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Background: The complement system is a major component of innate immunity and plays a vital role in experimental models of autoimmune pathogenesis. In patients with rheumatoid arthritis (RA), local activations of the complement pathways in the synovium will interact with macrophages and other synovial mesenchymal cells. However, it remains to be determined how specific complement components in the RA synovium modulate cell type functions to strengthen phagocytosis and inflammation resolution.

Methods: We have classified the spectrum of RA biopsies into six inflammatory phenotypes named CTAPs (Cell Type Abundance Phenotypes) using a comprehensive synovial single-cell multimodal cell atlas (> 314,000 cells, 70 RA patients) generated from NIH-funded AMP RA/SLE consortium. In this study, we linked complement activation pathways with cell-type heterogeneity and tested significant …