Dendritic cells facilitate accumulation of IL-17 T cells in the kidney following acute renal obstruction.
Dendritic cells facilitate accumulation of IL-17 T cells in the kidney following acute renal obstruction.
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DOI：
10.1038/ki.2008.394
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发表时间：
2008-11
影响因子：
19.6
通讯作者：
Griffin, Matthew D.
中科院分区：
文献类型：
--
作者：
Dong, Xiangyang;Bachman, Lori A.;Miller, Melinda N.;Nath, Karl A.;Griffin, Matthew D.
急性尿路梗阻可引起间质炎症，伴有白细胞聚集和可溶性介质的分泌。单侧输尿管结扎导致梗阻后24-72小时肾脏F4/80+和F4/80−树突状细胞、单核细胞、中性粒细胞和T细胞进行性增加。氯膦酸盐预处理使树突状细胞耗尽，表明这些细胞是梗阻肾中肿瘤坏死因子和其他促炎介质的最有效来源。F4/80+树突状细胞和T细胞共同分布于梗阻肾皮质髓质交界处和皮质。梗阻肾脏T细胞的细胞因子分泌模式和表面表型包括分泌干扰素γ的CD_4~+和CD_8~+记忆T细胞和分泌IL-17的CD_4~+记忆T细胞。在结扎前清除肾内树突状细胞并没有减少梗阻肾脏中的T细胞，但减弱了干扰素-γ和IL-17能力的T细胞。我们的研究表明，肾内树突状细胞是急性尿路梗阻后早期未知的促炎介质来源，在包括分泌IL-17的CD4+T细胞在内的效应记忆T细胞的募集和激活中发挥着特殊的作用。
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.
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影响因子：
32.4
作者：
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通讯作者：
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影响因子：
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作者：
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