Masuda K, Takei S, Nomura Y, Imanaka H, Sameshima K, Yoshinaga M
Department of Pediatrics, Faculty of Medicine, Kagoshima University, Kagoshima City, Sakuragaoka, Japan.
Pediatr Res. 1998 Jul;44(1):27-31. doi: 10.1203/00006450-199807000-00004.
Superantigens (SAs) are known to induce transient anergy followed by T cell activation. Recent reports have suggested that SAs are involved in the pathogenesis of Kawasaki disease (KD). In the present study, we investigated the peripheral T cell response to SAs by measuring proliferation and IL-2 production to determine whether the T cell anergy is induced by SAs in patients with KD. T cells were obtained from 45 Japanese patients with KD in different stages of the disease and were stimulated by streptococcal pyrogenic exotoxin (SPE)-A, SPE-C, and toxic shock syndrome toxin-1 (TSST-1). T cells from patients with KD in the acute or convalescent stage up to 2 mo showed significantly lower proliferation and IL-2 production than did T cells from healthy control subjects stimulated by SPE-C, but not SPE-A or TSST-1. The T cell response to SPE-C normalized within 1 y. The low T cell response to SPE-C in the acute stage correlated with a peak platelet count and the C-reactive protein-positive period. These findings suggest that the transient low T cell response to SPE-C in patients with KD may have been related to SA-induced anergy or disappearance of SPE-C-responding cells from the circulation. The present results suggested that SPE-C may be involved in the pathogenesis of KD.
已知超抗原（SAs）可诱导短暂的无反应性，随后激活T细胞。最近的报告表明，SAs参与了川崎病（KD）的发病机制。在本研究中，我们通过测量增殖和白细胞介素-2的产生来研究外周血T细胞对SAs的反应，以确定KD患者的T细胞无反应性是否由SAs诱导。从45名处于疾病不同阶段的日本KD患者中获取T细胞，并用链球菌致热外毒素（SPE）-A、SPE-C和中毒性休克综合征毒素-1（TSST-1）进行刺激。与健康对照受试者的T细胞相比，处于急性期或恢复期长达2个月的KD患者的T细胞对SPE-C刺激的增殖和白细胞介素-2产生显著降低，但对SPE-A或TSST-1刺激则不然。T细胞对SPE-C的反应在1年内恢复正常。急性期对SPE-C的低T细胞反应与血小板计数峰值和C反应蛋白阳性期相关。这些发现表明，KD患者对SPE-C的短暂低T细胞反应可能与SA诱导的无反应性或循环中对SPE-C有反应的细胞消失有关。目前的结果表明，SPE-C可能参与了KD的发病机制。
