{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,23]],"date-time":"2026-09-23T23:23:42Z","timestamp":1790205822760,"version":"4.1.0"},"reference-count":52,"publisher":"Wiley","issue":"12","license":[{"start":{"date-parts":[[2012,11,26]],"date-time":"2012-11-26T00:00:00Z","timestamp":1353888000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Clin Experimental Allergy"],"published-print":{"date-parts":[[2012,12]]},"abstract":"<jats:title>Summary<\/jats:title><jats:sec><jats:title>Background<\/jats:title><jats:p>Differentiation and activation of <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>4<jats:sup>+<\/jats:sup> T cells is controlled by various cytokines produced by innate immune cells. We have shown that eosinophils (<jats:styled-content style=\"fixed-case\">EOS<\/jats:styled-content>) have the potential to influence Th1 and Th2 cytokine generation by <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>4<jats:sup>+<\/jats:sup> cells, but their influence on <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201017A (<jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201017) has not been established.<\/jats:p><\/jats:sec><jats:sec><jats:title>Objective<\/jats:title><jats:p>The purpose of this study is to determine the effect of <jats:styled-content style=\"fixed-case\">EOS<\/jats:styled-content> on <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201017 production by lymphocytes.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Pre\u2010activated <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>4<jats:sup>+<\/jats:sup> T cells were cultured in the presence of either autologous EOS or EOS culture supernatants. Expression of IL\u201017 was determined by real\u2010time quantitative PCR (<jats:styled-content style=\"fixed-case\">qPCR<\/jats:styled-content>) after 5\u00a0h and protein level was measured after 48\u00a0h. To determine the effect of allergen\u2010induced airway <jats:styled-content style=\"fixed-case\">EOS<\/jats:styled-content> on <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201017, subjects with mild allergic asthma underwent bronchoscopic segmental bronchoprovocation with allergen (SBP\u2010Ag) after a treatment with an anti\u2010IL\u20105 neutralizing antibody (mepolizumab) to reduce airway eosinophilia. IL\u201017 <jats:styled-content style=\"fixed-case\">mRNA<\/jats:styled-content> was measured in bronchoalveolar lavage (BAL) cells by <jats:styled-content style=\"fixed-case\">qPCR<\/jats:styled-content>.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p><jats:italic>In vitro<\/jats:italic>,<jats:styled-content style=\"fixed-case\"> EOS<\/jats:styled-content> significantly increased <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201017 production by CD4<jats:sup>+<\/jats:sup> T cells. Addition of exogenous IL\u20101\u00df increased expression of IL\u201017 <jats:styled-content style=\"fixed-case\">mRNA<\/jats:styled-content> by <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>4<jats:sup>+<\/jats:sup> T cells. EOS expressed and released IL\u20101\u00df. Furthermore, levels of IL\u20101\u00df in EOS supernatants highly correlated with their ability to increase IL\u201017 expression by <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>4<jats:sup>+<\/jats:sup> T cells, and neutralizing antibody to IL\u20101\u00df reduced expression of IL\u201017 <jats:styled-content style=\"fixed-case\">mRNA<\/jats:styled-content>. <jats:italic>In vivo<\/jats:italic>, reduction of EOS in the airway using mepolizumab was associated with diminished IL\u201017 expression after SBP\u2010Ag.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions and clinical relevance<\/jats:title><jats:p>Our data demonstrate that <jats:styled-content style=\"fixed-case\">EOS<\/jats:styled-content> can promote <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201017 production through the release of <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20101\u00df. Enhanced <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201017 cytokine production is another mechanism by which <jats:styled-content style=\"fixed-case\">EOS<\/jats:styled-content> may participate in pathogenesis of allergic airway inflammation in asthma.<\/jats:p><\/jats:sec>","DOI":"10.1111\/j.1365-2222.2012.04060.x","type":"journal-article","created":{"date-parts":[[2012,7,6]],"date-time":"2012-07-06T17:25:24Z","timestamp":1341595524000},"page":"1756-1764","source":"Crossref","is-referenced-by-count":55,"title":["Human eosinophils release <scp>IL<\/scp>\u20101\u00df and increase expression of <scp>IL<\/scp>\u201017A in activated <scp>CD<\/scp>4<sup>+<\/sup> T lymphocytes"],"prefix":"10.1111","volume":"42","author":[{"given":"S.","family":"Esnault","sequence":"first","affiliation":[{"name":"Division of Allergy Pulmonary and Critical Care Medicine Department of Medicine University of Wisconsin School of Medicine and Public Health Madison WI 53792 USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"E. 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