ArticleRMD open2024
Induction of interleukin 21 receptor expression via enhanced intracellular metabolism in B cells and its relevance to the disease activity in systemic lupus erythematosus.
Article in RMD open, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Article
- GLUT1-mediated glucose flux constrains autoreactive but not foreign antigen-specific B-cell responses.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- Early-onset CLL is characterized by enhanced microenvironment-driven metabolic fitness, increased proliferative bias, and accelerated disease progression.Frontiers in immunology · 2026Article
- Immune regulation and cell metabolism in B cell subsets in patients with systemic lupus erythematosus.Frontiers in immunology · 2026Review
- Immunometabolic dysregulation in autoimmune rheumatic diseases: the central role of glycolytic reprogramming in pathogenesis and traditional Chinese medicine therapy.Frontiers in immunology · 2026Review
- Glucose metabolic reprogramming in systemic lupus erythematosus and lupus nephritis: theoretical foundations and therapeutic implications.Frontiers in immunology · 2026Review
- Validation and Functional Exploration of Exosome-Derived ITGA9-AS1 and WNT5A-AS1 as Candidate Diagnostic Biomarkers for Schizophrenia.Neuropsychiatric disease and treatment · 2026Article
Corrections and comments
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Authors and funding
14 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveTo elucidate the association between the changes in intracellular metabolism in the early stage of B cell activation and systemic lupus erythematosus (SLE) pathogenesis.
methodsCD19
resultsStimulation with CpG (Toll-like receptor 9 (TLR9) ligand) in vitro induced enhanced interleukin 21 (IL-21) receptor expression in CD19
conclusionIL-21R mRNA-GAPDH binding dissociation associated with rapid glycolytic enhancement by the TLR9 ligand in B cells may induce plasmocyte differentiation through IL-21 signals and be involved in exacerbating SLE.
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Registered trials
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