■为了研究程序性细胞死亡蛋白1（PD1）途径的免疫调节作用，抑制性免疫检查点,幼年特发性关节炎（JIA）。
■通过流式细胞术确定CD4和CD8T细胞上的PD1表达，通过ELISA确定PD1可溶形式（sPD1）水平，在JIA患者和健康对照（HCs）的外周血（PB）/血清和滑液（SF）样本中。我们搜索了生物标志物与JIA活性之间的任何关联。
■101名白种人患者（69名女性），12(8-15)岁,20个HCs参与了这项研究。在T细胞上的PBPD1表达在：a。JIA患者vsHCs（CD4：1.24％vs0.32％，p=0.007，CD8：1.6％vs0.4％，p=0.002)。B.活跃与不活跃的JIA（CD4：1.44%vs0.87%，p=0.072，CD8：2.1%vs0.93%，p=0.005)。T细胞上的SFPD1表达与疾病活动密切相关且呈正相关（CD4：ρ=0.55，p=0.022，CD8：ρ=0.555，p=0.026）。在治疗中的患者中，CD8T细胞上的SFPD1表达高于未治疗的患者（21.3％vs5.83％p=0.004）。sPD1水平在SF高于血清（801pg/mlvs367.2，p=0.013），与疾病活动无关。
■这些结果表明JIA中PD1途径的上调，至少在数量上,特别是在活动性疾病中。sPD1在发炎的关节处间隔产生。在较大的JIA患者样本中进行的进一步研究可能会验证这些观察结果，并有助于揭示PD1途径在关节炎症的发病机理和持久性中的确切作用。
UNASSIGNED: To investigate the immunoregulatory role of the Programmed-cell-Death-protein-1 (PD1) pathway, an inhibitory immune checkpoint, in Juvenile Idiopathic Arthritis (JIA).
UNASSIGNED: The PD1 expression on CD4+ and CD8+ T-cells was determined by flow cytometry and the PD1 soluble form (sPD1) levels by ELISA, in peripheral blood (PB)/serum and synovial fluid (SF) samples of JIA patients and healthy controls (HCs). We searched for any association in-between the biomarkers and with JIA activity.
UNASSIGNED: 101 Caucasian patients (69 female), aged 12 (8-15) years, and 20 HCs participated in this study. The PB PD1 expression on T-cells was higher in: a. JIA patients vs HCs (CD4: 1.24% vs 0.32%, p=0.007, CD8: 1.6% vs 0.4%, p=0.002). b. active vs inactive JIA (CD4: 1.44% vs 0.87%, p=0.072, CD8: 2.1% vs 0.93%, p=0.005). The SF PD1 expression on T-cells correlated strongly and positively with the disease activity (CD4: ρ=0.55, p=0.022, CD8: ρ=0.555, p=0.026). The SF PD1 expression on CD8 T-cells was higher in patients on-treatment vs those off-treatment (21.3% vs 5.83% p=0.004). The sPD1 levels were higher in the SF vs the serum (801pg/ml vs 367.2, p=0.013), without an association with disease activity.
UNASSIGNED: These results indicate an up-regulation of the PD1-pathway in JIA, at least quantitatively, especially in active disease. sPD1 is compartmentally produced at the inflamed joints. Further investigation in a larger sample of JIA patients may verify these observations and contribute to unravelling the precise role of the PD1 pathway in the pathogenesis and persistence of the joint inflammation.
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