Cross‐Priming is Under Control of the relB 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 relB gene, a regulato...

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Bibliographic Details
Published in:Scandinavian journal of immunology 2002-09, Vol.56 (3), p.219-223
Main Authors: CASTIGLIONI, P., JANSSEN, E. M., PRILLIMAN, K. R., GERLONI, M., SCHOENBERGER, S., ZANETTI, M.
Format: Article
Language:English
Subjects:
Animals
Antigen Presentation
Antigens - immunology
Antigens - metabolism
Bone Marrow Transplantation
Cells, Cultured
Cytotoxicity Tests, Immunologic
Langerhans Cells - immunology
Lymph Nodes - immunology
Lymphocyte Activation
Mice
Mice, Inbred C57BL
Mice, Knockout
Protein Transport
Proto-Oncogene Proteins - genetics
Proto-Oncogene Proteins - physiology
Spleen - cytology
Spleen - immunology
T-Lymphocytes, Cytotoxic - immunology
Transcription Factor RelB
Transcription Factors - genetics
Transcription Factors - physiology
Transplantation Chimera
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Summary: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 relB 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 relB(–/–) 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 relB(–/–) BM chimeras are unable to cross‐prime CD8+ T cells, suggesting that the relB gene regulates cross‐priming.
ISSN:0300-9475
1365-3083
DOI:10.1046/j.1365-3083.2002.01144.x