In addition, when DC from NOX2-deficient mice serve as APC, T cells produce more IL-17 after activation by toxic shock syndrome toxin-1 (TSST-1) (121); however, research into SKG mice (a spontaneous arthritis animal model caused by ZAP70 mutation) indicates that Ncf1 mutation-related ROS deficiency does not exhibit further alteration of T-cell activation or differentiation profile because of ZAP70 mutation, while transgenic restoration of functional Ncf1 in macrophages modified the arthritis in Ncf1-mutated SKG mice to the state observed in ROS-sufficient SKG mice. This evidence concerns the gene IL17A and arthritic joint disease.