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 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.