ArticleFrontiers in immunology2020
B Cell Subsets and Cellular Signatures and Disease Relapse in Lupus Nephritis.
Article in Frontiers in immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Single-Cell Transcriptomic and Metabolic Signatures in Exhausted and Classical Memory B Cells-An Exploratory Analysis in Systemic Lupus Erythematosus and Lupus Nephritis.Biomedicines · 2026Article
- Identification of genetic variants associated with lupus nephritis in a Taiwanese cohort through systematic genetic screening.Scientific reports · 2025Article
- The role of B lymphocyte subsets in nephrotic syndrome: functions, mechanisms, clinical significance and future perspectives.Frontiers in immunology · 2025Review
- Transcription factor BACH1 in cancer: roles, mechanisms, and prospects for targeted therapy.Biomarker research · 2024Review
- Association of Immune-Related Genetic and Epigenetic Alterations with Lupus Nephritis.Kidney diseases (Basel, Switzerland) · 2022Review
- Diagnostic test accuracy of novel biomarkers for lupus nephritis-An overview of systematic reviews.PloS one · 2022Review
- MicroRNA-98-5p inhibits human mesangial cell proliferation and TNF-α and IL-6 secretion by targeting BTB and CNC homology 1.Experimental and therapeutic medicine · 2021Article
- MicroRNAs in Lupus Nephritis-Role in Disease Pathogenesis and Clinical Applications.International journal of molecular sciences · 2021Review
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Renal relapses adversely affect the long-term outcomes of patients with lupus nephritis (LN), but the pathogenic mechanisms remain elusive. B cell signatures of miR-148a, BACH1, BACH2, and PAX5 expression are relevant to the regulation of B lymphocyte homeostasis. It is unknown whether B cell signature is related to the relapse of LN. Methods: We compared B lymphocyte subsets and cellular signatures during disease quiescence between LN patients with multiple relapses (MR, ≥3 LN relapses within 36 months) and those with no relapse (NR). Also, circulating B lymphocytes were isolated from treatment-naïve patients with active LN and treated with antagomir-148a Results: MR patients ( Conclusion: Altered B cell subsets and cellular signatures of miR-148a, BACH1, BACH2, and PAX5 may be associated with distinct patient phenotypes related to the risk of LN relapse.
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