{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,29]],"date-time":"2026-08-29T01:55:08Z","timestamp":1787968508090,"version":"build-2784847793"},"reference-count":56,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2015,6,27]],"date-time":"2015-06-27T00:00:00Z","timestamp":1435363200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/100010805","name":"FORSS","doi-asserted-by":"crossref","id":[{"id":"10.13039\/100010805","id-type":"DOI","asserted-by":"crossref"}]},{"name":"Futurum, academy for Health and Care J\u00f6nk\u00f6ping County Council, Sweden"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American J Rep Immunol"],"published-print":{"date-parts":[[2015,10]]},"abstract":"<jats:sec><jats:title>Problem<\/jats:title><jats:p>A deficiency in regulatory T (Treg) cells causing reduced immune regulatory capacity has been proposed in preeclampsia.<\/jats:p><\/jats:sec><jats:sec><jats:title>Objective<\/jats:title><jats:p>Utilizing recent advances in flow cytometry phenotyping, we aimed to assess whether a deficiency of Treg subpopulations occurs in preeclampsia.<\/jats:p><\/jats:sec><jats:sec><jats:title>Method of study<\/jats:title><jats:p>Six\u2010color flow cytometry was used for Treg phenotyping in 18 preeclamptic women (one early\u2010onset, one severe and 16 both), 20 women with normal pregnancy, and 20 non\u2010pregnant controls.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>No differences were found in major Treg populations including <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>127<jats:sup>low<\/jats:sup><jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>25<jats:sup>+<\/jats:sup>\/<jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>127<jats:sup>ow<\/jats:sup><jats:styled-content style=\"fixed-case\">FOXP<\/jats:styled-content>3<jats:sup>+<\/jats:sup>, resting (<jats:styled-content style=\"fixed-case\">FOXP<\/jats:styled-content>3<jats:sup>dim<\/jats:sup><jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>45<jats:styled-content style=\"fixed-case\">RA<\/jats:styled-content><jats:sup>+<\/jats:sup>), and activated (<jats:styled-content style=\"fixed-case\">FOXP<\/jats:styled-content>3<jats:sup>bright<\/jats:sup><jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>45<jats:styled-content style=\"fixed-case\">RA<\/jats:styled-content><jats:sup>\u2212<\/jats:sup>) Treg cells, whereas preeclamptic women showed increased <jats:styled-content style=\"fixed-case\">CTLA<\/jats:styled-content>\u20104<jats:sup>+<\/jats:sup> and <jats:styled-content style=\"fixed-case\">CCR<\/jats:styled-content>4<jats:sup>+<\/jats:sup> proportions within resting\/activated Treg populations. Corticosteroid treatment prior to blood sampling (<jats:italic>n<\/jats:italic>\u00a0=\u00a010) affected the distribution of Treg populations.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>Although we found no major alterations in circulating Treg frequencies, differences in <jats:styled-content style=\"fixed-case\">CTLA<\/jats:styled-content>\u20104<jats:sup>+<\/jats:sup> and <jats:styled-content style=\"fixed-case\">CCR<\/jats:styled-content>4<jats:sup>+<\/jats:sup> frequencies suggest a migratory defect of Treg cells in preeclampsia. 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