An update on the roles of transcription factor Ets1 in autoimmune diseases.

IF 4.6 3区 医学 Q2 MEDICINE, RESEARCH & EXPERIMENTAL WIREs Mechanisms of Disease Pub Date : 2023-11-01 Epub Date: 2023-08-10 DOI:10.1002/wsbm.1627
Lee Ann Garrett-Sinha
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Abstract

Transcription factors are crucial to regulate gene expression in immune cells and in other cell types. In lymphocytes, there are a large number of different transcription factors that are known to contribute to cell differentiation and the balance between quiescence and activation. One such transcription factor is E26 oncogene homolog 1 (Ets1). Ets1 expression is high in quiescent B and T lymphocytes and its levels are decreased upon activation. The human ETS1 gene has been identified as a susceptibility locus for many autoimmune and inflammatory diseases. In accord with this, gene knockout of Ets1 in mice leads to development of a lupus-like autoimmune disease, with enhanced activation and differentiation of both B cells and T cells. Prior reviews have summarized functional roles for Ets1 based on studies of Ets1 knockout mice. In recent years, numerous additional studies have been published that further validate ETS1 as a susceptibility locus for human diseases where immune dysregulation plays a causative role. In this update, new information that further links Ets1 to human autoimmune diseases is organized and collated to serve as a resource. This update also describes recent studies that seek to understand molecularly how Ets1 regulates immune cell activation, either using human cells and tissues or mouse models. This resource is expected to be useful to investigators seeking to understand how Ets1 may regulate the human immune response, particularly in terms of its roles in autoimmunity and inflammation. This article is categorized under: Immune System Diseases > Genetics/Genomics/Epigenetics Immune System Diseases > Molecular and Cellular Physiology.

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转录因子Ets1在自身免疫性疾病中作用的最新进展
转录因子对调节免疫细胞和其他细胞类型中的基因表达至关重要。在淋巴细胞中,已知有大量不同的转录因子有助于细胞分化以及静止和激活之间的平衡。一种这样的转录因子是E26癌基因同源物1(Ets1)。Ets1在静止的B和T淋巴细胞中表达高,并且其水平在激活时降低。人类ETS1基因已被鉴定为许多自身免疫性和炎症性疾病的易感基因座。与此一致,小鼠中Ets1的基因敲除导致狼疮样自身免疫性疾病的发展,同时增强了B细胞和T细胞的活化和分化。先前的综述基于对Ets1敲除小鼠的研究总结了Ets1的功能作用。近年来,发表了许多其他研究,进一步证实ETS1是免疫失调起致病作用的人类疾病的易感基因座。在这次更新中,组织和整理了将Ets1与人类自身免疫性疾病进一步联系起来的新信息,作为一种资源。这一更新还描述了最近的研究,这些研究试图从分子上理解Ets1如何调节免疫细胞激活,无论是使用人类细胞和组织还是小鼠模型。这一资源预计将对寻求了解Ets1如何调节人类免疫反应的研究人员有用,特别是在其在自身免疫和炎症中的作用方面。这篇文章分类在:免疫系统疾病>遗传学/基因组学/表观遗传学免疫系统疾病>分子和细胞生理学。
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来源期刊
WIREs Mechanisms of Disease
WIREs Mechanisms of Disease MEDICINE, RESEARCH & EXPERIMENTAL-
CiteScore
11.40
自引率
0.00%
发文量
45
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