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B cells play protective roles during inflammation as well. However, the roles of endogenous <jats:styled-content style=\"fixed-case\">PPAR<\/jats:styled-content>\u2010<jats:italic>\u03b3<\/jats:italic> in the regulatory properties of B cells to relieve inflammation remain unknown. Here, we developed B\u2010cell\u2010specific <jats:styled-content style=\"fixed-case\">PPAR<\/jats:styled-content>\u2010<jats:italic>\u03b3<\/jats:italic> knockout (B\u2010<jats:styled-content style=\"fixed-case\">PPAR<\/jats:styled-content>\u2010<jats:italic>\u03b3<\/jats:italic><jats:sup>\u2212\/\u2212<\/jats:sup>) mice and found that the conditional deletion of <jats:styled-content style=\"fixed-case\">PPAR<\/jats:styled-content>\u2010<jats:italic>\u03b3<\/jats:italic> in B cells resulted in exaggerated contact hypersensitivity (<jats:styled-content style=\"fixed-case\">CHS<\/jats:styled-content>). Meanwhile, interferon\u2010<jats:italic>\u03b3<\/jats:italic> (<jats:styled-content style=\"fixed-case\">IFN<\/jats:styled-content>\u2010<jats:italic>\u03b3<\/jats:italic>) of <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>4<jats:sup>+<\/jats:sup> <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>8<jats:sup>+<\/jats:sup> T cells was up\u2010regulated in B\u2010<jats:styled-content style=\"fixed-case\">PPAR<\/jats:styled-content>\u2010<jats:italic>\u03b3<\/jats:italic><jats:sup>\u2212\/\u2212<\/jats:sup> mice in <jats:styled-content style=\"fixed-case\">CHS<\/jats:styled-content>. This showed that the regulatory function of B cells in B\u2010<jats:styled-content style=\"fixed-case\">PPAR<\/jats:styled-content>\u2010<jats:italic>\u03b3<\/jats:italic><jats:sup>\u2212\/\u2212<\/jats:sup> mice declined <jats:italic>in vivo<\/jats:italic>. Whereas splenic <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>5<jats:sup>+<\/jats:sup> <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>1d<jats:sup>hi<\/jats:sup> regulatory B\u2010cell numbers and peripheral regulatory T\u2010cell numbers were not changed in naive B\u2010<jats:styled-content style=\"fixed-case\">PPAR<\/jats:styled-content>\u2010<jats:italic>\u03b3<\/jats:italic><jats:sup>\u2212\/\u2212<\/jats:sup> mice. Loss of <jats:styled-content style=\"fixed-case\">PPAR<\/jats:styled-content>\u2010<jats:italic>\u03b3<\/jats:italic> in B cells also did not affect either <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>86 or FasL expression in splenic <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>5<jats:sup>+<\/jats:sup> <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>1d<jats:sup>hi<\/jats:sup> regulatory B cells after activation. Notably, interleukin\u201010 (<jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201010) production in <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>5<jats:sup>+<\/jats:sup> <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>1d<jats:sup>hi<\/jats:sup> regulatory B cells reduced in B\u2010<jats:styled-content style=\"fixed-case\">PPAR<\/jats:styled-content>\u2010<jats:italic>\u03b3<\/jats:italic>\u2010deficient mice. In addition, functional <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201010\u2010producing <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>5<jats:sup>+<\/jats:sup> <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>1d<jats:sup>hi<\/jats:sup> regulatory B cells decreased in B\u2010<jats:styled-content style=\"fixed-case\">PPAR<\/jats:styled-content>\u2010<jats:italic>\u03b3<\/jats:italic><jats:sup>\u2212\/\u2212<\/jats:sup> mice in the <jats:styled-content style=\"fixed-case\">CHS<\/jats:styled-content> model. These findings were in accordance with augmented <jats:styled-content style=\"fixed-case\">CHS<\/jats:styled-content>. The current work indicated the involvement of endogenous <jats:styled-content style=\"fixed-case\">PPAR<\/jats:styled-content>\u2010<jats:italic>\u03b3<\/jats:italic> in the regulatory function of B cells by disturbing the expansion of <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201010\u2010positive regulatory B cells.<\/jats:p>","DOI":"10.1111\/imm.13027","type":"journal-article","created":{"date-parts":[[2018,11,24]],"date-time":"2018-11-24T16:34:09Z","timestamp":1543077249000},"page":"282-296","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":8,"title":["B\u2010cell\u2010specific\u2010peroxisome proliferator\u2010activated receptor <i>\u03b3<\/i> deficiency augments contact hypersensitivity with impaired regulatory B cells"],"prefix":"10.1111","volume":"156","author":[{"given":"Jianbing","family":"Su","sequence":"first","affiliation":[{"name":"Laboratory of Anti\u2010inflammatory and Immunomodulatory 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