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在慢性牙周炎病变中,IL-23 产生的 CD68(+) 巨噬细胞样细胞在 IL-17 极化浸润中占优势。

IL-23-producing CD68(+) macrophage-like cells predominate within an IL-17-polarized infiltrate in chronic periodontitis lesions.

机构信息

Department of Dermatology and Allergy, University of Bonn, Germany.

出版信息

J Clin Periodontol. 2011 Oct;38(10):879-86. doi: 10.1111/j.1600-051X.2011.01752.x. Epub 2011 Aug 31.

DOI:10.1111/j.1600-051X.2011.01752.x
PMID:21883359
Abstract

AIM

To analyse antigen-presenting cells (APCs), such as dendritic cells (DCs), macrophages (Mo) or B cells depending on the regional site of chronic periodontitis (CP), and to investigate their relation to Th17 cells.

MATERIAL AND METHODS

Biopsies from oral mucosa as well as the coronal and bottom regions of CP were analysed by immunhistochemistry, immunofluorescence, flow cytometry and real-time PCR.

RESULTS

A predominance of CD68(+) Mo-like cells and CD20(+) B cells and strong Th17 infiltration was observed in the bottom region of CP lesions, while CD1a(+) DCs were only detected in the coronal regions, where Th17 infiltration was low. Furthermore, CD68(+) Mo-like cells displayed CD163 expression as a typical Mo-marker, but expressed in parallel typical DCs markers, such as CD11c or CD209 and TLR4. Interestingly, Th17-inducing cytokine IL-23p19 was produced by CD68(+) Mo-like cells, but not CD20(+) B cells. Moreover, the stimulation of in vitro generated CD68(+) Mo-like cells by Porphyromonas gingivalis-derived (Pg) lipopolysaccharide resulted in the upregulation of their IL-23p19 mRNA expression, which was inhibited by the blockage of TLR4.

CONCLUSIONS

In view of these data, a picture emerges that IL-17-producing cells in CP could be in part directed by CD68(+) Mo-like cells, which produce IL-23p19 upon TLR4 activation by Pg.

摘要

目的

分析抗原呈递细胞(APC),如树突状细胞(DC)、巨噬细胞(Mo)或 B 细胞,具体取决于慢性牙周炎(CP)的区域性部位,并研究它们与 Th17 细胞的关系。

材料和方法

通过免疫组织化学、免疫荧光、流式细胞术和实时 PCR 分析口腔黏膜以及 CP 的冠部和底部区域的活检样本。

结果

CP 病变底部区域观察到 CD68(+)Mo 样细胞和 CD20(+)B 细胞的优势以及强烈的 Th17 浸润,而 CD1a(+)DC 仅在冠部区域检测到,那里的 Th17 浸润较低。此外,CD68(+)Mo 样细胞显示 CD163 表达作为典型的 Mo 标志物,但同时表达典型的 DC 标志物,如 CD11c 或 CD209 和 TLR4。有趣的是,Th17 诱导细胞因子 IL-23p19 由 CD68(+)Mo 样细胞产生,而不是由 CD20(+)B 细胞产生。此外,牙龈卟啉单胞菌(Pg)衍生的脂多糖(LPS)体外刺激 CD68(+)Mo 样细胞导致其 IL-23p19 mRNA 表达上调,该表达被 TLR4 阻断所抑制。

结论

鉴于这些数据,CP 中的 IL-17 产生细胞可能部分由 CD68(+)Mo 样细胞指导,这些细胞在 TLR4 被 Pg 激活时产生 IL-23p19。

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