Cross‐Priming is Under Control of the rel B Gene
Cross‐priming is an important mechanism of intercell transfer of antigenic material leading to the specific activation of cytotoxic T lymphocytes. Dendritic cells (DCs) are considered the central antigen‐presenting cell in cross‐priming. Here we decided to probe the role of the rel B gene, a regulat...
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| Veröffentlicht in: | Scandinavian journal of immunology 2002-09, Vol.56 (3), p.219-223 |
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| container_title | Scandinavian journal of immunology |
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| creator | CASTIGLIONI, P. JANSSEN, E. M. PRILLIMAN, K. R. GERLONI, M. SCHOENBERGER, S. ZANETTI, M. |
| description | Cross‐priming is an important mechanism of intercell transfer of antigenic material leading to the specific activation of cytotoxic T lymphocytes. Dendritic cells (DCs) are considered the central antigen‐presenting cell in cross‐priming. Here we decided to probe the role of the
rel
B gene, a regulator of DC differentiation, in the
in vivo
cross‐priming of a model tumour antigen, TAP(–/–) murine embryo cells (MEC), expressing human adenovirus type 5 early region 1. To this end, we used
rel
B(–/–) mutant mice to generate bone marrow (BM) chimeras as these possess few residual DC but are capable of initiating CD4
+
and CD8
+
T‐cell responses
in vivo
. Our results show that
rel
B(–/–) BM chimeras are unable to cross‐prime CD8
+
T cells, suggesting that the
rel
B gene regulates cross‐priming. |
| doi_str_mv | 10.1046/j.1365-3083.2002.01144.x |
| format | Article |
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rel
B gene, a regulator of DC differentiation, in the
in vivo
cross‐priming of a model tumour antigen, TAP(–/–) murine embryo cells (MEC), expressing human adenovirus type 5 early region 1. To this end, we used
rel
B(–/–) mutant mice to generate bone marrow (BM) chimeras as these possess few residual DC but are capable of initiating CD4
+
and CD8
+
T‐cell responses
in vivo
. Our results show that
rel
B(–/–) BM chimeras are unable to cross‐prime CD8
+
T cells, suggesting that the
rel
B gene regulates cross‐priming.</description><identifier>ISSN: 0300-9475</identifier><identifier>EISSN: 1365-3083</identifier><identifier>DOI: 10.1046/j.1365-3083.2002.01144.x</identifier><language>eng</language><ispartof>Scandinavian journal of immunology, 2002-09, Vol.56 (3), p.219-223</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c1359-5930ee6d6a79cf864b4ecbd82d11734809043b558796fe292193b7bb9557bfd13</citedby><cites>FETCH-LOGICAL-c1359-5930ee6d6a79cf864b4ecbd82d11734809043b558796fe292193b7bb9557bfd13</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27903,27904</link.rule.ids></links><search><creatorcontrib>CASTIGLIONI, P.</creatorcontrib><creatorcontrib>JANSSEN, E. M.</creatorcontrib><creatorcontrib>PRILLIMAN, K. R.</creatorcontrib><creatorcontrib>GERLONI, M.</creatorcontrib><creatorcontrib>SCHOENBERGER, S.</creatorcontrib><creatorcontrib>ZANETTI, M.</creatorcontrib><title>Cross‐Priming is Under Control of the rel B Gene</title><title>Scandinavian journal of immunology</title><description>Cross‐priming is an important mechanism of intercell transfer of antigenic material leading to the specific activation of cytotoxic T lymphocytes. Dendritic cells (DCs) are considered the central antigen‐presenting cell in cross‐priming. Here we decided to probe the role of the
rel
B gene, a regulator of DC differentiation, in the
in vivo
cross‐priming of a model tumour antigen, TAP(–/–) murine embryo cells (MEC), expressing human adenovirus type 5 early region 1. To this end, we used
rel
B(–/–) mutant mice to generate bone marrow (BM) chimeras as these possess few residual DC but are capable of initiating CD4
+
and CD8
+
T‐cell responses
in vivo
. Our results show that
rel
B(–/–) BM chimeras are unable to cross‐prime CD8
+
T cells, suggesting that the
rel
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rel
B gene, a regulator of DC differentiation, in the
in vivo
cross‐priming of a model tumour antigen, TAP(–/–) murine embryo cells (MEC), expressing human adenovirus type 5 early region 1. To this end, we used
rel
B(–/–) mutant mice to generate bone marrow (BM) chimeras as these possess few residual DC but are capable of initiating CD4
+
and CD8
+
T‐cell responses
in vivo
. Our results show that
rel
B(–/–) BM chimeras are unable to cross‐prime CD8
+
T cells, suggesting that the
rel
B gene regulates cross‐priming.</abstract><doi>10.1046/j.1365-3083.2002.01144.x</doi><tpages>5</tpages></addata></record> |
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| ispartof | Scandinavian journal of immunology, 2002-09, Vol.56 (3), p.219-223 |
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| language | eng |
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| source | Wiley Online Library Journals Frontfile Complete; Wiley Online Library Free Content; IngentaConnect Open Access Journals; EZB-FREE-00999 freely available EZB journals |
| title | Cross‐Priming is Under Control of the rel B Gene |
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