{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,20]],"date-time":"2026-05-20T13:52:27Z","timestamp":1779285147574,"version":"3.51.4"},"reference-count":31,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2015,11,30]],"date-time":"2015-11-30T00:00:00Z","timestamp":1448841600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Eur J Immunol"],"published-print":{"date-parts":[[2016,1]]},"abstract":"<jats:p>In mouse models of infection with the gastrointestinal parasite <jats:italic>Trichuris muris<\/jats:italic>, appropriate dendritic\u2010cell (DC) Ag sampling, migration, and presentation to T\u00a0cells are necessary to mount a protective Th2\u2010polarized adaptive immune response, which is needed to clear infection. SH2\u2010containing inositol 5\u2032\u2010phosphatase 1 (SHIP\u20101) has been shown to be an important regulator of DC function in vitro through the negative regulation of the phosphoinositide 3\u2010kinase (PI3K) pathway, but its role in vivo is relatively unexplored. In the current work, mice with a specific deletion of SHIP\u20101 in DCs (<jats:italic>Ship1<\/jats:italic><jats:sup>\u0394DC<\/jats:sup>) were infected with the parasite <jats:italic>T. muris<\/jats:italic>. <jats:italic>Ship1<\/jats:italic><jats:sup>\u0394DC<\/jats:sup> mice were susceptible to infection due to ineffective priming of Th2\u2010polarized responses. This is likely due to an increased production of interleukin (IL) 12p40 by SHIP\u20101\u2010deficient DCs, as in vivo antibody blockade of IL\u201012p40 was able to facilitate the clearing of infection in <jats:italic>Ship1<\/jats:italic><jats:sup>\u0394DC<\/jats:sup> mice. Our results describe a critical role for SHIP\u20101 in regulating the ability of DCs to efficiently prime Th2\u2010type responses.<\/jats:p>","DOI":"10.1002\/eji.201545628","type":"journal-article","created":{"date-parts":[[2015,10,31]],"date-time":"2015-10-31T09:24:51Z","timestamp":1446283491000},"page":"122-130","source":"Crossref","is-referenced-by-count":15,"title":["Dendritic\u2010cell expression of <i>Ship1<\/i> regulates Th2 immunity to helminth infection in mice"],"prefix":"10.1002","volume":"46","author":[{"given":"Matthew J.","family":"Gold","sequence":"first","affiliation":[{"name":"Biomedical Research Centre University of British Columbia  Vancouver Canada"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Frann","family":"Antignano","sequence":"additional","affiliation":[{"name":"Biomedical Research Centre University of British Columbia  Vancouver Canada"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Michael R.","family":"Hughes","sequence":"additional","affiliation":[{"name":"Biomedical Research Centre University of British Columbia  Vancouver Canada"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Colby","family":"Zaph","sequence":"additional","affiliation":[{"name":"Biomedical Research Centre University of British Columbia  Vancouver Canada"},{"name":"Infection and Immunity Program Monash Biomedicine Discovery Institute"},{"name":"Department of Biochemistry and Molecular Biology Monash University  Clayton Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kelly M.","family":"McNagny","sequence":"additional","affiliation":[{"name":"Biomedical Research Centre University of British Columbia  Vancouver Canada"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2015,11,30]]},"reference":[{"key":"e_1_2_7_2_1","doi-asserted-by":"publisher","DOI":"10.1002\/1521-4141(200007)30:7<2083::AID-IMMU2083>3.0.CO;2-3"},{"key":"e_1_2_7_3_1","doi-asserted-by":"crossref","first-page":"3453","DOI":"10.4049\/jimmunol.160.7.3453","article-title":"A critical role for IL\u201013 in resistance to intestinal nematode infection","volume":"160","author":"Bancroft A. 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