摘要
通过观察静脉注射免疫球蛋白（ＩＶＩＧ）对川崎病（ＫＤ）患儿淋巴细胞凋亡（ＡＰＯ）的影响，进一步探讨ＩＶＩＧ对免疫性疾病的作用机理。对２６例川崎病患儿和２０名健康儿童外周血单个核细胞（ＰＢＭＣ）经抗－ＣＤ３单克隆抗体刺激培养不同时间（０，１２，２４，４８，７２小时）ＡＰＯ百分率和ＤＮＡ片断化分析，２６例患儿随机分为两组，阿司匹林＋ＩＶＩＧ治疗组（ｎ＝１６）和阿司匹林治疗组（ｎ＝１０），并对ＰＢＭＣ经植物血凝素（ＰＨＡ）刺激淋巴细胞增殖反应进行了观察。结果：ＫＤ患儿ＡＰＯ百分率和ＤＮＡ片断化较正常儿童明显降低（Ｐ＜０．００１）和延迟；ＩＶＩＧ治疗后，降低的ＡＰＯ百分率和延迟的ＤＮＡ片断化被逆转，同时与单用阿司匹林组比较，临床症状明显改善。淋巴细胞增殖反应下调（Ｐ＜０．００１）。外周血淋巴细胞ＡＰＯ下调可能参与了ＫＤ的发病。ＩＶＩＧ治疗ＫＤ的机理可能部分归于对被抑制的淋巴细胞ＡＰＯ的逆转。ＩＶＩＧ对其它淋巴细胞凋亡不足的自身免疫性疾病治疗可能存在同样机理。
To observe the effect of intravenous immunoglobulin(IVIG) on peripheral blood mononuclear cell (PBMC) apoptosis (APO) in acute Kawasaki disease (KD) and to further explore the therapeutic mechanism of IVIG for immunomediated disease. PBMC from 26 children with KD and 20 agematched healthy children were stimulated by antiCD3 monoclonal antibody, and apoptovitic cell percentage and DNA fragmentation were assayed at 0, 12, 24, 48, 72h in vitro. The patients were randomly divided into 2 groups: combining IVIG with aspirin therapy (n=16) and aspirin alone (n=10), PBMC was stimulated by phytohemaglutinin (PHA) to evaluate lymphocyte proliferative response. Compared with normal controls, apoptotic cell percentage and the DNA fragmentation were markedly decreased (P<0.001) and delayed in PBMC from KD children. After IVIG treatment, the apoptotic cell percentage and delayed DNA fragmentation were reversed to the levels of normal controls, accompanied by a fast clinical remission as compared to the patients treated with aspirin alone. Lymphocyte proliferative response was also downregulated in vitro after IVIG therapy (P<0.001). Conclusions: The decreased peripheral lymphocyte APO might be involved in pathogenesis of KD. The therapeutic mechanism of IVIG for KD may be partially contributed to reversing the inhibited lymphocyte APO, IVIG appears to have the same effect in treatment of other autoimmune diseases with insufficient lymphocyte APO.
出处
《中华儿科杂志》
CAS
CSCD
北大核心
1997年第12期645-648,共4页
Chinese Journal of Pediatrics
关键词
粘膜皮肤
淋巴结综合征
免疫球蛋白类
静脉内
Mucocutaneous lymph node syndrome Immunoglobulins, intravenous phagocytosis
