网站首页期刊介绍通知公告编 委 会投稿须知电子期刊广告合作联系我们
最新消息:
Th17/Treg平衡与男性无症状高尿酸血症相关性研究及痛风风险评估
作者:秦安霖1  张丽卿2  温倩颖1 
单位:1. 山西医科大学 汾阳学院, 山西 汾阳 032200;
2. 山西医科大学附属汾阳医院 风湿免疫科, 山西 汾阳 032200
关键词:无症状高尿酸血症  痛风  Th17细胞  Treg细胞 
分类号:R593
出版年·卷·期(页码):2025·53·第五期(732-737)
摘要:

目的: 探讨辅助性T细胞17(Th17)/调节性T细胞(Treg)平衡在无症状高尿酸血症(aHUA)中的作用及其对痛风的预测价值。方法: 于山西医科大学附属汾阳医院体检中心数据库招募符合纳入排除标准的67例aHUA患者、79例健康对照组(HCs),收集基本信息、体检数据,检测实验室指标、外周血CD4+T淋巴细胞亚群,aHUA组随访6个月观察关节病变,双源CT检查受累关节尿酸盐晶体形成情况。采用SPSS 27.0统计软件分析,采用t检验、非参数检验、卡方检验进行组间临床资料与CD4+T淋巴细胞亚群比较,采用Logistic回归分析aHUA进展为痛风的影响因素。结果: aHUA组外周血Th17细胞计数[10.51(9.01,15.47)]较HCs组[8.71(6.17,12.28)]明显增高,差异有统计学意义(P<0.05); aHUA组的Th17/Treg[0.38(0.33,0.48)]与HCs组[0.29(0.21,0.37)]比较明显增高,差异有统计学意义(P<0.05)。Th17细胞(OR=1.382,95%CI 1.037~1.841,P=0.027)、尿酸(OR=1.020,95%CI 1.005~1.036,P=0.008)是aHUA发展为痛风的危险因素。结论: aHUA患者外周血Th17细胞、Th17/Treg较健康人升高,且Th17细胞、UA是aHUA发展为痛风的危险因素。

Objective: To investigate the role of the T helper 17(Th17)/regulatory T cell(Treg) balance in asymptomatic hyperuricemia(aHUA) and its predictive value for the progression to gout arthrolithiasis. Methods: A total of 67 aHUA patients and 79 healthy controls(HCs) meeting inclusion/exclusion criteria were recruited from the physical examination database of Shanxi Medical University Affiliated Fenyang Hospital. Demographic information, physical examination data, laboratory parameters, and peripheral blood CD4+ T lymphocyte subsets were collected. The aHUA group was followed for 6 months to observe joint lesions, and dual-source CT of affected joints was used for examining monosodium urate deposition. Statistical analysis was performed by SPSS 27.0. Independent t-tests, non-parametric tests, and chi-square tests were used to compare clinical data and CD4+ T lymphocyte subsets between two groups. Logistic regression analysis was applied to identify factors influencing the progression from aHUA to gout arthrolithiasis. Results: The peripheral Th17 cell count in the aHUA group[10.51(9.01, 15.47)] was significantly higher than that in the HCs group[8.71(6.17, 12.28)](P<0.05). The Th17/Treg ratio in the aHUA group[0.38(0.33, 0.48)] was also significantly elevated compared to the HCs group[0.29(0.21, 0.37)](P<0.05). Th17 cells(OR=1.382,95%CI 1.037-1.841,P=0.027) and uric acid(OR=1.020,95%CI 1.005-1.036,P=0.008) were identified as risk factors for the progression of aHUA to gout arthrolithiasis. Conclusion: Th17 cells and Th17/Treg in peripheral blood of aHUA patients were higher than those of healthy people, and Th17 cells and uric acid were independent risk factors for predicting the development of gout arthrolithiasis in aHUA patients.

参考文献:

[1] 中华医学会内分泌学分会.中国高尿酸血症与痛风诊疗指南(2019)[J].中华内分泌代谢杂志,2020,36(1):1-13.
[2] ZHOU Z,LI K,LI X,et al.Independent and joint associations of body mass index,waist circumference,waist-height ratio and their changes with risks of hyperuricemia in middle-aged and older Chinese individuals:a population-based nationwide cohort study[J].Nutr Metab(Lond),2021,18(1):62.
[3] SUN Q,ZHANG T,MANJI L,et al.Association between serum uric acid and non-alcoholic fatty liver disease:an updated systematic review and meta-analysis[J].Clin Epidemiol,2023,15:683-693.
[4] 梁露,周燕,韦瑾,等.高尿酸血症人群高血糖发生风险列线图预测模型的构建与评价[J].现代医学,2023,51(5):637-642.
[5] FITZGERALD J D,DALBETH N,MIKULS T,et al.2020 American college of rheumatology guideline for the management of gout[J].Arthritis Rheumatol,2020,72(6):879-895.
[6] WANG B,CHEN S,QIAN H,et al.Role of T cells in the pathogenesis and treatment of gout[J].Int Immunopharmacol,2020,88:106877.
[7] ZHAO L J,WANG H,GAO H Y,et al.Increase in different peripheral effector T subsets in acute and chronic gout[J].Transpl Immunol,2023,76:101763.
[8] ZI X,SU R,SU R,et al.Elevated serum IL-2 and Th17/Treg imbalance are associated with gout[J].Clin Exp Med,2024,24(1):9.
[9] PEI R,WANG J,HE P,et al.Risk factors for type 2 diabetes mellitus in Chinese rheumatoid arthritis patients from 2018 to 2022:a real-world,single-center,retrospective study[J].Front Immunol,2024,15:1445639.
[10] ALEXANDER M,ANG Q Y,NAYAK R R,et al.Human gut bacterial metabolism drives Th17 activation and colitis[J].Cell Host Microbe,2022,30(1):17-30.e9.
[11] BUGAUT H,ARACTINGI S.Major role of the IL17/23 axis in psoriasis supports the development of new targeted therapies[J].Front Immunol,2021,12:621956.
[12] ZONG Y,DENG K,CHONG W P.Regulation of Treg cells by cytokine signaling and co-stimulatory molecules[J].Front Immunol,2024,15:1387975.
[13] TANAKA A,SAKAGUCHI S.Regulatory T cells in cancer immunotherapy[J].Cell Res,2017,27(1):109-118.
[14] WANG Y,TU S,HUANG Y,et al.microRNA-181a regulates Treg functions via TGF-β1/Smad axis in the spleen of mice with acute gouty arthritis induced by MSU crystals[J].Braz J Med Biol Res,2022,55:e12002.
[15] LIU X,CHEN J,YUE S,et al.NLRP3-mediated IL-1β in regulating the imbalance between Th17 and Treg in experimental autoimmune prostatitis[J].Sci Rep,2024,14(1):18829.
[16] 陶金辉,程苗,刘勤,等.调节性T细胞在急慢性痛风患者中的变化及意义[J].中华风湿病学杂志,2019,23(6):406-409.
[17] DAI X J,TAO J H,FANG X,et al.Changes of treg/Th17 ratio in spleen of acute gouty arthritis rat induced by MSU crystals[J].Inflammation,2018,41(5):1955-1964.
[18] 杨虹,杨小红,钟晓武,等.辅助性T细胞17/调节性T细胞平衡在原发性痛风性关节炎发病机制中的作用[J].中华风湿病学杂志,2016,20(8):520-525.
[19] RAUCCI F,IQBAL A J,SAVIANO A,et al.IL-17A neutralizing antibody regulates monosodium urate crystal-induced gouty inflammation[J].Pharmacol Res,2019,147:104351.
[20] IMIELA A M,MIKOŁAJCZYK T P,SIEDLISKI M,et al.Th17/Treg imbalance in patients with primary hyperaldosteronism and resistant hypertension[J].Pol Arch Intern Med,2022,132(3):16171.
[21] LIU R,KLüCK V,KISCHKEL B,et al.Soluble urate-induced effects on cytokine production in vitro-Assessment of methodologies and cell types[J].Cytokine,2024,175:156502.
[22] KIM H W,YOON E J,JEONG S H,et al.Distinct gut microbiota in patients with asymptomatic hyperuricemia:a potential protector against gout development[J].Yonsei Med J,2022,63(3):241-251.
[23] CHEN P,TANG X.Gut microbiota as regulators of Th17/Treg balance in patients with myasthenia gravis[J].Front Immunol,2021,12:803101. 欢迎订阅 欢迎投稿

服务与反馈:
文章下载】【发表评论】【查看评论】【加入收藏
提示:您还未登录,请登录!点此登录
您是第 914402 位访问者


 ©《现代医学》编辑部
联系电话:025-83272481;83272479
电子邮件: xdyx@pub.seu.edu.cn

本系统由北京博渊星辰网络科技有限公司设计开发 技术支持电话:010-63361626

苏ICP备09058541