Hara Toshiro
Nihon Rinsho. 2014 Sep;72(9):1542-7.
Kawasaki disease (KD) is an acute self-limited systemic vasculitis, and could develop in association with innate immune disorders. An innate immune system appears to play a key role in the development of KD, because pathogen-associated molecular patterns(PAMPs) and damage-associated molecular patterns(DAMPs) are elevated in the sera at acute phase KD, and oral administration of innate immune Nod1 ligand induces KD-like coronary arteritis in mice. PAMPs can be produced massively from microbes in a certain condition. DAMPs are produced from the host cells by the stimulation of PAMPs. We propose a hypothesis that PAMPs and DAMPs activate innate immune system and vascular cells through innate immune pattern recognition receptors(PRR) to release chemokines and cytokines, and induce KD in genetically predisposed individuals.
川崎病（KD）是一种急性自限性全身性血管炎，可能与先天性免疫紊乱有关。先天性免疫系统似乎在KD的发病过程中起关键作用，因为在急性期KD患者的血清中，病原体相关分子模式（PAMPs）和损伤相关分子模式（DAMPs）水平升高，并且口服先天性免疫Nod1配体可在小鼠中诱导出类似KD的冠状动脉炎。在特定条件下，微生物可大量产生PAMPs。PAMPs刺激宿主细胞产生DAMPs。我们提出一个假说，即PAMPs和DAMPs通过先天性免疫模式识别受体（PRR）激活先天性免疫系统和血管细胞，释放趋化因子和细胞因子，并在遗传易感个体中诱发KD。
