citations in OpenAlex.
- The role of microRNAs in Kawasaki disease: a systematic review.European journal of pediatrics · 2026Pooled it
- Unraveling the inflammatory bridge: genomic evidence identifies TNFRSF9 as a potential biomarker linking Sjögren's syndrome to total risk non-Hodgkin lymphoma.Clinical rheumatology · 2026Article
- Sjögren's Syndrome: Epidemiology, Classification Criteria, Molecular Pathogenesis, Diagnosis, and Treatment.MedComm · 2025Review
- PRMT5 participates in B cell overactivation in patients with primary Sjogren's syndrome (pSS) through RSAD2-mediated NF-κB signaling.Immunity, inflammation and disease · 2023Article
Corrections and comments
- Retracted
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
objectiveThere are new evidences that protein arginine methyltransferase 5 (PRMT5) is widely involved in the progression of various diseases, but its effect is unclear on Primary Sjogren's syndrome (pSS). The main purpose of this study is to explore the regulatory effect of PRMT5 on pSS and its potential mechanisms.
methodsCD40L treated CD19 + B cells to construct a cell model of pSS. CCK-8 assay and Annexin V-FITC/PI kits were used to measure cell proliferation and apoptosis. ELISA assay was used to determine the contents of IL-6 and TNF-α in CD19 + B cells. And commercial kits were used to detect the levels of immunoglobins (IgG, IgM, and IgA) in CD40L-treated CD19 + B cells. And successfully constructed a pSS mouse model.
resultsThe results revealed an increase in the expression of PRMT5 in CD19 + B cells from patients with pSS. After CD40L treatment, the knockdown of PRMT5 prominently decreased cell viability, the production level of immunoglobulins (IgG, IgM, and IgA), and the content of IL-10, increased the content of IL-6 and IL-8, and promoted the apoptosis of pSS CD19 + B cells. Mechanistically, PRMT5 negatively regulated the RSAD2 and nuclear factor kappa-B (NF-κB) signaling pathway. Furthermore, overexpression of RSAD2 and p65 significantly rescued the effect of PRMT5 knockdown on proliferation, immunoglobin production and secreting cytokines in CD40L-treated CD19 + B cells. More importantly, inhibition of PRMT5 significantly inhibited the symptoms of pSS mice.
conclusionsLow-expression of PRMT5 through inactivation of RSAD2/NF-κB signalling pathway alleviates the hyperactivity of B cells, which may provide theoretical basis and potential therapeutic targets for clinical treatment of pSS.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.