Wang Shuhui, Qian Guanghui, Liu Ying, Li Xuan, Huang Hongbiao, Sun Ling, Lv Haitao
Department of Cardiology, Children's Hospital of Soochow University, Suzhou, Jiangsu, China.
Department of Pediatrics, Institute of Pediatric Research, Children's Hospital of Soochow University, Suzhou, Jiangsu, China.
Front Immunol. 2025 Jul 17;16:1582638. doi: 10.3389/fimmu.2025.1582638. eCollection 2025.
Kawasaki disease (KD) is a systemic immune vasculitis characterized by fever and is a common cause of acquired heart disease in children. The etiology of KD remains unclear, but it is generally believed to be an amplified inflammatory cascade caused by the combined action of infection and genetic susceptibility factors. Changes in T lymphocyte subsets and their abnormal activation play an important role in the immune response to KD. This review delves into the critical role of T cells in the pathogenesis of KD, with a particular focus on how the expansion of CD8+ T cells and the imbalance between Th17 and Tregs contribute to IVIG resistance and persistent inflammation. Our analysis suggests that interventions targeting T cell function could potentially improve the clinical prognosis for KD patients. This provides specific directions for future therapeutic strategies, including the use of novel immunomodulatory approaches such as cyclosporine and IL-17/IL-23 inhibitors, aimed at providing new insights into the pathogenesis and treatment of KD.
川崎病（KD）是一种以发热为特征的全身性免疫性血管炎，是儿童后天性心脏病的常见病因。KD的病因尚不清楚，但一般认为是由感染和遗传易感性因素共同作用引起的炎症级联反应增强所致。T淋巴细胞亚群的变化及其异常激活在KD的免疫反应中起重要作用。本综述深入探讨了T细胞在KD发病机制中的关键作用，特别关注CD8+T细胞的扩增以及Th17和Tregs之间的失衡如何导致静脉注射免疫球蛋白（IVIG）抵抗和持续性炎症。我们的分析表明，针对T细胞功能的干预措施可能会改善KD患者的临床预后。这为未来的治疗策略提供了具体方向，包括使用新型免疫调节方法，如环孢素和IL-17/IL-23抑制剂，旨在为KD的发病机制和治疗提供新的见解。
