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Though most infections are subclinical in immunocompetent individuals, congenital contraction can lead to severe consequences such as spontaneous abortion, stillbirth, and a range of cranio-cerebral and\/or ocular abnormalities. Previous studies reported that <jats:italic>T. gondii<\/jats:italic>-infected pregnancy mice unveiled a deficit in both the amount and suppressive functions of regulatory T (Treg) cells, accompanied with reduced levels of forkhead box p3 (Foxp3). Recently, accumulative studies have demonstrated that microRNAs (miRNAs) are, to some extent, relevant to <jats:italic>T. gondii<\/jats:italic> infection. However, the link between alterations in miRNAs and downregulation of Foxp3 triggered by <jats:italic>T. gondii<\/jats:italic> has been only sporadically studied.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Methods<\/jats:title>\n                <jats:p>Quantitative reverse transcription polymerase chain reaction (RT-qPCR), protein blotting and immunofluorescence were employed to evaluate the impact of <jats:italic>T. gondii<\/jats:italic> infection and antigens on miRNA transcription and Foxp3 expression. Dual-luciferase reporter gene assays were performed to examine the fluorescence activity in EL4 cells, which were transfected with recombinant plasmids containing full-length\/truncated\/mutant microRNA-142a-3p (miR-142a) promoter sequence or wild type\/mutant of Foxp3 3\u2019 untranslated region (3\u2019 UTR).<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Results<\/jats:title>\n                <jats:p>We found a pronounced increase in miR-142a transcription, concurrent with a decrease in Foxp3 expression in <jats:italic>T. gondii<\/jats:italic>-infected mouse placental tissue. Similarly, comparable findings have been experimentally confirmed through the treatment of EL4 cells with <jats:italic>T. gondii<\/jats:italic> antigens (<jats:italic>Tg<\/jats:italic>Ag) in vitro. Simultaneously, miR-142a mimics attenuated Foxp3 expression, whereas its inhibitors markedly augmented Foxp3 expression. miR-142a promoter activity was elevated upon the stimulation of <jats:italic>T. gondii<\/jats:italic> antigens, which mitigated co-transfection of mutant miR-142a promoter lacking P53 target sites. miR-142a mimics deceased the fluorescence activity of Foxp3 3\u2019 untranslated region (3\u2019 UTR), but it did not affect the fluorescence activity upon the co-transfection of mutant Foxp3 3\u2019 UTR lacking miR-142a target site.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Conclusion<\/jats:title>\n                <jats:p>In both in vivo and in vitro studies, a negative correlation was discovered between Foxp3 expression and miR-142a transcription. <jats:italic>Tg<\/jats:italic>Ag enhanced miR-142a promoter activity to facilitate miR-142a transcription through a P53-dependent mechanism. Furthermore, miR-142a directly targeted Foxp3 3\u2019 UTR, resulting in the downregulation of Foxp3 expression. Therefore, harnessing miR-142a may be a possible therapeutic approach for adverse pregnancy caused by immune imbalances, particularly those induced by <jats:italic>T. gondii<\/jats:italic> infection.<\/jats:p>\n              <\/jats:sec>","DOI":"10.1186\/s12879-024-09375-0","type":"journal-article","created":{"date-parts":[[2024,5,13]],"date-time":"2024-05-13T09:02:50Z","timestamp":1715590970000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["The role of microRNA-142a in Toxoplasma gondii infection-induced downregulation of Foxp3: implications for adverse pregnancy outcomes"],"prefix":"10.1186","volume":"24","author":[{"given":"Yue","family":"Zhong","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yining","family":"Cao","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Xiaoyu","family":"Geng","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Shujin","family":"Yang","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Tianmei","family":"Qian","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Chun","family":"Liu","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jinling","family":"Chen","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"297","published-online":{"date-parts":[[2024,5,13]]},"reference":[{"issue":"6","key":"9375_CR1","doi-asserted-by":"publisher","first-page":"3076","DOI":"10.3390\/ijms23063076","volume":"23","author":"MF Ragab","year":"2022","unstructured":"Ragab MF, Yoshifumi N. 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