Nisitani S, Tsubata T, Murakami M, Okamoto M, Honjo T
Department of Medical Chemistry, Faculty of Medicine, Kyoto University, Japan.
J Exp Med. 1993 Oct 1;178(4):1247-54. doi: 10.1084/jem.178.4.1247.
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.
为了检测bcl-2原癌基因的产物是否会阻止自身反应性B细胞的克隆清除,我们构建了携带bcl-2基因以及抗红细胞4C8抗体免疫球蛋白基因的转基因小鼠。在这些转基因小鼠中,尽管bcl-2基因有表达,但骨髓中自身反应性未成熟B细胞的克隆清除并未受到抑制。相反,转基因小鼠腹腔中自身抗原诱导的成熟自身反应性Ly-1 B(B1)细胞的克隆清除受到了抑制。这些结果表明,骨髓中未成熟自身反应性B细胞的克隆清除机制与外周成熟自身反应性B细胞的克隆清除机制不同。