Tumor Necrosis Factor–Induced Neuropilin‐2 in Fibroblast‐Like Synoviocytes Exacerbates Rheumatoid Arthritis
Authors' conclusion
TNF-induced NRP2 drives inflammatory persistence in RA and serves as a promising diagnostic biomarker.
Study context
- Population
- Patients with rheumatoid arthritis (RA), patients with osteoarthritis (OA) and healthy volunteers; NRP2 knockout mice with serum-transfer-induced arthritis (STIA); RA-FLS
- Comparison
- RA vs OA and healthy volunteers (NRP2 levels); NRP2 knockout vs wild-type in STIA models
- Healthy volunteersn = 30reference
- OAn = 20
Methodological detailshuman serum, synovial fluid and synovial tissue, systemic and conditional NRP2 knockout mice, serum-transfer-induced arthritis models, siRNA knockdown in RA-FLS, chromatin immunoprecipitation sequencing (ChIP-seq)
- Human serum, synovial fluid and synovial tissue
- Systemic and conditional NRP2 knockout mice
- Serum-transfer-induced arthritis models
- siRNA knockdown in RA-FLS
- ChIP-seq
Main finding
As reported in the abstract
- NRP2 levels in RA serum (n = 76) elevated and correlated with disease activity
- Tumor necrosis factor (TNF) up-regulated NRP2 expression in fibroblast-like synoviocytes (FLS) via transcription factor p65
- Elevated NRP2 amplified local inflammation and tissue damage by increasing FLS proliferation and promoting release of cytokines, chemokines and matrix metalloproteinases (MMPs)
- Systemic and conditional NRP2 knockout alleviated joint inflammation and damage in STIA models
- NRP2-mediated inflammatory regulation derived primarily from α+THY1+ subset within synovial sublining layer
Original publication
Tumor Necrosis Factor–Induced Neuropilin‐2 in Fibroblast‐Like Synoviocytes Exacerbates Rheumatoid Arthritis. Arthritis Rheumatol. Published 17 February 2026. doi:10.
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