{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T14:15:58Z","timestamp":1791296158481,"version":"4.1.0"},"reference-count":32,"publisher":"Oxford University Press (OUP)","issue":"1","license":[{"start":{"date-parts":[[2016,8,4]],"date-time":"2016-08-04T00:00:00Z","timestamp":1470268800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"funder":[{"DOI":"10.13039\/100000002","name":"U.S. National Institutes of Health","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["F30-DK104562"],"award-info":[{"award-number":["F30-DK104562"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["DK063222"],"award-info":[{"award-number":["DK063222"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000060","name":"NIH National Institute of Allergy and Infectious Diseases","doi-asserted-by":"publisher","award":["U19-AI083024"],"award-info":[{"award-number":["U19-AI083024"]}],"id":[{"id":"10.13039\/100000060","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2017,1,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>The liver contains 2 transcriptionally distinct group 1 ILC subsets: CD49a+ ILC1s and CD49b+ NK cells. However, little is known about how group 1 ILCs contribute to hepatic immune responses. Therefore, we characterized murine liver-resident group 1 ILCs and found that CD49a+ ILC1s express high levels of the inhibitory receptor NKG2A and localize near DCs in perivascular spaces surrounding the portal triads. Upon hepatic viral infection, NKG2A signaling in group 1 ILCs, especially in CD49a+ ILC1s, inhibits CXCL9 expression required for robust accumulation of IFN-\u03b3+CD49b+ NK cells. As a consequence, NKG2A\u2212\/\u2212 mice showed increased numbers of IFN-\u03b3-producing NK cells that preferentially activate liver CD103+ DCs, leading to the sustained proliferation of adoptively transferred, virus-specific CD8+ T cells. Collectively, these data suggest that group 1 ILCs play a role in maintaining the liver as a tolerogenic site by limiting the recruitment of peripheral NK cells during the early phase of viral infection. Furthermore, our findings implicate that the inhibition of NKG2A signaling on group 1 ILCs may be a novel vaccine strategy to induce robust CD8+ T cell responses against persistent liver pathogens.<\/jats:p>","DOI":"10.1189\/jlb.3a0516-225r","type":"journal-article","created":{"date-parts":[[2016,8,5]],"date-time":"2016-08-05T03:24:05Z","timestamp":1470367445000},"page":"329-338","source":"Crossref","is-referenced-by-count":47,"title":["Murine liver-resident group 1 innate lymphoid cells regulate optimal priming of anti-viral CD8+ T cells"],"prefix":"10.1093","volume":"101","author":[{"given":"Peter D","family":"Krueger","sequence":"first","affiliation":[{"name":"Beirne B. Carter Center for Immunology Research, University of Virginia , Charlottesville, Virginia , USA"},{"name":"Department of Microbiology, Immunology, and Cancer Biology, University of Virginia , Charlottesville, Virginia , USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sowmya","family":"Narayanan","sequence":"additional","affiliation":[{"name":"Beirne B. Carter Center for Immunology Research, University of Virginia , Charlottesville, Virginia , USA"},{"name":"Department of Microbiology, Immunology, and Cancer Biology, University of Virginia , Charlottesville, Virginia , USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fionna A","family":"Surette","sequence":"additional","affiliation":[{"name":"Beirne B. Carter Center for Immunology Research, University of Virginia , Charlottesville, Virginia , USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael G","family":"Brown","sequence":"additional","affiliation":[{"name":"Beirne B. Carter Center for Immunology Research, University of Virginia , Charlottesville, Virginia , USA"},{"name":"Department of Medicine, University of Virginia , Charlottesville, Virginia , USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sun-Sang J","family":"Sung","sequence":"additional","affiliation":[{"name":"Beirne B. Carter Center for Immunology Research, University of Virginia , Charlottesville, Virginia , USA"},{"name":"Department of Medicine, University of Virginia , Charlottesville, Virginia , USA"},{"name":"Center for Immunity, Inflammation and Regenerative Medicine, University of Virginia , Charlottesville, Virginia , USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Young S","family":"Hahn","sequence":"additional","affiliation":[{"name":"Beirne B. 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