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Recent studies have suggested a critical role of glucocorticoid-induced tumor necrosis factor receptor (TNFR) family-related protein (GITR) in the pathogenesis of autoimmune arthritis, but the underlying mechanisms by which GITR activation promotes arthritic progression remain largely unclear.In this study, we found that CIA mice treated with the ligand of GITR (GITRL) displayed an earlier onset of arthritis with markedly increased severity of arthritic symptoms and joint damage, in which significantly increased Th17 cells in spleen and draining lymph nodes (DLNs) were observed.