Dendritic cells facilitate accumulation of IL-17 T cells in the kidney following acute renal obstruction

Xiangyang Dong, Lori A. Bachman, Melinda N. Miller, Karl A. Nath, Matthew D. Griffin

Research output: Contribution to journalArticle

70 Scopus citations

Abstract

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-γ-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-γ 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.

Original languageEnglish (US)
Pages (from-to)1294-1309
Number of pages16
JournalKidney international
Volume74
Issue number10
DOIs
StatePublished - Nov 2008

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Keywords

  • Dendritic cells
  • Inflammation
  • Interleukin 17
  • Obstructive nephropathy
  • T cells
  • Tumor necrosis factor

ASJC Scopus subject areas

  • Nephrology

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