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Dong, XY,Bachman, LA,Miller, MN,Nath, KA,Griffin, MD
2008
November
Kidney International
Dendritic cells facilitate accumulation of IL-17 T cells in the kidney following acute renal obstruction
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obstructive nephropathy inflammation dendritic cells T cells tumor necrosis factor interleukin 17 ISCHEMIA-REPERFUSION INJURY MONOCYTE CHEMOATTRACTANT PROTEIN-1 UNILATERAL URETERAL OBSTRUCTION ISCHEMIA/REPERFUSION INJURY TNF-ALPHA FUNCTIONAL-CHARACTERIZATION MOLECULAR-MECHANISMS TUBULAR CELLS GENE-THERAPY FAILURE
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Acute urinary obstruction causes interstitial inflammation with leukocyte accumulation and the secretion of soluble mediators. Here we show that unilateral ureteral ligation caused a progressive increase in renal F4/80(+) and F4/80(-) dendritic cells, monocytes, neutrophils and T-cells 24-72 h following obstruction. Depletion of dendritic cells by clodronate pretreatment showed these cells to be the most potent source of tumor necrosis factor and other pro-inflammatory mediators in the obstructed kidney. F4/80(+) dendritic cells and T-cells co-localized in the cortico-medullary junction and cortex of the obstructed kidney. Cytokine secretion patterns and surface phenotypes of T-cells from obstructed kidneys were found to include interferon-gamma-secreting CD4(+) and CD8(+) memory T-cells as well as interleukin 17 (IL-17)-secreting CD4(+) memory T-cells. Depletion of the intra-renal dendritic cells prior to ligation did not numerically reduce T-cells in obstructed kidneys but attenuated interferon-gamma and IL-17-competent T-cells. Our study shows that intra-renal dendritic cells are a previously unidentified early source of proinflammatory mediators after acute urinary obstruction and play a specific role in recruitment and activation of effector-memory T-cells including IL-17-secreting CD4(+) T-cells.
DOI 10.1038/ki.2008.394
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