Young F, Mizoguchi E, Bhan A K, Alt F W
Howard Hughes Medical Institute and the Department of Genetics and Pediatrics, The Children's Hospital, Boston, Massachusetts 02115, USA.
Immunity. 1997 Jan;6(1):23-33. doi: 10.1016/s1074-7613(00)80239-3.
To test for effects on B cell differentiation, we introduced immunoglobulin mu heavy chain (HC) and Bcl-2 transgenes, separately or together, into recombination-activating gene 2 (RAG-2)-deficient mice. Transgenic Bcl-2 expression led to increased numbers of RAG-deficient pro-B cells, but did not promote their further differentiation. Expression of the mu HC transgene promoted the differentiation of RAG-deficient pro-B cells into pre-B cells that also expressed certain differentiation markers characteristic of even more mature B cell stages. However, the extent of the mu HC-dependent differentiation effects was greatly enhanced by coexpression of the transgenic Bcl-2 gene, and a subset of pre-B cells from both HC and HC, Bcl-2-transgenic RAG-2-deficient animals expressed surface mu HCs that were functional as judged by cross-linking experiments. These experiments demonstrate that the pro-B to pre-B transition in vivo cannot be effected by the expression of Bcl-2 alone, and that nontransformed immature B-lineage cells are competent to receive signals through a surface mu complex.
为了测试对B细胞分化的影响,我们将免疫球蛋白μ重链(HC)和Bcl-2转基因单独或一起导入重组激活基因2(RAG-2)缺陷小鼠体内。转基因Bcl-2的表达导致RAG缺陷前B细胞数量增加,但并未促进其进一步分化。μHC转基因的表达促进了RAG缺陷前B细胞分化为前B细胞,这些前B细胞也表达了更成熟B细胞阶段特有的某些分化标志物。然而,转基因Bcl-2基因的共表达极大地增强了μHC依赖性分化效应的程度,并且来自HC和HC、Bcl-2转基因RAG-2缺陷动物的一部分前B细胞表达了通过交联实验判断具有功能的表面μHC。这些实验表明,体内前B细胞到前B细胞的转变不能仅通过Bcl-2的表达来实现,并且未转化的未成熟B谱系细胞能够通过表面μ复合体接收信号。