Treg is essential to limit the extend and duration of the immune response, but its stability is still under debate. Here we demonstrate that IL-17-producing Treg cells (Th17-like cells) increased in peripheral blood of patients with Systemic Lupus Erythematosus (SLE). Notably, the Th17-like cells from patient with active SLE were characterized with some phenotype and function of Th17 cells. Upon stimulation, Helios-Foxp3 + CD4+ T cells decrease Foxp3 expression but increase expression of IL-17 and RORγt. Damage associated molecule pattern and inflammatory cytokines are important for induction of IL-17 expression in Treg cells. The Th17-like cells from patients with active SLE lose suppressive function and have robust response to stimulation of autoantigens. We also observed that the level of Th17-like cells in peripheral blood is closely associated with the clinical index of SLE. These findings suggest that instability of Treg plays a critical role in pathogenesis of autoimmune diseases.

中文翻译：

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活动性系统性红斑狼疮患者外周Foxp3 +调节性T细胞向Th17样细胞的重编程。

Treg对于限制免疫反应的范围和持续时间至关重要，但其稳定性仍在争论中。在这里，我们证明系统性红斑狼疮（SLE）患者外周血中产生IL-17的Treg细胞（Th17样细胞）增加。值得注意的是，活动性SLE患者的Th17样细胞具有Th17细胞的某些表型和功能。刺激后，Helios-Foxp3 + CD4 + T细胞降低Foxp3表达，但增加IL-17和RORγt的表达。损伤相关分子模式和炎性细胞因子对于诱导Treg细胞中IL-17表达很重要。活动性SLE患者的Th17样细胞失去抑制功能，对自身抗原刺激反应强烈。我们还观察到外周血中Th17样细胞的水平与SLE的临床指标密切相关。这些发现表明，Treg的不稳定性在自身免疫疾病的发病机理中起关键作用。