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Lack of Bcl-3 in bone marrow\u2013derived DCs blunted their ability to expand and promote effector functions of T cells upon Ag\/adjuvant challenge in vitro and after adoptive transfers in vivo. Importantly, the critical role of Bcl-3 for priming of T cells was exposed upon Ag\/adjuvant challenge of mice specifically ablated of Bcl-3 in DCs. Furthermore, Bcl-3 in endogenous DCs was necessary for contact hypersensitivity responses. Bcl-3 modestly aided maturation of DCs, but most consequentially, Bcl-3 promoted their survival, partially inhibiting expression of several antiapoptotic genes. Loss of Bcl-3 accelerated apoptosis of bone marrow\u2013derived DCs during Ag presentation to T cells, and DC survival was markedly impaired in the context of inflammatory conditions in mice specifically lacking Bcl-3 in these cells. Conversely, selective overexpression of Bcl-3 in DCs extended their lifespan in vitro and in vivo, correlating with increased capacity to prime T cells. These results expose a previously unidentified function for Bcl-3 in DC survival and the generation of adaptive immunity.<\/jats:p>","DOI":"10.4049\/jimmunol.1401505","type":"journal-article","created":{"date-parts":[[2014,9,23]],"date-time":"2014-09-23T07:24:00Z","timestamp":1411457040000},"page":"4303-4311","source":"Crossref","is-referenced-by-count":23,"title":["The NF-\u03baB Regulator Bcl-3 Governs Dendritic Cell Antigen Presentation Functions in Adaptive Immunity"],"prefix":"10.1093","volume":"193","author":[{"given":"Ilaria","family":"Tassi","sequence":"first","affiliation":[{"name":"Laboratory of Molecular Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health , Bethesda, MD 20892"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Estefania","family":"Claudio","sequence":"additional","affiliation":[{"name":"Laboratory of Molecular Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health , Bethesda, MD 20892"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hongshan","family":"Wang","sequence":"additional","affiliation":[{"name":"Laboratory of Molecular Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health , Bethesda, MD 20892"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wanhu","family":"Tang","sequence":"additional","affiliation":[{"name":"Laboratory of Molecular Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health , Bethesda, MD 20892"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hye-lin","family":"Ha","sequence":"additional","affiliation":[{"name":"Laboratory of Molecular Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health , Bethesda, MD 20892"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sun","family":"Saret","sequence":"additional","affiliation":[{"name":"Laboratory of Molecular Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health , Bethesda, MD 20892"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Madhu","family":"Ramaswamy","sequence":"additional","affiliation":[{"name":"Immunoregulation Section, Autoimmunity Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health , Bethesda, MD 20892"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Richard","family":"Siegel","sequence":"additional","affiliation":[{"name":"Immunoregulation Section, Autoimmunity Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health , Bethesda, MD 20892"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ulrich","family":"Siebenlist","sequence":"additional","affiliation":[{"name":"Laboratory of Molecular Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health , Bethesda, MD 20892"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2014,11,1]]},"reference":[{"key":"2025030707421206200_r1","doi-asserted-by":"crossref","first-page":"1160","DOI":"10.1126\/science.1122545","article-title":"Dendritic cell apoptosis in the maintenance of immune tolerance","volume":"311","author":"Chen","year":"2006","journal-title":"Science"},{"key":"2025030707421206200_r2","doi-asserted-by":"crossref","first-page":"629","DOI":"10.1016\/j.immuni.2007.03.016","article-title":"Elimination of antigen-presenting cells and autoreactive T cells by Fas contributes to prevention of autoimmunity","volume":"26","author":"Stranges","year":"2007","journal-title":"Immunity"},{"key":"2025030707421206200_r3","doi-asserted-by":"crossref","first-page":"176","DOI":"10.1038\/nm1697","article-title":"Dcir deficiency causes development of autoimmune diseases in mice due to excess expansion of dendritic cells","volume":"14","author":"Fujikado","year":"2008","journal-title":"Nat. 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