Periglomerular accumulation of dendritic cells in rat crescentic glomerulonephritis.
Periglomerular accumulation of dendritic cells in rat crescentic glomerulonephritis.
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DOI：
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发表时间：
2007-05
影响因子：
3.4
通讯作者：
H. Fujinaka;M. Nameta;P. Kovalenko;Asako Matsuki;Nobutaka Kato;G. Nishimoto;Y. Yoshida;Eishin Yaoita-Eis
中科院分区：
文献类型：
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作者：
H. Fujinaka;M. Nameta;P. Kovalenko;Asako Matsuki;Nobutaka Kato;G. Nishimoto;Y. Yoshida;Eishin Yaoita-Eis
在WKY大鼠抗肾小球基底膜（anti-GBM）新月体肾小球肾炎（GN）过程中，观察到肾小球和肾小球周围肾小球中主要组织相容性复合物（MHC）II类阳性细胞（OX-6+细胞）数量增加。本研究旨在证明肾小球周围OX-6+细胞是树突状细胞（DC），并阐明其在该GN发病机制中的作用。方法采用免疫组织化学方法对OX-6和大鼠DC标记物OX-62进行染色，免疫电镜观察肾小球周围OX-6+细胞。采用逆转录聚合酶链反应（RT-PCR）和原位杂交检测肾组织CXCL 12 mRNA的表达，采用原位杂交检测肾组织IL-1 β mRNA的表达。结果免疫组化显示肾小球周围OX-6+细胞大多数为艾德-1阴性。OX-62+细胞在正常肾组织中稀疏分布，在肾小球周围的肾小球中更常见。免疫电镜证实OX-6+艾德-1-细胞具有DC形态。RT-PCR显示病变肾小球中CXCL 12 mRNA表达增加。原位杂交结果显示，CXCL 12 mRNA表达的肾小球细胞为壁上皮细胞和脏层上皮细胞，与OX-6阳性细胞定位位置接近。原位杂交显示肾小球周围细胞表达IL-1 β mRNA。结论：OX-6+艾德-1- DCs在WKY大鼠抗GBM新月体肾炎肾小球周围分布。这些DC可能被CXCL 12聚集在肾小球周围的肾小球中，并通过产生IL-1 β而参与肾小球肾炎的发生和发展。
BACKGROUND An increased number of major histocompatibility complex (MHC) class II-positive cells (OX-6+ cells) were observed in the glomerulus and periglomerular interstitium during the course of anti-glomerular basement membrane (anti-GBM) crescentic glomerulonephritis (GN) in WKY rats. This study aimed to demonstrate that periglomerular OX-6+ cells are dendritic cells (DCs) and to clarify their roles in the pathogenesis of this GN. METHODS Kidney sections were stained with the OX-6 and the rat DC marker OX-62 by immunohistochemistry, and periglomerular OX-6+ cells were observed by immunoelectron microscopy. Renal mRNA expression for CXCL12 was examined by reverse transcriptase polymerase chain reaction (RT-PCR) and in situ hybridization, and that for IL-1beta was examined by in situ hybridization. RESULTS Immunohistochemistry revealed that most periglomerular OX-6+ cells in this GN were ED-1-negative. OX-62+ cells were observed sparsely in normal kidney interstitium, and considerably more frequently in periglomerular interstitium in this GN. Immunoelectron microscopy confirmed the periglomerular OX-6+ED-1- cells had DC morphology. The increased expression of CXCL12 mRNA in the diseased glomerulus was shown by RT-PCR. By in situ hybridization, CXCL12 mRNA-expressing glomerular cells were the parietal and visceral epithelial cells, which were close to the site of periglomerular OX-6+ cell localization. The intense expression of IL-1beta mRNA by periglomerular cells was demonstrated by in situ hybridization. CONCLUSIONS The periglomerular distribution of OX-6+ED-1- DCs was demonstrated in anti-GBM crescentic GN in WKY rats. These DCs might be accumulated in periglomerular interstitium by CXCL12, and play a role in the initiation and progression of this GN by producing IL-1beta.