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The etiology of RA has not yet been fully elucidated, but a large number of studies have shown that the initiation of inflammation in RA is closely related to T-cell activation, the production of a variety of pro-inflammatory cytokines, macrophage M1/M2 imbalance, homeostatic imbalance of the intestinal flora, fibroblast-like synoviocytes (FLSs) and synovial tissue macrophages (STMs) in the synovial lumen of joints that exhibit an aggressive phenotype

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