Continued RAG expression in late stages of B cell development and no apparent re-induction after immunizion

Wong Yu, Hitoshi Nagaoka, Mila Jankovic, Ziva Misulovin, Heikyung Suh, Antonius Rolink, Fritz Melchers, Eric Meffre and Michel C. Nussenzweig ()
Additional contact information
Wong Yu: Laboratory of Molecular Immunology
Hitoshi Nagaoka: Laboratory of Molecular Immunology
Mila Jankovic: Laboratory of Molecular Immunology
Ziva Misulovin: Laboratory of Molecular Immunology
Heikyung Suh: Laboratory of Molecular Immunology
Antonius Rolink: Basel Institute for Immunology
Fritz Melchers: Basel Institute for Immunology
Eric Meffre: Laboratory of Molecular Immunology
Michel C. Nussenzweig: Laboratory of Molecular Immunology

Nature, 1999, vol. 400, issue 6745, 682-687

Abstract: Abstract Models of B-cell development in the immune system suggest that only those immature B cells in the bone marrow that undergo receptor editing express V (D)J -recombination-activating genes (RAGs)1,2,3. Here we investigate the regulation of RAG expression in transgenic mice carrying a bacterial artificial chromosome that encodes a green fluorescent protein reporter instead of RAG2 (ref. 4). We find that the reporter is expressed in all immature B cells in the bone marrow and spleen. Endogenous RAG messenger RNA is expressed in immature B cells in bone marrow and spleen and decreases by two orders of magnitude as they acquire higher levels of surface immunoglobulin M (IgM). Once RAG expression is stopped it is not re-induced during immune responses. Our findings may help to reconcile a series of apparently contradictory observations, and suggest a new model for the mechanisms that regulate allelic exclusion, receptor editing and tolerance.

Date: 1999
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DOI: 10.1038/23287

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