{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T12:58:03Z","timestamp":1791205083056,"version":"4.1.0"},"reference-count":50,"publisher":"Oxford University Press (OUP)","issue":"6","license":[{"start":{"date-parts":[[2015,3,1]],"date-time":"2015-03-01T00:00:00Z","timestamp":1425168000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2015,3,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>NK cells are an important component of host immune defense against malignancy and infection. NK cells are educated by MHC class I ligands to ensure self-tolerance while also promoting lytic competency against altered self and damaged self targets. However, the intracellular molecular events that culminate in tolerance and functional competency of educated NK cells remain undefined. Mice with germline deficiency in SHIP1 were shown to have a defective NK cell compartment. However, SHIP1 is expressed in all hematopoietic lineages, and consequently several hematolymphoid phenotypes have already been identified in certain cell types that are the result of SHIP1 deficiency in cells in separate and distinct lineages, that is, cell-extrinsic phenotypes. Thus, it was previously impossible to determine the NK cell\u2013intrinsic role of SHIP1. In the present study, through the creation of an NK cell\u2013specific deletion mouse model of SHIP1, we show that SHIP1 plays a profound NK lineage\u2013intrinsic role in NK cell homeostasis, development, education, and cytokine production. Moreover, we show SHIP1 expression by NK cells is required for in vivo\u2013mismatched bone marrow allograft rejection as well as for NK memory responses to hapten.<\/jats:p>","DOI":"10.4049\/jimmunol.1402930","type":"journal-article","created":{"date-parts":[[2015,2,17]],"date-time":"2015-02-17T03:05:50Z","timestamp":1424142350000},"page":"2847-2854","source":"Crossref","is-referenced-by-count":33,"title":["SHIP1 Intrinsically Regulates NK Cell Signaling and Education, Resulting in Tolerance of an MHC Class I\u2013Mismatched Bone Marrow Graft in Mice"],"prefix":"10.1093","volume":"194","author":[{"given":"Matthew","family":"Gumbleton","sequence":"first","affiliation":[{"name":"Department of Microbiology and Immunology, State University of New York Upstate Medical University , Syracuse, NY 13210"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Eric","family":"Vivier","sequence":"additional","affiliation":[{"name":"Centre d\u2019Immunologie de Marseille\u2013Luminy, Aix-Marseille University Unit\u00e9 Mixte 2 , 13288 Marseille ,","place":["France"]},{"name":"INSERM Unit\u00e9 1104 , 13288 Marseille ,","place":["France"]},{"name":"Centre National de la Recherche Scientifique Unit\u00e9 Mixte de Recherche 7280 , 13288 Marseille ,","place":["France"]},{"name":"Service d\u2019Immunologie, Assistance Publique\u2013H\u00f4pitaux de Marseille, H\u00f4pital de la Conception , 13385 Marseille ,","place":["France"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4720-7135","authenticated-orcid":false,"given":"William G","family":"Kerr","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, State University of New York Upstate Medical University , Syracuse, NY 13210"},{"name":"Department of Pediatrics, State University of New York Upstate Medical University , Syracuse, NY 13210"},{"name":"Department of Chemistry, Syracuse University , Syracuse, NY 13210"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2015,3,15]]},"reference":[{"key":"2025030705305670500_r1","doi-asserted-by":"crossref","first-page":"44","DOI":"10.1126\/science.1198687","article-title":"Innate or adaptive immunity? 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