krn-7000 and Acute-Kidney-Injury

Although activation of mouse natural killer T (NKT) cells by α-galactosylceramide (α-GalCer) causes failure of multiple organs, including the kidneys, the precise mechanisms underlying kidney injury remain unclear. Here, we showed that α-GalCer-activated mouse NKT cells injured both kidney vascular endothelial cells and tubular epithelial cells in vitro, causing acute kidney injury (AKI) with hematuria in middle-aged mice. The perforin-mediated pathway was mainly involved in glomerular endothelial cell injury, whereas the TNF-α/Fas ligand pathway played an important role in the injury of tubular epithelial cells. Kidney injury in young mice was mild but could be significantly exacerbated if NKT cells were strongly activated by NK cell depletion alone or in combination with IL-12 pretreatment. When stimulated by a combination of IL-2 and IL-12, human CD56

Topics: Acute Kidney Injury; Age Factors; Animals; CD56 Antigen; Cell Line; Coculture Techniques; Cytotoxicity, Immunologic; Endothelial Cells; Epithelial Cells; Fas Ligand Protein; Female; Galactosylceramides; Hematuria; Humans; Kidney Tubules, Proximal; Lymphocyte Activation; Male; Mice, Inbred C57BL; Natural Killer T-Cells; Phenotype; Pore Forming Cytotoxic Proteins; Sex Factors; Signal Transduction; Tumor Necrosis Factor-alpha