Department of Pathology, Immunology, and Laboratory Medicine, University of Florida, Gainesville, FL, United States.
Front Immunol. 2022 May 26;13:887489. doi: 10.3389/fimmu.2022.887489. eCollection 2022.
Immune homeostasis is a constant balancing act between effector T cells and regulatory T cells defined by expression, the transcription factor that drives their differentiation and immunosuppressive activity. Immune homeostasis is altered when Treg cells are not generated or maintained in sufficient numbers. Treg cells rendered unstable by loss of expression, known as ex-Treg cells, gain pro-inflammatory functions. Treg cells may also become dysfunctional and lose their suppressive capabilities. These alterations can cause an imbalance between effector and regulatory subsets, which may ultimately lead to autoimmunity. This review discusses recent studies that identified genetic factors that maintain Treg cell stability as well as preserve their suppressive function. We focus on studies associated with systemic lupus erythematosus and highlight their findings in the context of potential therapeutic gene targeting in Treg cells to reverse the phenotypic changes and functional dysregulation inducing autoimmunity.
免疫稳态是效应 T 细胞和调节性 T 细胞之间的一种持续平衡，由表达和转录因子驱动其分化和免疫抑制活性来定义。当 Treg 细胞不能以足够的数量产生或维持时，免疫稳态就会发生改变。表达缺失导致的不稳定的 Treg 细胞，称为 ex-Treg 细胞，获得促炎功能。Treg 细胞也可能功能失调并失去其抑制能力。这些改变会导致效应细胞和调节性细胞亚群之间的失衡，最终可能导致自身免疫。这篇综述讨论了最近的研究，这些研究确定了维持 Treg 细胞稳定性和维持其抑制功能的遗传因素。我们专注于与系统性红斑狼疮相关的研究，并突出其在 Treg 细胞潜在治疗性基因靶向中的发现，以逆转诱导自身免疫的表型变化和功能失调。
