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单核细胞亚群在巨细胞动脉炎免疫病理学中的作用。

Involvement of Monocyte Subsets in the Immunopathology of Giant Cell Arteritis.

机构信息

Department of Rheumatology and Clinical Immunology, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.

Department of Pathology and Medical Biology, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.

出版信息

Sci Rep. 2017 Jul 26;7(1):6553. doi: 10.1038/s41598-017-06826-4.

DOI:10.1038/s41598-017-06826-4
PMID:28747747
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5529580/
Abstract

Monocytes/macrophages are critical in systemic and local inflammation in giant cell arteritis (GCA) and possibly in clinically overlapping polymyalgia rheumatica (PMR). Therefore, we aimed to understand the contribution of monocyte subsets and the CX3CR1-CX3CL1 and CCR2-CCL2 migratory pathways, to the pathology of GCA. Peripheral blood monocytes were enumerated in samples from newly-diagnosed, untreated GCA and PMR patients and after prednisone-induced remission. The distribution of classical (CD14CD16) and the more pro-inflammatory, intermediate (CD14CD16+) and non-classical (CD14CD16+) monocyte subsets was analysed by flow cytometry. The phenotype of macrophages in temporal artery biopsies (TABs) from GCA patients was studied by immunohistochemistry and immunofluorescence. A clear monocytosis was seen in newly diagnosed GCA and PMR patients caused by elevated numbers of classical monocytes. Prednisone treatment suppressed numbers of non-classical monocytes. Both chemokine CX3CL1 and CCL2 were highly expressed in the TAB. Most macrophages in the TAB of GCA patients expressed non-classical monocyte markers CD16 and CX3CR1 whereas co-localisation of CD16 with classical monocyte marker CCR2 was infrequent. In conclusion, we report an altered distribution of monocyte subsets in both GCA and PMR patients. The majority of macrophages in TABs of GCA patients were CD68 + CD16 + CX3CR1 + CCR2- and thereby resembled the phenotype of non-classical monocytes.

摘要

单核细胞/巨噬细胞在巨细胞动脉炎（GCA）的全身和局部炎症中起着关键作用，在临床上与之重叠的多发性肌痛（PMR）中也可能起作用。因此，我们旨在了解单核细胞亚群以及 CX3CR1-CX3CL1 和 CCR2-CCL2 趋化途径对 GCA 病理学的贡献。在新诊断、未经治疗的 GCA 和 PMR 患者以及泼尼松诱导缓解后，对其外周血单核细胞进行计数。通过流式细胞术分析经典（CD14CD16）和更具炎症性的中间（CD14CD16+）和非经典（CD14CD16+）单核细胞亚群的分布。通过免疫组织化学和免疫荧光研究 GCA 患者颞动脉活检（TAB）中的巨噬细胞表型。新诊断的 GCA 和 PMR 患者出现明显的单核细胞增多症，这是由于经典单核细胞数量增加所致。泼尼松治疗抑制了非经典单核细胞的数量。TAB 中趋化因子 CX3CL1 和 CCL2 表达水平均较高。GCA 患者 TAB 中的大多数巨噬细胞表达非经典单核细胞标志物 CD16 和 CX3CR1，而 CD16 与经典单核细胞标志物 CCR2 的共定位则很少见。总之，我们报告了 GCA 和 PMR 患者单核细胞亚群分布的改变。GCA TAB 中的大多数巨噬细胞为 CD68+CD16+CX3CR1+CCR2-，因此类似于非经典单核细胞的表型。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/998d/5529580/dd7e66c3cd68/41598_2017_6826_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/998d/5529580/ace0c853e26b/41598_2017_6826_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/998d/5529580/2f568155d3c0/41598_2017_6826_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/998d/5529580/596c539e5141/41598_2017_6826_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/998d/5529580/af29e92b97d7/41598_2017_6826_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/998d/5529580/dd7e66c3cd68/41598_2017_6826_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/998d/5529580/ace0c853e26b/41598_2017_6826_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/998d/5529580/2f568155d3c0/41598_2017_6826_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/998d/5529580/596c539e5141/41598_2017_6826_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/998d/5529580/af29e92b97d7/41598_2017_6826_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/998d/5529580/dd7e66c3cd68/41598_2017_6826_Fig5_HTML.jpg

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