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Rückerl, F. ; Bachl, J.

Activation-induced cytidine deaminase fails to induce a mutator phenotype in the human pre-B cell line Nalm-6.

Eur. J. Immunol. 35, 290-298 (2005)
DOI
Open Access Green as soon as Postprint is submitted to ZB.
Activation-induced cytidine deaminase (AID) plays a key role in the induction of somatic hypermutation and class switching at the immunoglobulin loci of B lymphocytes. AID overexpression can induce a mutator phenotype in lymphoid and nonlymphoid cell lines, suggesting that AID by itself is sufficient to trigger hypermutation and class switching. AID expression in vivo is considered to be restricted to germinal center B lymphocytes, yet AID expression is also seen in many B cell lymphomas, hinting at a potential role for the development of these malignancies. We used a GFP-based reversion assay to efficiently evaluate the activation of mutator phenotypes. As expected, AID overexpression in the human Burkitt lymphoma cell line BL70 caused hypermutation. Surprisingly, AID overexpression in the human pre-B cell line Nalm-6 failed to induce a detectable mutator phenotype, indicating that Nalm-6 cells are probably lacking an essential factor(s) to confer AID-induced mutagenesis. This finding supports the concept that AID overexpression by itself must not automatically lead to the onset of a mutator phenotype. In addition, treating Nalm-6 transfectants with thymidine, a potential mutagenic drug, caused profound mutation rates on the GFP transgene. Thus, the GFP-based mutation assay might prove a powerful tool to study protein- and chemical-induced mutator phenotypes in cell lines.
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Publication type Article: Journal article
Document type Scientific Article
Keywords human; B lymphocytes; repertoire development; antibodies
ISSN (print) / ISBN 0014-2980
e-ISSN 1521-4141
Journal European Journal of Immunology
Quellenangaben Volume: 35, Issue: 1, Pages: 290-298 Article Number: , Supplement: ,
Publisher Wiley
Publishing Place Hoboken
Reviewing status Peer reviewed
Institute(s) Institute of Clinical Molecular Biology and Tumor Genetics (K.MOLBI)