背景:关于银屑病关节炎(PsA)中调节性T(Treg)细胞水平的研究一直存在争议,导致关于Treg细胞在疾病发病机理中的作用存在分歧。明确PsA患者Treg细胞的状态,我们进行了一项荟萃分析,以确定PsA患者中Treg细胞和血清Treg相关细胞因子的水平.
方法:根据PubMed发布的数据,WebofScience,Embase,临床试验.gov,MEDLINE,WebofKnowledge,科克伦图书馆,和FDA.gov,我们测定了PsA患者的Treg和Treg细胞因子水平。使用随机效应模型汇集效应估计值。
结果:这项荟萃分析包括12项研究。与健康对照(HC)相比,PsA患者中Treg细胞的比例没有显着差异(基于标准化平均值[SMD]=-1.038,95%置信区间[CI]=-2.165至0.089,p=0.071)。在子群分析的基础上,PsA患者的CD4+Treg细胞百分比(SMD=-1.501,95%CI-2.799~-0.202,p=0.023)低于OKT8+Treg(SMD=0.568,95%CI-2.127~3.263,p=0.679).此外,在PsA患者的PBMC水平上,CD4CD25CD25FoxP3Treg细胞和CD4CD25highCD127lowTreg细胞均显着降低(SMD=-0.764,95%CI-1.404至-0.125,p=0.019;SMD=-5.184,95%CI-6.955至-3.412,p<0.001)。滑液中CD4+CD25+FoxP3+Treg细胞含量高于外周血(SMD=3.288,95%CI2.127to4.449,p<0.001)。外周血中CD4+CD25+Treg细胞和CD4+T细胞中CD4+CD25+FoxP3+Treg细胞比例差异无统计学意义(SMD=-2.498,95%CI-7.720~2.725,p=0.349;SMD=-0.719,95%CI-2.525~1.086,p=0.435)。PsA患者的细胞因子如转化生长因子β(TGFβ)降低(SMD=-2.199,95%CI-3.650至-0.749,p=0.003)。
结论:Treg定义标志物影响PsA患者Treg细胞的规模。PsA的发病可能归因于Treg群体不足或功能不良。
Studies on the level of regulatory T (
Treg) cells in psoriatic arthritis (PsA) have been controversial, leading to disagreement regarding the role Treg cells play in the pathogenesis of the disease. To clarify the status of Treg cells in patients with PsA, we performed a meta-analysis to determine the levels of
Treg cells and serum
Treg-associated cytokines in PsA patients.
According to published data from PubMed, Web of Science, Embase, Clinical Trials.gov, MEDLINE, Web of Knowledge, Cochrane Library, and FDA.gov, we determined the Treg and
Treg cytokine levels in patients with PsA. The effect estimates were pooled using a random-effects model.
This meta-analysis included 12 studies. Compared to healthy controls (HCs), the proportions of Treg cells had no significant difference in patients with PsA (based on standardized means[SMD] = - 1.038, 95% confidence intervals[CI] = - 2.165 to 0.089, p = 0.071). On the basis of subgroup analysis, patients with PsA had a lower percentage of CD4+ Treg cells (SMD = - 1.501, 95% CI - 2.799 to - 0.202, p = 0.023) than OKT8+ Treg (SMD = 0.568, 95% CI - 2.127 to 3.263, p = 0.679). Besides, CD4+CD25+FoxP3+
Treg cells and CD4+CD25highCD127low
Treg cells were both significantly decreased on the levels of PBMCs in patients with PsA (SMD = - 0.764, 95% CI - 1.404 to - 0.125, p = 0.019; SMD = - 5.184, 95% CI - 6.955 to - 3.412, p < 0.001). CD4+CD25+FoxP3+ Treg cells were particularly more abundant in the synovial fluid thanin peripheral blood (SMD = 3.288, 95% CI 2.127 to 4.449, p < 0.001). No significant difference was observed in the proportion of CD4+CD25+ Treg cells in peripheral blood and CD4+CD25+FoxP3+ Treg cells in CD4+ T cells (SMD = - 2.498, 95% CI - 7.720 to 2.725, p = 0.349; SMD = - 0.719, 95% CI - 2.525 to 1.086, p = 0.435). PsA patients had decreased cytokines such as transforming growth factor-β (TGFβ) (SMD = - 2.199, 95% CI - 3.650 to - 0.749, p = 0.003).
Treg definition markers influence the scale of
Treg cells in patients with PsA. Pathogenesis of PsA may be attributed to an insufficient or malfunctioning Treg population.