Systemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by abnormal activation of T cells and caused by an imbalance in the production and clearance of apoptotic cells. We previously showed that the transcription regulator Bach2 regulated abnormal B‐cell activation in SLE. Here, we investigated whether Bach2 was also involved in Th9 cell differentiation in SLE. We found that the proportion of Th9 cells was enhanced in the peripheral blood mononuclear cells (PBMC) of SLE patients. The PBMC and CD4⁺ T cells of SLE patients exhibited a decrease of Bach2 expression and an increase of IL‐9 expression. Furthermore, Bach2 overexpression significantly repressed the levels of PU.1, IRF4, IL‐9, and Th9 cells in the CD4⁺ T cells of SLE patients and healthy volunteers. In addition, Bach2 overexpression inhibited the levels of IL‐9 and Th9 cells, whereas IRF4 upregulation enhanced the levels of IRF4 and IL‐9 and Th9 cells in the CD4⁺ T cells of SLE patients and healthy volunteers. The effect of IRF4 up‐regulation was abolished by Bach2 overexpression. In summary, our work suggests that Bach2 overexpression represses Th9 cell differentiation by suppressing IRF4 expression in SLE, and thus, Bach2 may be a novel potential target for SLE treatment.

中文翻译：

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Bach2过表达通过抑制系统性红斑狼疮中IRF4的表达来抑制Th9细胞分化

系统性红斑狼疮 (SLE) 是一种慢性自身免疫性疾病，其特征是 T 细胞异常活化，由凋亡细胞的产生和清除失衡引起。我们之前发现转录调节因子 Bach2 调节 SLE 中的异常 B 细胞活化。在这里，我们研究了 Bach2 是否也参与 SLE 中的 Th9 细胞分化。我们发现 SLE 患者外周血单个核细胞 (PBMC) 中 Th9 细胞的比例增加。SLE患者的PBMC和CD4 ⁺ T细胞表现出Bach2表达减少和IL-9表达增加。此外，Bach2 过表达显着抑制 CD4 ^{+中 PU.1、IRF4、IL-9 和 Th9 细胞的水平。}SLE患者和健康志愿者的T细胞。此外，Bach2 过表达抑制了 IL-9 和 Th9 细胞的水平，而 IRF4 上调提高了 SLE 患者和健康志愿者 CD4 ⁺ T 细胞中 IRF4 和 IL-9 和 Th9 细胞的水平。Bach2 过表达消除了 IRF4 上调的作用。总之，我们的工作表明，Bach2 过表达通过抑制 SLE 中 IRF4 的表达来抑制 Th9 细胞分化，因此，Bach2 可能是 SLE 治疗的一个新的潜在靶点。