C3a– C3aR1 –Mediated Interactions Between Fibroblast–Like Synoviocytes and Macrophages Promote the Progression of Rheumatoid Arthritis
Authors' conclusion
Our study suggests that FLS promotes synovial inflammation via interaction with macrophages through a C3a-C3aR1 signaling-mediated positive feedback regulation.
Study context
- Population
- Rheumatoid arthritis (RA) synovium (OA synovium as comparator); Collagen-induced arthritis (CIA) mouse model
- Comparison
- RA synovium vs OA synovium; C3a-C3aR1 signalling blockade in CIA mice
Methodological detailsimaging mass cytometry, single-cell RNA sequencing, CIA mouse model
- Imaging mass cytometry
- Single-cell RNA sequencing
- CIA mouse model
Main finding
As reported in the abstract
- Cellular neighborhoods (CNs) enriched with FLSs and immune cells, particularly FLSs and macrophages, more frequent in RA synovium vs OA
- FLSs specifically up-regulated complement C3; macrophages showed high levels of the C3 receptor C3aR1
- FLS-derived C3a enhanced the type I interferon response in macrophages; C3a-C3aR1 blockade reduced macrophage interferon β secretion, thereby affecting FLS activation
- Inhibition of C3a-C3aR1 signalling attenuated CIA severity, with decreased immune cell infiltration, reduced FLS activation and lessened bone destruction
Original publication
C3a– C3aR1 –Mediated Interactions Between Fibroblast–Like Synoviocytes and Macrophages Promote the Progression of Rheumatoid Arthritis. Arthritis Rheumatol. Published 4 November 2025. doi:10.
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