Amino Acids Fueling Fibroblast‐Like Synoviocyte Activation and Arthritis By Regulating Chemokine Expression and Leukocyte Migration
Authors' conclusion
AA deprivation reduces the severity of arthritis by suppressing the expression of IRF1-STAT1-driven chemokines, which are crucial for leukocyte recruitment to the arthritic joint.
Study context
- Population
- Rheumatoid arthritis (RA) fibroblast-like synoviocytes and mice with K/BxN serum transfer arthritis
- Comparison
- Amino acid (AA) availability vs AA deprivation in tumor necrosis factor (TNF)-stimulated RA FLSs; low-protein vs normal diet in mice
Methodological detailsin vitro FLS stimulation, K/BxN serum transfer arthritis mouse model
- In vitro FLS stimulation
- K/BxN serum transfer arthritis mouse model
Main finding
As reported in the abstract
- AA deprivation decreased expression of a specific gene subset, incl. chemokines CXCL10, CCL2 and CCL5, in TNF-stimulated FLSs
- AAs required for TNF-induced activation of an IRF1-STAT1 signalling circuit driving chemotactic factor expression
- IRF1 and IRF1-dependent gene set expression in FLSs highly correlated with presence of inflammatory cells in human RA
- Low-protein diet mice expressed less IRF1 in inflamed synovium and developed reduced clinical and histologic signs of arthritis
Original publication
Amino Acids Fueling Fibroblast‐Like Synoviocyte Activation and Arthritis By Regulating Chemokine Expression and Leukocyte Migration. Arthritis Rheumatol. Published 17 January 2024. doi:10.
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