Uchiyama T, Kato H
Department of Microbiology and Immunology, School of Medicine, Tokyo Women's Medical University, Japan.
Jpn J Infect Dis. 1999 Aug;52(4):141-5.
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.
川崎病(KD)是一种发生于婴幼儿和儿童的急性发热性疾病,伴有包括冠状动脉瘤在内的全身性临床症状。KD患者出现的一些表现,如T细胞浸润至血管病变、血清中可溶性白细胞介素2受体升高、T细胞亚群失衡以及CD11/CD18阳性的T细胞短暂耗竭,提示T细胞活化参与了KD的发病机制。1992年,有人提出了一种有趣的机制,即某种超抗原激活T细胞参与了KD的发病机制。人们已进行了广泛的研究以证实这一假说。然而,我们仍然没有支持上述假说的可靠证据。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与系统性假结核耶尔森菌感染之间的关系,这种感染表现出与KD非常相似的临床症状。