ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2025
Target Fibroblast-B cell crosstalk via MIF signaling drives pathogenic B cell differentiation and joint damage in knee osteoarthritis.
Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Multi-Omics Integration Identifies PTGS2 as a Candidate Diagnostic Biomarker and Precise Therapeutic Target Related to Schisandra chinensis for Osteoarthritis.Chemical biology & drug design · 2026Article
- The vicious cycle from inflammation to pyroptosis: the core role of macrophage polarization imbalance in the pathogenesis of knee osteoarthritis.Molecular biology reports · 2026Review
- APOA4 Protects Chondrocytes and Modulates Wnt Signaling in Osteoarthritis.Journal of inflammation research · 2026Article
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Authors and funding
11 authors.
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Abstract
backgroundB cells play a critical role in knee osteoarthritis (KOA), however, the heterogeneity, activation mechanisms, and their contribution to cartilage damage in KOA joints are still not fully understood.
methodsWe performed single-cell RNA sequencing (scRNA-seq) on joint tissues from 9 healthy controls and 21 KOA patients, integrating transcriptomic profiling, pseudotime trajectory analysis, and ligand-receptor interaction mapping. Key findings were validated using immunohistochemistry, Western blotting, in vitro co-culture systems, and a murine KOA model induced by anterior cruciate ligament transection and destabilization of the medial meniscus (ACLT + DMM).
resultsscRNA-seq analysis identified 31 cell clusters, with B cells showing marked enrichment in subchondral bone and synovium of KOA joints, particularly in older and female patients. Re-clustering of B cells revealed eight distinct subgroups, including pathogenic DERL3
conclusionThis study unveils a fibroblast-B cell crosstalk axis mediated by MIF signaling in KOA pathogenesis. Targeting MIF signaling may represent a promising therapeutic strategy to mitigate B cell-associated joint inflammation and structural alterations in KOA.
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