ArticleInflammation2025
SYK Activation Enhances Dendritic Cell Functions in Spontaneous Rheumatoid Arthritis.
Article in Inflammation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Defective autophagy in diabetic nephropathy sensitizes podocytes to hyperuricemia induced injury by amplifying inflammasome activation.Clinical and experimental nephrology · 2026Article
- Dapagliflozin mitigates acute pancreatitis induced by L-arginine in Rats through modulation of TLR-4/NF-κB/NLRP3 pathway: integrated biochemical, histopathological, and in silico study.Inflammopharmacology · 2026Article
- Repurposing Product Nkabinde for Hepatitis B Virus Therapy: A Network Pharmacology and Molecular Docking Investigation.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Pathological mechanisms and treatment strategies for immune checkpoint inhibitor-associated myocarditis: insights from single-cell sequencing.Basic research in cardiology · 2026Review
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
The pathogenesis of rheumatoid arthritis (RA) involves an aberrant number and/or activation of dendritic cells (DCs) within the synovial microenvironment. Targeting synovial DCs represents an attractive approach for the treatment of RA. Spleen tyrosine kinase (SYK), a pivotal molecule in immune cell receptor signaling pathways, is known to play a critical role in RA progression. However, the impact of SYK on DC biology under RA-specific pathological conditions remains incompletely understood. In this study, we employed a spontaneous RA mouse model carrying a gain-of-function SYK variant (SYKS544Y) to investigate the effects of SYK activation on DCs. Our findings demonstrate that SYK activation promotes the expansion of the DCs population (CD11C+MHCII+), particularly the CD11C+MHCII+CD11B+CD8a− subtype, in blood, spleen, and ankle. Furthermore, SYK activation enhances DC maturation and endocytosis by upregulating CD40 and CD86. Additionally, bone-marrow-derived DCs from SYKS544Y mice exhibit increased T-cell proliferative activity. Collectively, these results suggest that gain-of-function SYK may contribute to RA pathogenesis by promoting DC expansion and maturation, thereby modulating immune responses in the synovial environment.
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Registered trials
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