Results of flow cytometric detection of gamma-deltaT cells in peripheral blood of patients with ankylosing spondylitis: a pilot study.

IF 1.9 4区 医学 Q3 PHYSIOLOGY
Physiological research Pub Date : 2023-12-31
Si-Liang Man, Peng Dong, Wei Liu, Hong-Chao Li, Liang Zhang, Xiao-Jian Ji, Li-Dong Hu, Hui Song
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引用次数: 0

Abstract

Previous studies have suggested that gamma-delta T cells play an important role in the pathogenesis of ankylosing spondylitis (AS). In this pilot study, the peripheral blood mononuclear cells (PBMCs) of patients with ankylosing spondylitis (AS) and healthy volunteers were stained and analyzed by flow cytometry to distinguish gamma-delta T cells and its subtypes, and then to report the distribution of gamma-delta T cells and iyts subtypes and their correlation with ankylosing spondylitis. A total of 17 patients with active AS and 10 age- and gender- matched healthy volunteers were enrolled in this study, and their peripheral blood were drawn to collect mononuclear cells (PBMCs). Flow cytometry was used to analyze gamma-delta T cell subpopulations by measuring the surface and intracellular expressions of phenotypic markers. Serum levels of inflammatory and bone turnover markers were measured, and their correlations with subpopulations of gamma-delta T cells were evaluated. In patients with AS, the Vdelta2 fractions within gamma-delta T cells and CD3+ T cells decreased significantly, in particular, the proportions of CD27+ Vdelta2 T cells, CD86+CD80+ Vdelta1 T cells, and IL17A-secreting and TNFalpha-secreting Vdelta1 T cells within the parental cells decreased significantly. gamma-delta T cells/PBMCs, Vdelta2 cells/gamma-delta T cells, and Vdelta2 cells/CD3+ T cells were negatively correlated with CRP, whereas Vdelta1 cells/CD3+ T cells were negatively correlated with ESR. Vdelta1 cells/gamma-delta T cells were positively correlated with CRP, gamma-deltaT cells/PBMCs were positively correlated with beta-CTx, CD69+CD25+ and IL-17A-secreting Vdelta1 cells were positively correlated with TP1NP, and CD69+CD25+ Vdelta1 and Vdelta2 cells were positively correlated with osteocalcin. Decreases in peripheral Vdelta2, CD27+ Vdelta2, CD86+CD80+ Vdelta1, and IL17A or TNFalpha-secreting Vdelta1 T cells are associated with AS. The correlations between gamma-delta T cell subpopulations and CRP and the CD69+CD25+ subpopulation with TP1NP or osteocalcin suggest that an imbalance in peripheral gamma-delta T cell subpopulations contributes to the pathogenesis of AS.

强直性脊柱炎患者外周血中 gamma-deltaT 细胞的流式细胞术检测结果:一项试点研究。
以往的研究表明,γ-δ T 细胞在强直性脊柱炎(AS)的发病机制中起着重要作用。在这项试验性研究中,研究人员对强直性脊柱炎(AS)患者和健康志愿者的外周血单核细胞(PBMCs)进行了染色,并通过流式细胞术分析了γ-δT细胞及其亚型,然后报告了γ-δT细胞和iyts亚型的分布及其与强直性脊柱炎的相关性。本研究共招募了17名活动性强直性脊柱炎患者和10名年龄与性别匹配的健康志愿者,并抽取他们的外周血采集单核细胞(PBMCs)。流式细胞术通过测量表型标记物的表面和细胞内表达来分析γ-δ T 细胞亚群。测量了血清中炎症和骨转换标记物的水平,并评估了它们与γ-δT细胞亚群的相关性。在强直性脊柱炎患者中,γ-ΔT细胞和CD3+ T细胞中的Vdelta2部分明显减少,尤其是母细胞中CD27+ Vdelta2 T细胞、CD86+CD80+ Vdelta1 T细胞以及分泌IL17A和TNFα的Vdelta1 T细胞的比例明显减少。γ-δT细胞/PBMCs、Vdelta2细胞/γ-δT细胞和Vdelta2细胞/CD3+ T细胞与CRP呈负相关,而Vdelta1细胞/CD3+ T细胞与ESR呈负相关。Vdelta1 细胞/γ-delta T 细胞与 CRP 呈正相关,γ-deltaT 细胞/PBMCs 与 beta-CTx 呈正相关,CD69+CD25+ 和分泌 IL-17A 的 Vdelta1 细胞与 TP1NP 呈正相关,CD69+CD25+ Vdelta1 和 Vdelta2 细胞与骨钙素呈正相关。外周 Vdelta2、CD27+ Vdelta2、CD86+CD80+ Vdelta1 和分泌 IL17A 或 TNFalpha 的 Vdelta1 T 细胞的减少与强直性脊柱炎有关。γ-δT细胞亚群与CRP、CD69+CD25+亚群与TP1NP或骨钙素之间的相关性表明,外周γ-δT细胞亚群的失衡是强直性脊柱炎的发病机制之一。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Physiological research
Physiological research 医学-生理学
CiteScore
4.00
自引率
4.80%
发文量
108
审稿时长
3 months
期刊介绍: Physiological Research is a peer reviewed Open Access journal that publishes articles on normal and pathological physiology, biochemistry, biophysics, and pharmacology. Authors can submit original, previously unpublished research articles, review articles, rapid or short communications. Instructions for Authors - Respect the instructions carefully when submitting your manuscript. Submitted manuscripts or revised manuscripts that do not follow these Instructions will not be included into the peer-review process. The articles are available in full versions as pdf files beginning with volume 40, 1991. The journal publishes the online Ahead of Print /Pre-Press version of the articles that are searchable in Medline and can be cited.
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