Shenzhen Graduate School, School of Chemical Biology and Biotechnology, State Key Laboratory of Chemical Oncogenomics, Key Laboratory of Chemical Genome, Peking University, Shenzhen, 518055, China.
Department of Rheumatology and Immunology, Shenzhen Children's Hospital, 7019 Yitian Road, Shenzhen, 518026, China.
Clin Exp Med. 2021 Aug;21(3):407-414. doi: 10.1007/s10238-021-00695-y. Epub 2021 Feb 25.
Kawasaki disease is a kind of self-limited systemic vasculitis involving middle and small arteries, which usually occurs in children under 5 years old. Excessive inflammatory response caused by activation of monocytes is one of the important mechanisms of Kawasaki disease. Activated monocytes secrete large amounts of inflammatory mediators such as TNF-α and IL-1β. Activin A, a member of transforming growth factor-β superfamily, is a multifunctional growth and transforming factor. Several experimental evidences pinpoint that Activin A can regulate multiple biological function of the immune system. However, whether Activin A is involved in regulation of activation of monocytes in Kawasaki disease was not well characterized. Here, this study showed that the expression of Activin A in serum decreased in acute-phase Kawasaki disease. Furthermore, Activin A inhibits activin type IIA receptor, activin type IB receptor, CD86 and CD80 expression in over-activated monocytes. In addition, Activin A inhibited Smad3 expression and NF-κB signaling pathways. Specific function and mechanism of Activin A in acute-phase Kawasaki disease need further study.
川崎病是一种累及中、小动脉的自限性全身性血管炎，多发生于 5 岁以下儿童。单核细胞的激活导致过度炎症反应是川崎病的重要发病机制之一。活化的单核细胞可分泌大量的炎症介质，如 TNF-α 和 IL-1β。激活素 A 是转化生长因子-β超家族的成员，是一种多功能的生长和转化因子。有几项实验证据表明激活素 A 可以调节免疫系统的多种生物学功能。然而，激活素 A 是否参与川崎病中单核细胞的激活调节尚不清楚。本研究表明，川崎病急性期患者血清中激活素 A 的表达降低。此外，激活素 A 可抑制过度激活的单核细胞中激活素Ⅱ型 A 受体、激活素 I 型 B 受体、CD86 和 CD80 的表达。此外，激活素 A 还抑制 Smad3 表达和 NF-κB 信号通路。激活素 A 在川崎病急性期的具体作用和机制还需要进一步研究。
