{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,2]],"date-time":"2026-06-02T06:11:05Z","timestamp":1780380665090,"version":"3.54.1"},"reference-count":50,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2016,1,12]],"date-time":"2016-01-12T00:00:00Z","timestamp":1452556800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/3.0\/"}],"funder":[{"DOI":"10.13039\/501100000265","name":"Medical Research Council","doi-asserted-by":"publisher","award":["G0701437"],"award-info":[{"award-number":["G0701437"]}],"id":[{"id":"10.13039\/501100000265","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100004440","name":"Wellcome Trust","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100004440","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Immunol Cell Biol"],"published-print":{"date-parts":[[2016,4]]},"abstract":"<jats:p>Dendritic cells (DCs) are the key initiators of T\u2010helper (Th) 2 immune responses against the parasitic helminth <jats:italic>Schistosoma mansoni<\/jats:italic>. Although the liver is one of the main sites of antigen deposition during infection with this parasite, it is not yet clear how distinct DC subtypes in this tissue respond to <jats:italic>S. mansoni<\/jats:italic> antigens <jats:italic>in vivo<\/jats:italic>, or how the liver microenvironment might influence DC function during establishment of the Th2 response. In this study, we show that hepatic DC subsets undergo distinct activation processes <jats:italic>in vivo<\/jats:italic> following murine infection with <jats:italic>S. mansoni<\/jats:italic>. Conventional DCs (cDCs) from schistosome\u2010infected mice upregulated expression of the costimulatory molecule CD40 and were capable of priming naive CD4<jats:sup>+<\/jats:sup> T cells, whereas plasmacytoid DCs (pDCs) upregulated expression of MHC class II, CD86 and CD40 but were unable to support the expansion of either naive or effector\/memory CD4<jats:sup>+<\/jats:sup> T cells. Importantly, <jats:italic>in vivo<\/jats:italic> depletion of pDCs revealed that this subset was dispensable for either maintenance or regulation of the hepatic Th2 effector response during acute <jats:italic>S. mansoni<\/jats:italic> infection. Our data provides strong evidence that <jats:italic>S. mansoni<\/jats:italic> infection favors the establishment of an immunogenic, rather than tolerogenic, liver microenvironment that conditions cDCs to initiate and maintain Th2 immunity in the context of ongoing antigen exposure.<\/jats:p>","DOI":"10.1038\/icb.2015.114","type":"journal-article","created":{"date-parts":[[2015,12,11]],"date-time":"2015-12-11T09:20:57Z","timestamp":1449825657000},"page":"400-410","source":"Crossref","is-referenced-by-count":27,"title":["A central role for hepatic conventional dendritic cells in supporting Th2 responses during helminth infection"],"prefix":"10.1111","volume":"94","author":[{"given":"Rachel J","family":"Lundie","sequence":"first","affiliation":[{"name":"Institute of Immunology and Infection Research, Centre for Immunity, Infection and Evolution, University of Edinburgh  Edinburgh UK"},{"name":"Centre for Biomedical Research, Burnet Institute  Melbourne VIC 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