Expression of CD40 ligand on CD4+ T-cells and platelets correlated to the coronary artery lesion and disease progress in Kawasaki disease -: art. no. e140
Expression of CD40 ligand on CD4+ T-cells and platelets correlated to the coronary artery lesion and disease progress in Kawasaki disease -: art. no. e140
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DOI：
10.1542/peds.111.2.e140
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发表时间：
2003-02-01
期刊：
影响因子：
8
通讯作者：
Yang, KD
中科院分区：
文献类型：
--
作者：
Wang, CL;Wu, YT;Yang, KD
客观的。川崎病（KD）是一种儿童急性发热性血管炎综合征。 CD40 配体 (CD40L) 与某些类型的血管炎有关。我们提出CD40L 表达可能与KD 中的冠状动脉病变相关。方法。在静脉注射免疫球蛋白 (IVIG) 治疗前和治疗后 3 天，从 43 名 KD 患者身上采集了血液样本。 43 名年龄匹配的患有各种疾病的发热儿童作为对照进行平行研究。采用流式细胞术检测T细胞和血小板上CD40L的表达，采用酶联免疫吸附法测定可溶性CD40L（sCD40L）水平。结果。我们发现，KD 患者中 CD4(+) T 细胞上的 CD40L 表达显着高于发热对照组 (FC) 组（28.69 +/- 1.17% vs 4.37 +/- 0.36%）。 IVIG 给药后 3 天，CD40L 表达显着下降（28.69 +/- 1.17% vs 13.53 +/- 0.55%）。 KD 患者血小板上的 CD40L 表达也显着高于 FC 组（8.20 +/- 0.41% vs 1.26 +/- 0.12%），并且在 IVIG 治疗后下降。患有 FC 的 KD 患者中 sCD40L 水平也显着较高（9.69 +/- 0.45 ng/mL vs 2.25 +/- 0.19 ng/mL），但 3 天后不受 IVIG 治疗的影响（9.69 +/- 0.45 ng/mL vs 9.03 +/- 0.32 ng/mL）。更有趣的是，我们发现在KD患者中，CD4（+）T细胞和血小板上的CD40L表达与冠状动脉病变的发生相关，而CD8（+）T细胞或sCD40L上不表达。结论。 CD40L 可能在 KD 的免疫发病机制中发挥作用。 IVIG 治疗可能下调 CD40L 表达，从而减少川崎病中 CD40L 介导的血管损伤。这意味着调节 CD40L 表达可能有益于治疗 KD 血管炎。
Objective. Kawasaki disease (KD) is an acute febrile vasculitic syndrome in children. CD40 ligand (CD40L) has been implicated in certain types of vasculitis. We proposed that CD40L expression might be correlated with coronary artery lesions in KD.Methods. Blood samples were collected from 43 patients with KD before intravenous immunoglobulin (IVIG) treatment and 3 days afterward. Forty-three age-matched febrile children with various diseases were studied in parallel as controls. CD40L expression on T-cells and platelets were detected by flow cytometry, and soluble CD40L (sCD40L) levels were measured by enzyme-linked immunosorbent assay.Results. We found that CD40L expression on CD4(+) T-cells was significantly higher in patients with KD than in the febrile control (FC) group (28.69 +/- 1.17% vs 4.37 +/- 0.36%). CD40L expression decreased significantly 3 days after IVIG administration (28.69 +/- 1.17% vs 13.53 +/- 0.55%). CD40L expression on platelets from patients with KD was also significantly higher than in the FC group (8.20 +/- 0.41% vs 1.26 +/- 0.12%) and decreased after IVIG therapy. sCD40L levels were also significantly higher in KD patients with those of FC (9.69 +/- 0.45 ng/ mL vs 2.25 +/- 0.19 ng/ mL) but were not affected by IVIG treatment 3 days afterward (9.69 +/- 0.45 ng/ mL vs 9.03 +/- 0.32 ng/ mL). More interesting, we found that in KD patients, CD40L expression on CD4(+) T-cells and platelets but not on CD8(+) T-cells or sCD40L was correlated with the occurrence of coronary artery lesions.Conclusions. CD40L might play a role in the immunopathogenesis of KD. IVIG therapy might downregulate CD40L expression, resulting in decrease of CD40L-mediated vascular damage in KD. This implicates that modulation of CD40L expression may benefit to treat KD vasculitis.