易岂建 李成荣 杨锡强 刘恩梅
中国图书分类号 R593.2
摘 要 目的:探讨川崎病(KD)的免疫发病机理。方法:对26例KD患者和20名正常儿童外周血单个核细胞(PBMC)经anti-CD3诱导体外培养不同时间的凋亡进行计数凋亡细胞百分率和片段DNA分析。结果:KD患者凋亡细胞百分率和片段DNA出现时间较正常对照降低(P<0.001)和延迟,PBMC体外培养产生IL-6水平较正常对照显著升高(P<0.001);加抗IL-6单抗培养或静脉注射免疫球蛋白(IVIG)治疗可显著降低IL-6水平,逆转凋亡细胞百分率的降低和DNA片段化延迟。结论:KD患者PBMC凋亡下调可能与本病IL-6水平异常增高有关。
关键词 川崎病 细胞凋亡 IL-6
Preliminary study on the decreased apoptosis of lymphocytes in acute kawasaki disease
YI Qi-Jian,LI Cheng-Rong, YANG Xi-Qiang et al.
Children s Hospital Chongqing University of Medical Sciences,Chongqing 400014
Abstract Objective:To further explore the pathogenesis of kawasaki disease (KD).Methods:Calculating percentage of apoptotic cells and assaying DNA fragmentation in peripheral blood mononuclear cell(PBMC)stimulated by anti-CD3 for 0,12,24,48,72 h in vitro from 30 patients with KD and 20 age-matched health children.Results:Apoptotic cell percentage and DNA fragmentation were markedly decreased(P<0.001) and delayed (compared with those in normal controls),which could reach the states of control group only by 72 h cultured.Remarkabely increased production of IL-6 in cultured supernatants of PBMC induced by phytohemagglutinin(PHA) from KD patients was found in comparison with those of PBMC from controls(P<0.001).Adding anti-IL-6 mAb to the cultures or using intravenous immunoglobulin(IVIG)in vivo led to significantly decreased production of IL-6(P<0.001),and reversed decreased apoptotic cell percentage and delayed DNA fragmentation to be compatible with normal controls.Conclusion:Over-produced IL-6 might be involved in down-regulation of peripheral blood lymphocyte apoptosis in KD.
Key words Kawasaki disease Apoptosis IL-6
细胞凋亡(Apoptosis)是细胞生理性死亡的主要形式[1]。机体细胞增殖和死亡过程达到动态平衡是维持其自身恒定的必要条件。细胞凋亡过度或不足都会引起细胞数量失衡,导致临床疾病[2]。已推测凋亡可能与系统性红斑狼疮(SLE)等自身免疫性疾病有关。川崎病(Kawasaki disease,KD)是一原因不明的急性血管炎,其发病可能为感染或其他因素触发的异常免疫反应。本文拟对KD患者外周血单个核细胞(PBMC)体外培养时的凋亡进行观察,并对有关因素进行探讨。
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