Platelets release mitochondrial antigens in systemic lupus erythematosus.

摘要: The accumulation of DNA and nuclear components in blood their recognition by autoantibodies play a central role the pathophysiology systemic lupus erythematosus (SLE). Despite efforts, sources circulating autoantigens SLE are still unclear. Here, we show that SLE, platelets release mitochondrial DNA, majority which is associated with extracellular organelle. Mitochondrial patients correlates platelet degranulation. This process requires stimulation FcγRIIA, receptor for immune complexes. Because mice lack FcγRIIA murine completely devoid capable binding IgG-containing complexes, used transgenic expressing our vivo investigations. expression lupus-prone led to recruitment kidneys mitochondria vivo. Using reporter mouse red fluorescent protein targeted mitochondrion, confirmed as source driven its cosignaling fibrinogen α2bβ3 These findings suggest might be key antigens therapeutic target treating SLE.