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Objective
We analyzed the impact of amino acid (AA) availability on the inflammatory response in arthritis.
Methods
We stimulated rheumatoid arthritis (RA) fibroblast‐like synoviocytes (FLSs) with tumor necrosis factor (TNF) in the presence or absence of proteinogenic AAs and measured their response by QuantSeq 3′ messenger RNA sequencing, quantitative polymerase chain reaction, and enzyme‐linked...
Accumulating evidence suggests that metabolic master regulators, including mTOR, regulate adaptive and innate immune responses. Resident mesenchymal tissue components are increasingly recognized as key effector cells in inflammation. Whether mTOR also controls the inflammatory response in fibroblasts is insufficiently studied. Here, we show that TNF signaling co-opts the mTOR pathway to shift synovial...
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