State Key Laboratory of Chemical Oncogenomics, Key Laboratory of Chemical Genome, Peking University, Shenzhen Graduate School, School of Chemical Biology & Biotechnology, Shenzhen, 518055, China.
Department of Rheumatology and Immunology, Shenzhen Children's Hospital, 7019 Yitian Road, Shenzhen, 518026, China.
BMC Immunol. 2021 Feb 23;22(1):17. doi: 10.1186/s12865-021-00407-x.
Kawasaki disease is an autoimmune disease characterized by systemic vasculitis of unknown aetiology and most commonly occurs in children under 5 years old. Previous studies have found that the over-activation of lymphocytes is an important mechanism of Kawasaki disease. Activin A, also known as immunosuppressive factor P, is a multifunctional growth and transforming factor. However, whether activin A is involved in the regulation of peripheral lymphocytes activity in Kawasaki disease is unclear. Thus, we aimed to investigate the effect of activin A on the activity of peripheral lymphocytes in acute-phase Kawasaki disease.
Seven patients with Kawasaki disease and seven healthy controls were studied. Peripheral blood lymphocytes were isolated by Ficoll density gradient centrifugation. The activation of CD4 and CD8 T cells and CD19 B cells was investigated by flow cytometry. The expression of activin type IIA receptors was investigated by flow cytometry.
Immune imbalance in CD4 and CD8 lymphocytes were detected in acute-phase Kawasaki disease. The expression of activin type IIA receptors on CD8 T cells and CD19 B cells was increased in acute-phase Kawasaki disease and decreased following treatment with activin A. Activin A suppressed the expression of CD25 and CD69 on CD8 T cells and the expression of CD69 on CD19 B cells.
The expression of activin type IIA receptor was increased on CD8 T cells and CD19 B cells in Kawasaki disease. Activin A suppressed the expression of CD25, CD69 and activin type IIA receptors on peripheral CD8 T lymphocyte. Activin A plays different roles in different lymphocyte subsets and suppresses peripheral CD8 T lymphocyte activity in acute-phase Kawasaki disease.
川崎病是一种病因不明的全身性自身免疫性血管炎，多发生于 5 岁以下儿童。既往研究发现，淋巴细胞过度激活是川崎病的重要发病机制。激活素 A 又称免疫抑制因子 P，是一种多功能生长转化因子。然而，激活素 A 是否参与川崎病患者外周淋巴细胞活性的调节尚不清楚。因此，本研究旨在探讨激活素 A 对川崎病急性期外周淋巴细胞活性的影响。
选取 7 例川崎病患者和 7 例健康对照者，采用 Ficoll 密度梯度离心法分离外周血淋巴细胞，流式细胞术检测 CD4、CD8 T 细胞和 CD19 B 细胞的激活情况，流式细胞术检测激活素 IIA 型受体的表达。
川崎病急性期存在 CD4、CD8 淋巴细胞免疫失衡，CD8 T 细胞和 CD19 B 细胞激活素 IIA 型受体表达增加，经激活素 A 治疗后表达降低。激活素 A 可抑制 CD8 T 细胞 CD25、CD69 和 CD19 B 细胞 CD69 的表达。
川崎病患者 CD8 T 细胞和 CD19 B 细胞激活素 IIA 型受体表达增加，激活素 A 可抑制外周血 CD8 T 淋巴细胞 CD25、CD69 和激活素 IIA 型受体的表达，在不同的淋巴细胞亚群中发挥不同的作用，抑制川崎病急性期外周血 CD8 T 淋巴细胞的活性。
