The pathogenesis of Kawasaki disease and superantigens.
The pathogenesis of Kawasaki disease and superantigens.
复制标题
川崎病的发病机制和超抗原。
DOI：
10.7883/yoken.52.141
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发表时间：
1999
影响因子：
2.2
通讯作者：
H. Kato
中科院分区：
文献类型：
--
作者：
T. Uchiyama;H. Kato
川崎病(KD)是一种婴儿和儿童的急性发热性疾病，具有包括冠状动脉动脉瘤在内的全身临床症状。在KD患者中发现T细胞在血管病变中的浸润，血清中可溶性白介素2受体的升高，T细胞亚群的失衡，以及T细胞与CD11/CD18的一过性耗竭，提示T细胞的激活参与了KD的发病机制。1992年，一种有趣的机制被提出，即某种超抗原激活的T细胞参与了KD的发病。已经进行了广泛的检验，以证实所提出的假设。然而，我们仍然没有可靠的证据支持上述假设。在本文中，我们回顾了支持或排除上述观点的研究论文。此外，我们还讨论了KD与表现出与KD相似的临床症状的系统性假结核耶尔森菌感染的关系。
Kawasaki disease (KD) is an acute febrile illness in infants and children with systemic clinical symptoms, including coronary artery aneurysms. Findings seen in KD patients such as infiltration of T cells into vascular lesions, elevation of soluble interleukin 2 receptors in serum, an imbalance of T cell subsets, and transient depletion of T cells with CD11/CD18 suggest that the activation of T cells is involved in the pathogenesis of KD. In 1992, an interesting mechanism was proposed in which T cell activation by a certain superantigen is involved in the pathogenesis of KD. Examinations have been undertaken extensively to confirm the proposed hypothesis. We, however, still do not have reliable evidence supporting the above hypothesis. In the present paper we review the research papers which support or rule out the view described above. In addition, we discuss the relation between KD and systemic Yersinia pseudotuberculosis infection that manifests clinical symptoms quite similar to those in KD.