This mechanism may at least partly explain previous studies showing that CX3CR1 deficiency or blockade alleviated inflammation and fibrosis in ischemia-reperfusion injury (44), hypertensive interstitial fibrosis (45) and crescentic glomerulonephritis (21); also, susceptibility of CX3CR1-deficient mice to renal Candida albicans infection (46) and to sepsis-induced kidney damage (47) could be due to a defect of macrophage formation. This evidence concerns the gene CX3CR1 and Sepsis.