Macrophage metabolic exhaustion and PANoptotic cell death drive chronic tissue inflammation in rheumatoid arthritis

In the autoimmune disease rheumatoid arthritis, the inflammatory response evolves from protective to pathogenic, causing tissue destruction. Rheumatoid synovitis persists despite the presence of pro-repair SELENOP^hiMerTK⁺CD206⁺ macrophages, suggesting that these cells acquire pro-arthritogenic functions. Patient-derived synovial SELENOP^hiMerTK⁺CD206⁺ macrophages produced high concentrations of the complement component C1q and conc