An update on the roles of transcription factor Ets1 in autoimmune diseases.
Lee Ann Garrett-SinhaPublished in: WIREs mechanisms of disease (2023)
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.
Keyphrases
- transcription factor
- genome wide identification
- endothelial cells
- dna binding
- gene expression
- immune response
- induced pluripotent stem cells
- pluripotent stem cells
- multiple sclerosis
- dna methylation
- mouse model
- genome wide
- copy number
- healthcare
- systematic review
- mental health
- randomized controlled trial
- mesenchymal stem cells
- bone marrow
- skeletal muscle
- binding protein
- dendritic cells
- genome wide analysis
- celiac disease