{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T16:27:07Z","timestamp":1791217627432,"version":"4.1.0"},"reference-count":57,"publisher":"Oxford University Press (OUP)","issue":"2","license":[{"start":{"date-parts":[[2013,9,30]],"date-time":"2013-09-30T00:00:00Z","timestamp":1380499200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"funder":[{"DOI":"10.13039\/100000062","name":"Intramural Research Programs of the NIDDK","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000901","name":"Juvenile Diabetes Research Foundation","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100000901","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2013,9,30]]},"abstract":"<jats:title>ABSTRACT<\/jats:title><jats:p>DCs are important mediators of peripheral tolerance for the prevention of autoimmunity. Chimeric \u03b1DEC-205 antibodies with attached antigens allow in vivo antigen-specific stimulation of T cells by CD8+ DCs, resulting in tolerance in nonautoimmune mice. However, it is not clear whether DC-mediated tolerance induction occurs in the context of ongoing autoimmunity. We assessed the role of CD8+ DCs in stimulation of autoreactive CD4+ T cells in the NOD mouse model of type 1 diabetes. Targeting of antigen to CD8+ DCs via \u03b1DEC-205 led to proliferation and expansion of \u03b2-cell specific BDC2.5 T cells. These T cells also produced IL-2 and IFN-\u03b3 and did not up-regulate FoxP3, consistent with an activated rather than tolerant phenotype. Similarly, endogenous BDC peptide-reactive T cells, identified with I-Ag7 tetramers, did not become tolerant after antigen delivery via \u03b1DEC-205: no deletion or Treg induction was observed. We observed that CD8+ DCs from NOD mice expressed higher surface levels of CD40 than CD8+ DCs from C57BL\/6 mice. Blockade of CD40\u2013CD40L interactions reduced the number of BDC2.5 T cells remaining in mice, 10 days after antigen targeting to CD8 DCs, and blocked IFN-\u03b3 production by BDC2.5 T cells. These data indicate that the ability of autoreactive CD4+ T cells to undergo tolerance mediated by CD8+ DCs is defective in NOD mice and that blocking CD40\u2013CD40L interactions can restore tolerance induction.<\/jats:p>","DOI":"10.1189\/jlb.0113013","type":"journal-article","created":{"date-parts":[[2013,10,1]],"date-time":"2013-10-01T06:09:21Z","timestamp":1380607761000},"page":"325-336","source":"Crossref","is-referenced-by-count":33,"title":["CD8+ dendritic cell-mediated tolerance of autoreactive CD4+ T cells is deficient in NOD mice and can be corrected by blocking CD40L"],"prefix":"10.1093","volume":"95","author":[{"given":"Jeffrey D","family":"Price","sequence":"first","affiliation":[{"name":"Immune Tolerance Section, Diabetes, Endocrinology and Obesity Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health , Bethesda, Maryland, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nicole M","family":"Beauchamp","sequence":"additional","affiliation":[{"name":"Immune Tolerance Section, Diabetes, Endocrinology and Obesity Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health , Bethesda, Maryland, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gwendoline","family":"Rahir","sequence":"additional","affiliation":[{"name":"Immune Tolerance Section, Diabetes, Endocrinology and Obesity Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health , Bethesda, Maryland, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yongge","family":"Zhao","sequence":"additional","affiliation":[{"name":"Immune Tolerance Section, Diabetes, Endocrinology and Obesity Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health , Bethesda, Maryland, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Cosima C","family":"Rieger","sequence":"additional","affiliation":[{"name":"Immune Tolerance Section, Diabetes, Endocrinology and Obesity Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health , Bethesda, Maryland, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Annie W","family":"Lau-Kilby","sequence":"additional","affiliation":[{"name":"Immune Tolerance Section, Diabetes, Endocrinology and Obesity Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health , Bethesda, Maryland, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kristin V","family":"Tarbell","sequence":"additional","affiliation":[{"name":"Immune Tolerance Section, Diabetes, Endocrinology and Obesity Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health , Bethesda, Maryland, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2013,9,30]]},"reference":[{"key":"2023032711075587000_","doi-asserted-by":"crossref","first-page":"685","DOI":"10.1146\/annurev.immunol.21.120601.141040","article-title":"Tolerogenic dendritic cells","volume":"21","author":"Steinman","year":"2003","journal-title":"Ann. 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