作者: K. Ikeda , K. Yamaguchi , T. Tanaka , Y. Mizuno , A. Hijikata
DOI: 10.1111/J.1365-2249.2009.04073.X
关键词:
摘要: Although Kawasaki disease (KD) is characterized by a marked activation of the immune system with elevations serum proinflammatory cytokines and chemokines at acute phase, major sources for these chemical mediators remain controversial. We analysed status peripheral blood mononuclear cells (PBMCs) flow cytometry, DNA microarray quantitative reverse transcription-polymerase chain reaction. The proportions CD69+ in both natural killer gammadeltaT acute-phase KD were significantly higher than those convalescent-phase KD. Microarray analysis revealed that five genes such as NAIP, IPAF, S100A9, FCGR1A GCA up-regulated pathways involved phase related closely to innate system. relative expression levels damage-associated molecular pattern molecule (DAMP) (S100A9 S100A12) PBMCs KD, while TNFA, IL1B IL6 not different between patients healthy controls. Intracellular production tumour necrosis factor-alpha, interleukin-10 interferon-gamma was observed patients. present data have indicated showed unique high DAMP but low cytokine genes, appears play role pathogenesis pathophysiology