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B\u2010cell deficient (B<jats:sup>\u2013\/\u2013<\/jats:sup>) mice are resistant to <jats:styled-content style=\"fixed-case\">SAT<\/jats:styled-content> but develop <jats:styled-content style=\"fixed-case\">SAT<\/jats:styled-content> if regulatory T (Treg) cells are transiently depleted. We established a transfer model using splenocytes from <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>28<jats:sup>\u2013\/\u2013<\/jats:sup>\u00a0B<jats:sup>\u2013\/\u2013<\/jats:sup> mice (effector cells and antigen\u2010presenting cells) cultured with or without sorted Treg cells from Foxp3\u2010<jats:styled-content style=\"fixed-case\">GFP<\/jats:styled-content> wild\u2010type (<jats:styled-content style=\"fixed-case\">WT<\/jats:styled-content>) or B<jats:sup>\u2013\/\u2013<\/jats:sup> mice. After transfer to mice lacking T cells, mice given Treg cells from B<jats:sup>\u2013\/\u2013<\/jats:sup> mice had significantly lower <jats:styled-content style=\"fixed-case\">SAT<\/jats:styled-content> severity scores than mice given Treg cells from <jats:styled-content style=\"fixed-case\">WT<\/jats:styled-content> mice, indicating that Treg cells in B<jats:sup>\u2013\/\u2013<\/jats:sup> mice are more effective suppressors of <jats:styled-content style=\"fixed-case\">SAT<\/jats:styled-content> than Treg cells in <jats:styled-content style=\"fixed-case\">WT<\/jats:styled-content> mice. Treg cells from B<jats:sup>\u2013\/\u2013<\/jats:sup> mice differ from <jats:styled-content style=\"fixed-case\">WT<\/jats:styled-content> Treg cells in expression of <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>27, tumour necrosis factor receptor (<jats:styled-content style=\"fixed-case\">TNFR<\/jats:styled-content>) <jats:styled-content style=\"fixed-case\">II<\/jats:styled-content> p75, and glucocorticoid\u2010induced <jats:styled-content style=\"fixed-case\">TNFR<\/jats:styled-content>\u2010related protein (<jats:styled-content style=\"fixed-case\">GITR<\/jats:styled-content>). After transient depletion using anti\u2010<jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>25 or diphtheria toxin, the repopulating Treg cells in B<jats:sup>\u2013\/\u2013<\/jats:sup> mice lack suppressor function, and expression of <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>27, <jats:styled-content style=\"fixed-case\">GITR<\/jats:styled-content> and p75 is like that of <jats:styled-content style=\"fixed-case\">WT<\/jats:styled-content> Treg cells. If B<jats:sup>\u2013\/\u2013<\/jats:sup> Treg cells develop with B cells in bone marrow chimeras, their phenotype is like that of <jats:styled-content style=\"fixed-case\">WT<\/jats:styled-content> Treg cells. Addition of B cells to cultures of B<jats:sup>\u2013\/\u2013<\/jats:sup> Treg and T effector cells abrogates their suppressive function and their phenotype is like that of <jats:styled-content style=\"fixed-case\">WT<\/jats:styled-content> Treg cells. These results establish for the first time that Treg cells in <jats:styled-content style=\"fixed-case\">WT<\/jats:styled-content> and B<jats:sup>\u2013\/\u2013<\/jats:sup> mice differ both functionally and in expression of particular cell surface markers. Both properties are altered after transient depletion and repopulation of B<jats:sup>\u2013\/\u2013<\/jats:sup> Treg cells, and by the presence of B cells during Treg cell development or during interaction with effector T cells.<\/jats:p>","DOI":"10.1111\/imm.12410","type":"journal-article","created":{"date-parts":[[2014,10,15]],"date-time":"2014-10-15T14:10:17Z","timestamp":1413382217000},"page":"598-610","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":11,"title":["Regulatory T cells in B\u2010cell\u2010deficient and wild\u2010type mice differ functionally and in expression of cell surface markers"],"prefix":"10.1111","volume":"144","author":[{"given":"Jason S.","family":"Ellis","sequence":"first","affiliation":[{"name":"Department of Medicine University of Missouri Columbia MO USA"},{"name":"Department of Molecular Microbiology &amp; Immunology University of Missouri Columbia MO 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