STAT5A and MKL-1 activate the activity of luciferase reporter plasmid containing FOXP3 gene promoter

Abstract

Idiopathic thrombocytopenic purpura (ITP) is a chronic acquired organ-specific autoimmune hemorrhagic disease, It has been proved that the reduce of regulatory T cells (Treg) (CD4+CD25+FOXP3+) was an important cause of ITP, and the transcriptional factor FOXP3 played an important role in the proliferation and differentiation of Treg cells. However, the definite transcription mechanism of foxp3 gene is unclear. In this study, human foxp3 promoter luciferase reporter construct was successfully constructed. Then transfected one of the two overexpression vectors of human MKL-1 and human STAT5A or both into 293T cells, and detected the activation of the foxp3 promoter by luciferase reporter assay. The result showed that transfected each of the overexpression vectors can enhance the transcriptional activity of FOXP3, and this activity effect can be enhancing when the two vectors were cotransfected. Our research will further reveal the proliferation and differentiation of Treg cells and may provide theoretical foundations for methods to cure ITP.