Apart from previously proposed mechanisms contributing to lupus susceptibility in NCF1-deficient mice, we suggest another mechanism that intrinsic ROS produced by pDCs limit AKT/mTOR-dependent pDC generation, CCR2-mediated tissue accumulation, and pDC hyperactivation through type I IFN signaling, thereby protecting against lupus development. This evidence concerns the gene CCR2 and systemic lupus erythematosus.