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Cross‐Priming is Under Control of the rel B Gene
Author(s) -
CASTIGLIONI P.,
JANSSEN E. M.,
PRILLIMAN K. R.,
GERLONI M.,
SCHOENBERGER S.,
ZANETTI M.
Publication year - 2002
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1046/j.1365-3083.2002.01144.x
Subject(s) - priming (agriculture) , cytotoxic t cell , biology , antigen , cd8 , microbiology and biotechnology , t cell , in vitro , immune system , immunology , genetics , botany , germination
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.