{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,15]],"date-time":"2026-05-15T09:44:41Z","timestamp":1778838281431,"version":"3.51.4"},"reference-count":40,"publisher":"Oxford University Press (OUP)","issue":"1","license":[{"start":{"date-parts":[[2018,1,1]],"date-time":"2018-01-01T00:00:00Z","timestamp":1514764800000},"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":[[2018,1,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Although prophylactic vaccines provide protective humoral immunity against infectious agents, vaccines that elicit potent CD8 T cell responses are valuable tools to shape and drive cellular immunity against cancer and intracellular infection. In particular, IFN-\u03b3\u2013polarized cytotoxic CD8 T cell immunity is considered optimal for protective immunity against intracellular Ags. Suppressor of cytokine signaling (SOCS)1 is a cross-functional negative regulator of TLR and cytokine receptor signaling via degradation of the receptor\u2013signaling complex. We hypothesized that loss of SOCS1 in dendritic cells (DCs) would improve T cell responses by accentuating IFN-\u03b3\u2013directed immune responses. We tested this hypothesis using a recombinant Listeria monocytogenes vaccine platform that targets CD11c+ DCs in mice in which SOCS1 is selectively deleted in all CD11c+ cells. Unexpectedly, in mice lacking SOCS1 expression in CD11c+ cells, we observed a decrease in CD8+ T cell response to the L. monocytogenes vaccine. NK cell responses were also decreased in mice lacking SOCS1 expression in CD11c+ cells but did not explain the defect in CD8+ T cell immunity. We found that DCs lacking SOCS1 expression were functional in driving Ag-specific CD8+ T cell expansion in vitro but that this process was defective following infection in vivo. Instead, monocyte-derived innate TNF-\u03b1 and inducible NO synthase\u2013producing DCs dominated the antibacterial response. Thus, loss of SOCS1 in CD11c+ cells skewed the balance of immune response to infection by increasing innate responses while decreasing Ag-specific adaptive responses to infectious Ags.<\/jats:p>","DOI":"10.4049\/jimmunol.1700909","type":"journal-article","created":{"date-parts":[[2017,11,17]],"date-time":"2017-11-17T19:50:28Z","timestamp":1510948228000},"page":"177-185","source":"Crossref","is-referenced-by-count":9,"title":["Amplifying IFN-\u03b3 Signaling in Dendritic Cells by CD11c-Specific Loss of SOCS1 Increases Innate Immunity to Infection while Decreasing Adaptive Immunity"],"prefix":"10.1093","volume":"200","author":[{"given":"Alejandro F","family":"Alice","sequence":"first","affiliation":[{"name":"Earle A. Chiles Research Institute, Robert W. Franz Cancer Center, Providence Portland Medical Center , Portland, OR 97213"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Gwen","family":"Kramer","sequence":"additional","affiliation":[{"name":"Earle A. Chiles Research Institute, Robert W. Franz Cancer Center, Providence Portland Medical Center , Portland, OR 97213"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Shelly","family":"Bambina","sequence":"additional","affiliation":[{"name":"Earle A. Chiles Research Institute, Robert W. Franz Cancer Center, Providence Portland Medical Center , Portland, OR 97213"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jason R","family":"Baird","sequence":"additional","affiliation":[{"name":"Earle A. Chiles Research Institute, Robert W. Franz Cancer Center, Providence Portland Medical Center , Portland, OR 97213"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Keith S","family":"Bahjat","sequence":"additional","affiliation":[{"name":"Earle A. Chiles Research Institute, Robert W. Franz Cancer Center, Providence Portland Medical Center , Portland, OR 97213"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5575-0074","authenticated-orcid":false,"given":"Michael J","family":"Gough","sequence":"additional","affiliation":[{"name":"Earle A. Chiles Research Institute, Robert W. Franz Cancer Center, Providence Portland Medical Center , Portland, OR 97213"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Marka R","family":"Crittenden","sequence":"additional","affiliation":[{"name":"Earle A. Chiles Research Institute, Robert W. Franz Cancer Center, Providence Portland Medical Center , Portland, OR 97213"},{"name":"The Oregon Clinic , Portland, OR 97213"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"286","published-online":{"date-parts":[[2018,1,1]]},"reference":[{"key":"2025030610004473300_r1","doi-asserted-by":"crossref","first-page":"160","DOI":"10.1111\/j.1600-065X.2010.00993.x","article-title":"Cell biology and immunology of Listeria monocytogenes infections: novel insights","volume":"240","author":"Stavru","year":"2011","journal-title":"Immunol. 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