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 Objective: To explore the pathogenesis of Kawasaki disease (KD). Methods: Peripheral blood mononuclear cells (PBMCs) from 26 KD patients and 20 normal children were counted and the percentage of apoptotic cells and fragment DNA were counted by anti-CD3 induction of apoptosis in vitro. Results: The percentages of apoptotic cells and DNA fragments in KD patients were lower than those in normal controls (P <0001) and delayed. The levels of IL6 produced by PBMC in vitro were significantly higher than those in normal controls (P <0001) Anti-IL 6 monoclonal antibody culture or intravenous immunoglobulin (IVIG) treatment can significantly reduce IL 6 levels, reverse the percentage of apoptotic cells and DNA fragmentation delay. Conclusion: The down-regulation of PBMC apoptosis in KD patients may be related to the abnormal increase of IL-6 level in this disease