Macrophages suppress T cell responses and arthritis development in mice by producing reactive oxygen species

摘要: Reduced capacity to produce ROS increases the severity of T cell-dependent arthritis in both mice and rats with polymorphisms neutrophil cytosolic factor 1 (Ncf1) (p47phox). Since cells cannot exert oxidative burst, we hypothesized that cell responsiveness is downregulated by produced APCs. Macrophages have highest burst among APCs, so study effect macrophage on activation, developed transgenic expressing functional Ncf1 restricted macrophages. Macrophage-restricted expression restored resistance level wild-type a collagen-induced model but not cell-independent anti-collagen antibody-induced model. activation was skewed toward Th2 mice. In vitro, IL-2 production proliferation were suppressed ROS, irrespective origin. IFN-gamma production, however, independent dependent These effects antigen collagen type II. conclusion, macrophage-derived play role selection, maturation, differentiation, also suppressive thereby mediate protection against autoimmune diseases like arthritis.