Spondyloarthritis & psoriatic arthritis
Interleukin-33 drives abnormal bone remodeling in ankylosing spondylitis via inhibition of osteoclast differentiation
Authors' conclusion
These findings demonstrate that IL-33 is a key mediator that links systemic inflammation to local enthesopathy and pathological bone formation in patients with AS.
Study context
- Population
- Patients diagnosed with ankylosing spondylitis (AS) and healthy controls (HCs); surgically harvested human enthesis tissues; curdlan-treated SKG mice to mimic AS
- Comparison
- Patients with AS vs HCs; anti-IL-33 neutralizing antibodies in curdlan-treated SKG mice
Methodological detailshuman serum, enthesis tissue and primary enthesis cells, curdlan-treated SKG mouse model, bulk RNA sequencing and Western blotting, osteoblast and osteoclast differentiation assays
- Human serum, enthesis tissue and primary enthesis cells
- Curdlan-treated SKG mouse model
- Bulk RNA sequencing and Western blotting
- Osteoblast and osteoclast differentiation assays
Main finding
As reported in the abstract
- Serum IL-33 significantly elevated in AS with high inflammatory burden; positively correlated with tumor necrosis factor (TNF), IL-17A and radiographic progression
- IL-33 expression in AS enthesis tissues and primary cells markedly higher than in HCs
- Synergistic TNF + IL-17A stimulation significantly upregulated IL-33 at transcriptomic and protein levels, particularly in AS enthesis cells
- Anti-IL-33 significantly attenuated clinical arthritis severity, enthesitis scores and enthesophyte formation in a mouse model of AS
- IL-33 significantly inhibited osteoclastogenesis by suppressing p38 MAPK-NFATc1 signalling in osteoclast precursors
Original publication
Interleukin-33 drives abnormal bone remodeling in ankylosing spondylitis via inhibition of osteoclast differentiation. Joint Bone Spine. Published 21 July 2026. doi:10.
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