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Journal of Experimental Medicine, Vol 178, 1247-1254, Copyright © 1993 by Rockefeller University Press
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S Nisitani, T Tsubata, M Murakami, M Okamoto and T Honjo
Department of Medical Chemistry, Faculty of Medicine, Kyoto University, Japan.
To test whether the product of the bcl-2 proto-oncogene blocks clonal deletion of self-reactive B cells, we have generated transgenic mice carrying the bcl-2 gene and the immunoglobulin genes for the anti- erythrocyte 4C8 antibody. In these transgenic mice, clonal deletion of self-reactive immature B cells in the bone marrow was not inhibited in spite of expression of the bcl-2 gene. In contrast, self-antigen- induced clonal deletion of mature self-reactive Ly-1 B (B1) cells in the peritoneal cavity was inhibited in the transgenic mice. These results indicate that the mechanism for clonal deletion of immature self-reactive B cells in the bone marrow differs from that of mature self-reactive B cells in the periphery.
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