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Войти в исследования Scandinavian journal of rheumatology · 2026
Therapeutic potential of interleukin-33 blockade in mitigating synovial inflammation and cartilage damage.
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Feng Y, Wu S, Li D, Jiang Y, Liu X
Аннотация
OBJECTIVE: To investigate the therapeutic potential of anti-interleukin-33 (anti-IL-33) in a collagen-induced arthritis (CIA) model and its biological effects on the aggressive phenotype of rheumatoid arthritis fibroblast-like synoviocytes (RA-FLSs).
METHOD: The CIA model was established in DBA/1 mice, which were treated with anti-IL-33, methotrexate, or vehicle. Arthritis severity was monitored via clinical scoring. Joint histopathology, cartilage damage, bone erosion, and synovial cell proliferation were assessed using H&E staining, Safranin O-fast green staining, and micro-computed tomography (micro-CT), respectively. In vitro, human RA-FLSs were stimulated with tumour necrosis factor-α (TNF-α) and treated with anti-IL-33. Cell proliferation, apoptosis, cell-cycle distribution, migration, invasion, and IL-6 production were evaluated using the 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl-tetrazolium (MTT) assay, immunofluorescence assay, flow cytometry, terminal deoxynucleotidyl transferase dUTP nick end labelling (TUNEL), Transwell assays, and enzyme-linked immunosorbent assay.
RESULTS: Anti-IL-33 treatment significantly attenuated the clinical severity of arthritis and delayed disease progression in CIA mice. Histological and micro-CT analyses revealed that IL-33 blockade reduced synovial inflammation, pannus formation, and bone destruction, while preserving cartilage. In vitro, anti-IL-33 suppressed the proliferation, migration, and invasion of TNF-α-stimulated RA-FLSs. Furthermore, it promoted apoptosis, induced cell-cycle arrest at the G1 phase, and significantly down-regulated the secretion of the pro-inflammatory cytokine IL-6.
CONCLUSION: IL-33 blockade effectively mitigates synovial inflammation and joint destruction by suppressing the proliferation, migration, and invasion of RA-FLSs while promoting their apoptosis. Targeting IL-33 may represent a promising strategy for the treatment of rheumatoid arthritis.
METHOD: The CIA model was established in DBA/1 mice, which were treated with anti-IL-33, methotrexate, or vehicle. Arthritis severity was monitored via clinical scoring. Joint histopathology, cartilage damage, bone erosion, and synovial cell proliferation were assessed using H&E staining, Safranin O-fast green staining, and micro-computed tomography (micro-CT), respectively. In vitro, human RA-FLSs were stimulated with tumour necrosis factor-α (TNF-α) and treated with anti-IL-33. Cell proliferation, apoptosis, cell-cycle distribution, migration, invasion, and IL-6 production were evaluated using the 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl-tetrazolium (MTT) assay, immunofluorescence assay, flow cytometry, terminal deoxynucleotidyl transferase dUTP nick end labelling (TUNEL), Transwell assays, and enzyme-linked immunosorbent assay.
RESULTS: Anti-IL-33 treatment significantly attenuated the clinical severity of arthritis and delayed disease progression in CIA mice. Histological and micro-CT analyses revealed that IL-33 blockade reduced synovial inflammation, pannus formation, and bone destruction, while preserving cartilage. In vitro, anti-IL-33 suppressed the proliferation, migration, and invasion of TNF-α-stimulated RA-FLSs. Furthermore, it promoted apoptosis, induced cell-cycle arrest at the G1 phase, and significantly down-regulated the secretion of the pro-inflammatory cytokine IL-6.
CONCLUSION: IL-33 blockade effectively mitigates synovial inflammation and joint destruction by suppressing the proliferation, migration, and invasion of RA-FLSs while promoting their apoptosis. Targeting IL-33 may represent a promising strategy for the treatment of rheumatoid arthritis.