{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,21]],"date-time":"2026-09-21T16:42:34Z","timestamp":1790008954121,"version":"4.0.1"},"reference-count":45,"publisher":"National Academy of Sciences","issue":"33","license":[{"start":{"date-parts":[[2017,2,1]],"date-time":"2017-02-01T00:00:00Z","timestamp":1485907200000},"content-version":"vor","delay-in-days":184,"URL":"http:\/\/www.pnas.org\/preview_site\/misc\/userlicense.xhtml"}],"funder":[{"DOI":"10.13039\/100000002","name":"HHS | National Institutes of Health","doi-asserted-by":"publisher","award":["PO1 AI065687"],"award-info":[{"award-number":["PO1 AI065687"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"HHS | National Institutes of Health","doi-asserted-by":"publisher","award":["RO1 AI42269"],"award-info":[{"award-number":["RO1 AI42269"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"HHS | National Institutes of Health","doi-asserted-by":"publisher","award":["R37 AI49954"],"award-info":[{"award-number":["R37 AI49954"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["www.pnas.org"],"crossmark-restriction":true},"short-container-title":["Proc. Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2016,8,16]]},"abstract":"<jats:title>Significance<\/jats:title>\n                  <jats:p>\n                    Systemic lupus erythematosus (SLE) is characterized by compromised IL-2 production and regulatory T-cell function. Studies in human SLE and in murine lupus models report that IL-2 replenishment ameliorates clinical lupus manifestations. Here we show that engagement of signaling lymphocytic activation molecule family 3 (SLAMF3), a coregulatory receptor of T cells, restores the sensitivity of SLE CD4\n                    <jats:sup>+<\/jats:sup>\n                    T cells to IL-2, increasing their response to exogenous IL-2 via up-regulation of the IL-2R\u03b1 subunit. Moreover, activation of na\u00efve CD4\n                    <jats:sup>+<\/jats:sup>\n                    T cells with a monoclonal antibody directed against SLAMF3 promotes T helper cell differentiation toward a suppressive phenotype. These data suggest that the SLAMF3 receptor may be a promising therapeutic target in SLE.\n                  <\/jats:p>","DOI":"10.1073\/pnas.1605081113","type":"journal-article","created":{"date-parts":[[2016,8,1]],"date-time":"2016-08-01T23:24:06Z","timestamp":1470093846000},"page":"9321-9326","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":41,"title":["Engagement of SLAMF3 enhances CD4\n                    <sup>+<\/sup>\n                    T-cell sensitivity to IL-2 and favors regulatory T-cell polarization in systemic lupus erythematosus"],"prefix":"10.1073","volume":"113","author":[{"given":"Denis","family":"Comte","sequence":"first","affiliation":[{"name":"Division of Rheumatology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02115;"},{"name":"Division of Immunology and Allergy, Centre Hospitalier Universitaire Vaudois, CH 1011 Lausanne, 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