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The extracellular citrulline autoantigen present in the joints of RA patients is mainly derived from the increased NET, which can cause the inflammatory response of synovial fibroblasts in patients and release a series of inflammatory mediators (such as pro-inflammatory cytokines, adhesion molecules and chemokines) to drive the progression of RA (205)
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Genetically modified Glp1r / mice displayed greater levels of epithelial damage in comparison to wild-type (WT) mice following inflammatory stimulation
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