Bain G, Robanus Maandag E C, te Riele H P, Feeney A J, Sheehy A, Schlissel M, Shinton S A, Hardy R R, Murre C
Department of Biology, University of California, San Diego, La Jolla 92093, USA.
Immunity. 1997 Feb;6(2):145-54. doi: 10.1016/s1074-7613(00)80421-5.
The E2A gene products, E12 and E47, are required for proper B cell development. Mice lacking the E2A gene products generate only a very small number of B220+ cells, which lack immunoglobulin DJ(H) rearrangements. We have now generated mice expressing either E12 or E47. B cell development in mice expressing E12 but lacking E47 is perturbed at the pro-B cell stage, and these mice lack IgM+B220+ B cells in both bone marrow and spleen. IgM+B220+ B cells can be detected, albeit at significantly reduced levels, in the bone marrow and spleen of mice lacking E12. Ectopic expression of both E12 and E47 in a null mutant background shows that E12 and E47 act in concert to promote B lineage development. Taken together, the data indicate that both E12 and E47 allow commitment to the B cell lineage and act synergistically to promote B lymphocyte maturation.
E2A基因产物E12和E47是B细胞正常发育所必需的。缺乏E2A基因产物的小鼠仅产生极少数B220⁺细胞，这些细胞缺乏免疫球蛋白DJ(H)重排。我们现已培育出表达E12或E47的小鼠。在表达E12但缺乏E47的小鼠中，B细胞发育在前B细胞阶段受到干扰，并且这些小鼠在骨髓和脾脏中均缺乏IgM⁺B220⁺B细胞。在缺乏E12的小鼠的骨髓和脾脏中可以检测到IgM⁺B220⁺B细胞，尽管其水平显著降低。在无突变背景下E12和E47的异位表达表明，E12和E47协同作用促进B细胞系发育。综上所述，数据表明E12和E47均促使细胞定向分化为B细胞系，并协同作用促进B淋巴细胞成熟。
