Author
Listed:
- Xiao-Feng Qin
(Laboratory of Molecular Immunology, The Rockefeller University)
- Stephan Schwers
(Institute for Genetics, University of Cologne)
- Wong Yu
(Laboratory of Molecular Immunology, The Rockefeller University)
- Fotini Papavasiliou
(Laboratory of Molecular Immunology, The Rockefeller University)
- Heikyung Suh
(Laboratory of Molecular Immunology, The Rockefeller University
Howard Hughes Medical Institute The Rockefeller University)
- Andre Nussenzweig
(Experimental Immunology Branch, National Cancer Institute, National Institutes of Health)
- Klaus Rajewsky
(Institute for Genetics, University of Cologne)
- Michel C. Nussenzweig
(Laboratory of Molecular Immunology, The Rockefeller University
Howard Hughes Medical Institute The Rockefeller University)
Abstract
B-1 B cells are a self-renewing population of B cells that differ from conventional B cells (B-2 cells) in that they are particularly predisposed to auto-antibody production1,2,3. Although much is known about the signalling pathways that control B-1-cell growth and development (reviewed in ref. 4), less is known about why these cells are prone to produce autoreactive antibodies. Here we show that B-1 cells, like germinal-centre B cells5,6,7,8, can express recombinase-activating genes 1 and 2 (RAG1 and RAG2) and undergo secondary V(D)J recombination of immunoglobulin genes. In addition, B cells from autoimmune-prone NZB mice show high levels of RAG messenger RNA and recombination. We propose that secondary immunoglobulin-gene rearrangements outside organized lymphoid organs may contribute to the development of autoreactive antibodies.
Suggested Citation
Xiao-Feng Qin & Stephan Schwers & Wong Yu & Fotini Papavasiliou & Heikyung Suh & Andre Nussenzweig & Klaus Rajewsky & Michel C. Nussenzweig, 1999.
"Secondary V(D)J recombination in B-1 cells,"
Nature, Nature, vol. 397(6717), pages 355-359, January.
Handle:
RePEc:nat:nature:v:397:y:1999:i:6717:d:10.1038_16933
DOI: 10.1038/16933
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