{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,23]],"date-time":"2026-09-23T08:36:07Z","timestamp":1790152567015,"version":"4.0.1"},"reference-count":64,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2015,4,14]],"date-time":"2015-04-14T00:00:00Z","timestamp":1428969600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"name":"Science Foundation Ireland and the National Children's Research Centre"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Eur J Immunol"],"published-print":{"date-parts":[[2015,6]]},"abstract":"<jats:p>B\u00a0cells have been described as having the capacity to regulate cellular immune responses and suppress inflammatory processes. One such regulatory B\u2010cell population is defined as IL\u201010\u2010producing CD19<jats:sup>+<\/jats:sup>CD1d<jats:sup>hi<\/jats:sup> cells. Previous work has identified an expansion of these cells in mice infected with the helminth, <jats:italic>Schistosoma mansoni<\/jats:italic>. Here, microarray analysis of CD19<jats:sup>+<\/jats:sup>CD1d<jats:sup>hi<\/jats:sup> B\u00a0cells from mice infected with <jats:italic>S. mansoni<\/jats:italic> demonstrated significantly increased <jats:italic>Tlr7<\/jats:italic> expression, while CD19<jats:sup>+<\/jats:sup>CD1d<jats:sup>hi<\/jats:sup> B\u00a0cells from uninfected mice also demonstrated elevated <jats:italic>Tlr7<\/jats:italic> expression. Using IL\u201010 reporter, <jats:italic>Il10<jats:sup>\u2212\/\u2212<\/jats:sup><\/jats:italic> and <jats:italic>Tlr7<jats:sup>\u2212\/\u2010<\/jats:sup><\/jats:italic> mice, we formally demonstrate that TLR7 ligation of CD19<jats:sup>+<\/jats:sup>CD1d<jats:sup>hi<\/jats:sup> B\u00a0cells increases their capacity to produce IL\u201010. In a mouse model of allergic lung inflammation, the adoptive transfer of TLR7\u2010elicited CD19<jats:sup>+<\/jats:sup>CD1d<jats:sup>hi<\/jats:sup> B\u00a0cells reduced airway inflammation and associated airway hyperresponsiveness. Using DEREG mice to deplete FoxP3<jats:sup>+<\/jats:sup> T regulatory cells in allergen\u2010sensitized mice, we show that that TLR7\u2010elicited CD19<jats:sup>+<\/jats:sup>CD1d<jats:sup>hi<\/jats:sup> B\u00a0cells suppress airway hyperresponsiveness via a T regulatory cell dependent mechanism. These studies identify that TLR7 stimulation leads to the expansion of IL\u201010\u2010producing CD19<jats:sup>+<\/jats:sup>CD1d<jats:sup>hi<\/jats:sup> B\u00a0cells, which can suppress allergic lung inflammation via T regulatory cells.<\/jats:p>","DOI":"10.1002\/eji.201445211","type":"journal-article","created":{"date-parts":[[2015,3,12]],"date-time":"2015-03-12T10:21:12Z","timestamp":1426155672000},"page":"1842-1854","source":"Crossref","is-referenced-by-count":35,"title":["Ligation of TLR7 on CD19<sup>+<\/sup>CD1d<sup>hi<\/sup> B\u00a0cells suppresses allergic lung inflammation via regulatory T cells"],"prefix":"10.1002","volume":"45","author":[{"given":"Adnan R.","family":"Khan","sequence":"first","affiliation":[{"name":"Trinity Biomedical Sciences Institute School of Medicine Trinity College Dublin  Dublin Ireland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sylvie","family":"Amu","sequence":"additional","affiliation":[{"name":"Institute of Molecular Medicine 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