Our data from FACS also showed that HMGB1 might upregulate CD3+CD8−IL-17+T cells in RA patients, and also in our in vitro study, we observed that HMGB1 directly acted on CD4+ T cells to enhance IL-17 production following activation by CD3 and CD28 mAbs, which was consistent with our recent report [33]. Here, CD4 is linked to rheumatoid arthritis.