{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,23]],"date-time":"2026-09-23T22:20:54Z","timestamp":1790202054183,"version":"4.1.0"},"reference-count":93,"publisher":"Oxford University Press (OUP)","issue":"9","license":[{"start":{"date-parts":[[2004,5,1]],"date-time":"2004-05-01T00:00:00Z","timestamp":1083369600000},"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":[[2004,5,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>The CTL response to the HLA-A*0201-restricted, HIV-1 p17 Gag77\u201385 epitope (SLYNTVATL; SL9) has been extensively studied in patients. Although this reactivity is exceptionally prominent in chronically infected patients and inversely correlated to viral load, SL9-specific CTLs (SL9-CTLs) are rarely detected in acute infection. To explore the cellular basis for this unusual manifestation, SL9-CTLs primed ex vivo from naive circulating CD8+ T cells of healthy, seronegative donors were generated and characterized. SL9 appeared to differ from other well-studied A*0201-restricted epitopes in several significant respects. In contrast to published reports for influenza and melanoma peptides and the HIV gag IV9 epitope studied here in parallel, SL9-CTLs were primed by immature but not mature autologous dendritic cells. Highly activated SL9-CTLs produce sufficient autocrine mediators to sustain clonal expansion and CTL differentiation for months without CD4+ T cells or exogenous IL-2. Moreover, SL9-CTLs were sensitive to paracrine IL-2-induced apoptosis. IL-2 independence and sensitivity to paracrine IL-2 were also characteristic of SL9-CTLs immunized by dendritic cells transduced by a nonreplicating lentiviral vector encoding full-length Gag. In vitro-primed SL9-CTLs resembled those derived from patients in degeneracy of recognition and functional avidities for both SL9 and its natural mutations. Together, these data show that SL9 is a highly immunogenic, help-independent HIV epitope. The scarcity of SL9-CTLs in acute infection may result from cytokine-induced apoptosis with the intense activation of the innate immunity. In contrast, SL9-CTLs that constitutively produce autocrine help would predominate during CD4-diminished chronic infection.<\/jats:p>","DOI":"10.4049\/jimmunol.172.9.5249","type":"journal-article","created":{"date-parts":[[2014,4,20]],"date-time":"2014-04-20T20:08:23Z","timestamp":1398024503000},"page":"5249-5261","source":"Crossref","is-referenced-by-count":33,"title":["The HIV-1 HLA-A2-SLYNTVATL Is a Help-Independent CTL Epitope"],"prefix":"10.1093","volume":"172","author":[{"given":"June","family":"Kan-Mitchell","sequence":"first","affiliation":[{"name":"Karmanos Cancer Institute, Departments of Pathology and Immunology\/Microbiology, Wayne State University , Detroit, MI 48201"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Brygida","family":"Bisikirska","sequence":"additional","affiliation":[{"name":"Karmanos Cancer Institute, Departments of Pathology and Immunology\/Microbiology, Wayne State University , Detroit, MI 48201"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Flossie","family":"Wong-Staal","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of California , San Diego, La Jolla, CA 90033"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Keri L","family":"Schaubert","sequence":"additional","affiliation":[{"name":"Karmanos Cancer Institute, Departments of Pathology and Immunology\/Microbiology, Wayne State University , Detroit, MI 48201"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Melissa","family":"Bajcz","sequence":"additional","affiliation":[{"name":"Karmanos Cancer Institute, Departments of Pathology and Immunology\/Microbiology, Wayne State University , Detroit, MI 48201"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michal","family":"Bereta","sequence":"additional","affiliation":[{"name":"Karmanos Cancer Institute, Departments of Pathology and Immunology\/Microbiology, Wayne State University , Detroit, MI 48201"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2004,5,1]]},"reference":[{"key":"2026020211291104100_R1","first-page":"230","volume-title":"Stem Cells","year":"2000"},{"key":"2026020211291104100_R2","first-page":"33","volume-title":"N. 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