Wu Yongzhuo, Zhou Yali, Zhu Qinghuan, Liu Yingying, Deng Danqi, Zhang Jianzhong
Department of Dermatology, The Second Affiliated Hospital of Kunming Medical University, Kunming, 650101, PR China.
Department of Dermatology, Peking University People's Hospital, Beijing, 100044, PR China.
Heliyon. 2024 Aug 8;10(16):e35949. doi: 10.1016/j.heliyon.2024.e35949. eCollection 2024 Aug 30.
Systemic lupus erythematosus (SLE) is largely caused by B cell dysfunction. JunD is an activator protein 1 family protein that has been linked to the regulation of apoptotic and proliferative activities. However, the precise mechanism(s) by which JunD functions remains to be fully elucidated. Accordingly, this study aimed to clarify the functional importance of JUND gene expression in SLE, with further analyses of the functional role that JunD plays as a regulator of B cell proliferation and immune function.
Reverse transcriptase quantitative polymerase chain reaction techniques were used to analyze JunD expression in B cells of patients with SLE and healthy subjects. Cell Counting Kit-8 (CCK-8) assays and flow cytometry methods were used to characterise proliferative activity, cell cycle progression, and apoptosis of B cells in which JunD was either knocked down or overexpressed. The immune status and autophagic activity of these cells were assessed using Western immunoblotting and enzyme-linked immunosorbent assay (ELISA). Additionally, a JunD knockdown mouse model was established, and the functional role of B cell JunD expression in the pathogenesis of SLE was assessed using Western immunoblotting, ELISA, and haematoxylin and eosin staining.
B cells from patients with SLE exhibited upregulation of JunD, with overexpression facilitating cellular proliferation and modulation of the immune and autophagic status of these B cells. JunD knockdown was also sufficient to modulate immune function and the autophagic status of B cells.
JunD was upregulated in the B cells of patients with SLE, where it regulates proliferation, autophagy, and immunity.
系统性红斑狼疮（SLE）主要由B细胞功能障碍引起。JunD是一种激活蛋白1家族蛋白，与细胞凋亡和增殖活性的调节有关。然而，JunD发挥作用的确切机制仍有待充分阐明。因此，本研究旨在阐明JUND基因表达在SLE中的功能重要性，并进一步分析JunD作为B细胞增殖和免疫功能调节因子所起的作用。
采用逆转录定量聚合酶链反应技术分析SLE患者和健康受试者B细胞中JunD的表达。使用细胞计数试剂盒-8（CCK-8）检测和流式细胞术方法来表征JunD被敲低或过表达的B细胞的增殖活性、细胞周期进程和凋亡情况。使用蛋白质免疫印迹法和酶联免疫吸附测定（ELISA）评估这些细胞的免疫状态和自噬活性。此外，建立了JunD敲低小鼠模型，并使用蛋白质免疫印迹法、ELISA和苏木精-伊红染色评估B细胞JunD表达在SLE发病机制中的作用。
SLE患者的B细胞中JunD表达上调，过表达促进了这些B细胞的增殖以及免疫和自噬状态的调节。JunD敲低也足以调节B细胞的免疫功能和自噬状态。
JunD在SLE患者的B细胞中上调，在其中调节增殖、自噬和免疫。
