摘要
目的拟通过对急性期川崎病(KD)患者外周血淋巴细胞凋亡的观察,进一步探讨KD的免疫发病机理。方法26例KD患者和20名正常儿童外周血单个核细胞(PBMC)经抗-CD3诱导处理,部分用IL-6单抗处理,之后培养不同时间(0,12,24,48,72小时)测定凋亡细胞百分率。结果KD患者凋亡细胞百分率和DNA片段化均较正常对照降低(P<0.001)和延迟。PHA刺激PBMC培养上清IL-6水平较正常对照明显升高(P<0.001)。加抗IL-6的单抗培养或静脉注射免疫球蛋白可显著降低IL-6水平,凋亡细胞百分率降低和DNA片段化延迟发生逆转。结论KD患者PBMC存在有凋亡降低或延迟。
For further exploration of the pathogenesis of Kawasaki disease(KD),the cellular morphological change,calculation of percentage of apoptotic cells and assaying DNA fragmentation in peripheral blood mononuclear cells(PBMC) stimulated by anti-CD3 for 0,12,24,48,72h in vitro in 26 KD patients and 20 agematched health children were observed.The results revealed that apoptotic cell percentage and DNA fragmentation were markedly decreased(P<0.001) and delayed(in comparison with those in normal controls),which could reach the state of the control group only by stimulation of antiCD3 for 72h.Remarkably increased production of IL6 in cultured supernatants of PBMC induced by phytohemagglutinin(PHA) from KD patients was found in comparison with those of PBMC from controls(P<0001).Adding antiIL6 McAb to the cultures or using intravenous immunoglobulin(IVIG)in vivo led to significantly decreased production of IL 6(P<0001) and reversed decreased apoptotic cell percentage and delayed DNA fragmentation which were compatible with normal controls.It concluded that peripheral lymphocyte apoptosis was inhibited in KD and overproduced IL6 might be involved in this process.
出处
《中华微生物学和免疫学杂志》
CAS
CSCD
北大核心
1998年第1期37-40,共4页
Chinese Journal of Microbiology and Immunology
关键词
川崎病
细胞凋亡
白细胞介素6
淋巴细胞
Apoptosis\ \ Interleukin6\ \ Kawasaki disease\ \ Lymphocyte