In mouse SLE models, short-term ischemia/reperfusion injury of convoluted tubule epithelial cells has been shown to induce colony-stimulating factor 1 (CSF-1) production and cause an M1/M2 macrophage imbalance with a predominance of proinflammatory phenotype (M1-like) in lupus-resistant mice (MRL-Faslpr) and M2-like phenotype in lupus-susceptible mice (Sle 123), resulting in impaired tissue regeneration and accelerating the progression of lupus nephritis [64]. Here, CSF1 is linked to lupus nephritis.