摘要
目的:通过检测川崎病患儿静脉输注丙球治疗前后外周血T细胞表面CD40L(CD154)表达,探讨川崎病冠状动脉损伤的发病机制。方法:采用流式细胞仪检测26例川崎病患儿静脉输注丙球治疗前后、16例其他发热性疾病患儿、15例正常儿童外周血T细胞表面的CD40L表达。采用酶联免疫吸附试验检测相应血清中可溶性CD40L。结果:川崎病患儿CD4+T细胞表面CD40L表达(66.26±6.71)%显著高于其他发热性疾病对照组(58.11±6.35)%及正常儿童对照组(46.96±4.27)%,川崎病患儿静脉输注丙球治疗后明显下降(58.86±7.49)%。川崎病患儿血清中可溶性CD40L(17.36±5.72)ng/ml亦显著高于其他发热性疾病对照组(12.17±4.28)ng/ml及正常儿童对照组(7.48±3.59)ng/ml,静脉输注丙球治疗后无明显下降(16.46±5.12)ng/ml。CD4+T细胞表面CD40L表达与川崎病冠状动脉损伤有关,而CD8+T细胞表面CD40L的表达及可溶性CD40L与冠状动脉损伤无关。川崎病患儿CD4+T细胞表面CD40L表达与C反应蛋白(CRP)水平正相关(r=0.553,P<0.05)。结论:CD40L异常表达在川崎病发病机制中其起重要作用。静脉输注丙球能下调CD40L表达,且有利于治疗血管炎。
Objective： To explore the pathogenesis of coronary artery lesions in Kawasaki disease （KD） by detecting expression of CD40L on T-cells from patients with KD. Mothods： Blood samples were collected from 26 patients with KD before and after intravenous immunoglobulin （IVIG） treatment. Sixteen age-matcbed febrile sixteen children with various diseases were studied in parallel as controls. Fifteen age-matched normal control fifteen children were studied as controls. CD40L expression on T-cells was detected by flow cytometry, and soluble CIMOL （sCD40L） levels were measured by enzyme-linked immunosorbent assay. Results： CD40L expression on CD4^＋-cells was significantly higher in patients with KD than that in the febrile control （FC） group （66.26 ± 6.71% vs 58.11 ±6.35%） and normal group （66.26 ±6.71% vs 46.96 ± 4.27%）. CD40L expression decreased significantly 2-3 days after IVIG administration （66.26 ±6.71% vs 58.86 ± 7.49%）. sCD40L levels were also significantly higher in KD patients than those of FC （17.36± 5.72 vs 12.17± 4.28 ng/ml） and normal group （17.36 ~ 5.72 vs 7.48 ± 3.59 ng/ml）, but were not affected by IVIG treatment （17.36 ±5.72 vs16.46 ± 5.12 ng/ml）. In KD patients, CD40L expression on CD4^＋T-cells but not on CD8^＋T-cells or sCD40L was correlated with the occurrence of coronary artery lesions. There was a significantly positive correlation between CD40L expression on CD4^＋T-cells in patients with KD and CRP （r = 0.553 , P 〈 0.05）. Conclusion： CD40L might play a role in the immunopathogenesis of KD. IVIG therapy might downregulate CIMOL expression and may benefit to recovery of KD vasculitis.
出处
《南京医科大学学报（自然科学版）》
CAS
CSCD
北大核心
2005年第11期835-838,共4页
Journal of Nanjing Medical University(Natural Sciences)
基金
南京医科大学科技发展基金项目资助(NY03051)
