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Defective generation or function of regulatory T cells (Tregs) may account for those adverse pregnancy outcomes. Forkhead box p3 (Foxp3), which is the key\u00a0transcriptional factor of Tregs, modulates its development and maintains inhibitory function. We previously demonstrated that ESA inhibited Foxp3 expression by attenuating transforming growth factor \u03b2 RII\/Smad2\/Smad3\/Smad4 pathway. In this study, we propose to study the role of ESA on the activity of Foxp3 promoter and explore potential mechanisms. We demonstrated that ESA suppressed Foxp3 promoter activity using dual\u2010luciferase reporter assay. ESA functioned at \u2212443\/\u221296 region of Foxp3 promoter to suppress its activity using truncated fragments of Foxp3 promoter. Further analysis revealed that suppressive role of ESA on Foxp3 promoter activity is related to specificity protein 1 (SP1). Transfection of expression plasmid of pcDNA3.1\u2010SP1 could restore the down\u2010regulation of Foxp3 induced by ESA. In conclusion, this study provides a new mechanism by which ESA could inhibit the Foxp3 promoter activity via SP1.<\/jats:p>","DOI":"10.1111\/jcmm.15703","type":"journal-article","created":{"date-parts":[[2020,7,30]],"date-time":"2020-07-30T05:55:50Z","timestamp":1596088550000},"page":"10785-10791","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":5,"title":["<i>Toxoplasma gondii<\/i> excreted\u2010secreted antigens suppress Foxp3 promoter activity via a SP1\u2010dependent mechanism"],"prefix":"10.1111","volume":"24","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-2992-6571","authenticated-orcid":false,"given":"Jinling","family":"Chen","sequence":"first","affiliation":[{"name":"Department of Pathogen Biology School of Medicine Nantong University Nantong China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jingjing","family":"Wang","sequence":"additional","affiliation":[{"name":"Department of Pathogen Biology 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