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外周 T 细胞中 CCR2 上调,但骨髓中未上调。

CCR2 upregulated on peripheral T cells in osteoarthritis but not in bone marrow.

机构信息

Department of Medicine, Immunology and Allergy Unit, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden.

Department of Surgery and Perioperative Science, Urology and Andrology Unit, Umeå University, Umeå, Sweden.

出版信息

Scand J Immunol. 2018 Dec;88(6):e12722. doi: 10.1111/sji.12722. Epub 2018 Oct 28.

DOI:10.1111/sji.12722
PMID:30403025
Abstract

Osteoarthritis (OA) is a condition affecting millions of patients around the world, causing pain and disability and often resulting in joint replacement surgery. The aetiology of OA has long been attributed to mechanical wear mainly due to the increased prevalence of OA in load bearing joints among older patients. However, recent studies reveal a complex molecular disease causality in which inflammation, nutritional deficit and angiogenesis lead to the destruction of the joint structure. The aim of this study was to examine chemokine receptor expression in peripheral blood and bone marrow in OA patients. We devised a protocol for extracting healthy bone marrow from patients undergoing hip arthroplasty due to coxarthrosis. Flow cytometry was used to determine the expression of 18 chemokine receptors on CD4 and CD8 T cells from bone marrow and blood from 7 osteoarthritis patients and peripheral blood from 9 healthy controls. We found a significantly increased fraction of CCR2 expressing CD4 and CD8 T cell in peripheral blood compared to healthy controls. Also, there was a significant decrease in CXCR3 (Th1) (P < 0.01) expressing T cells in peripheral blood from OA patients. Finally, multivariate analysis was used to separate T cell profiles from healthy controls and OA patients and demonstrate that the divergence of chemokine receptor expression occurs in the mature T cell subsets. In conclusion, we find increased CCR2 expression in peripheral blood from OA patients that possibly may be targeted in future clinical studies.

摘要

骨关节炎(OA)是一种影响全球数以百万计患者的疾病,导致疼痛和残疾,并且通常导致关节置换手术。OA 的病因长期以来归因于机械磨损,主要是由于老年患者负重关节中 OA 的患病率增加。然而,最近的研究揭示了一种复杂的分子疾病因果关系,其中炎症、营养缺乏和血管生成导致关节结构破坏。本研究旨在检查 OA 患者外周血和骨髓中的趋化因子受体表达。我们设计了一种从因髋关节骨关节炎接受髋关节置换术的患者中提取健康骨髓的方案。流式细胞术用于确定来自 7 名 OA 患者和 9 名健康对照者的骨髓和血液中的 CD4 和 CD8 T 细胞上的 18 种趋化因子受体的表达。我们发现与健康对照组相比,外周血中表达 CCR2 的 CD4 和 CD8 T 细胞的比例明显增加。此外,OA 患者外周血中 CXCR3(Th1)(P<0.01)表达的 T 细胞显著减少。最后,使用多元分析将健康对照者和 OA 患者的 T 细胞图谱分离,并证明趋化因子受体表达的差异发生在成熟的 T 细胞亚群中。总之,我们发现 OA 患者外周血中 CCR2 表达增加,这可能是未来临床研究的目标。

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