To investigate the roles and mechanisms of IL-34-mediated FLS-macrophage crosstalk in osteoclastogenesis-associated bone erosion in rheumatoid arthritis (RA).
Approach:
Key Findings:
Upregulated serum IL-34 levels in RA patients correlate with disease severity and bone erosion.
IL-34 overexpression in FLS promotes proliferation, migration, and invasion while inhibiting apoptosis.
Conditioned medium from IL-34-overexpressing FLS enhances macrophage recruitment and M1 polarization.
rhIL-34-stimulated FLS-macrophage coculture results in higher RANKL production and increased osteoclast differentiation.
IL-34 blockade reduces RA severity, synovial hyperplasia, macrophage M1 polarization, inflammatory infiltration, and bone erosion in CIA mice.
Interpretation:
Limitations:
The study primarily focuses on in vitro and animal models, which may not fully replicate human RA conditions.
Further clinical studies are needed to validate the therapeutic potential of IL-34 blockade in RA patients.
