Background: Systemic sclerosis (SSc) is a chronic, immune-mediated, connective tissue disease causing microvascular abnormalities and fibrosis. The cytoplasmic calcium influx kinetics in T lymphocytes governs lymphocyte activation in this inflammatory process. The inhibition of Kv1.3 and IKCa1 potassium channels reduces calcium influx. Methods: This study aimed to analyze cytoplasmic calcium influx kinetics following activation in Th1, Th2, and CD8 cells in peripheral blood of 12 healthy individuals and 16 patients with systemic sclerosis using flow cytometry. We also evaluated the effect of the specific inhibition of the Kv1.3 and IKCa1 potassium channels. Results: We observed higher levels of activation in CD8 compared with Th1 cells in SSc. However, the activation of CD8 cells was lower in SSc compared to healthy controls. Moreover, activation of Th1 lymphocytes was slower in SSc than in healthy controls. The inhibition of IKCa1 channels decreased the activation of Th1 cells, while the inhibition of Kv1.3 channels modified the dynamics of activation of Th1 and Th2 lymphocytes in SSc. Conclusion: Th1 and CD8 cells demonstrate specific activation dynamics and sensitivity to potassium channel inhibition in SSc, distinguishing this condition both from healthy controls and other autoimmune diseases.

中文翻译：

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系统性硬化症外周T淋巴细胞钙内流动力学及钾通道特征

背景：系统性硬化症 (SSc) 是一种慢性、免疫介导的结缔组织疾病，可导致微血管异常和纤维化。T 淋巴细胞中的细胞质钙流入动力学控制着该炎症过程中的淋巴细胞活化。Kv1.3 和 IKCa1 钾通道的抑制减少了钙内流。方法：本研究旨在使用流式细胞术分析 12 名健康个体和 16 名系统性硬化症患者外周血中 Th1、Th2 和 CD8 细胞激活后的细胞质钙流入动力学。我们还评估了 Kv1.3 和 IKCa1 钾通道的特异性抑制作用。结果：我们观察到与 SSc 中的 Th1 细胞相比，CD8 中的活化水平更高。然而，与健康对照相比，SSc 中 CD8 细胞的活化较低。而且，SSc 中 Th1 淋巴细胞的活化比健康对照慢。IKCa1 通道的抑制降低了 Th1 细胞的活化，而 Kv1.3 通道的抑制改变了 SSc 中 Th1 和 Th2 淋巴细胞的活化动力学。结论：Th1 和 CD8 细胞在 SSc 中表现出特定的激活动力学和对钾通道抑制的敏感性，将这种情况与健康对照和其他自身免疫性疾病区分开来。