Hertz M, Nemazee D
Department of Pediatrics, National Jewish Medical and Research Center, Denver, Colorado 80206, USA.
Immunity. 1997 Apr;6(4):429-36. doi: 10.1016/s1074-7613(00)80286-1.
The ability of BCR cross-linking to stimulate receptor editing was analyzed in vitro using bone marrow B cells from immunoglobulin (Ig) transgenic (Tg) and non-Tg mice. In cultured Ig-Tg cells, BCR ligation induced receptor editing as measured by up-regulation of RAG gene expression, light chain gene DNA rearrangements, and expression of lambda-light chain protein in cells that previously expressed kappa. In the culture conditions used, BCR ligation induced light chain rearrangements in most immature IgM+IgD- bone marrow B cells in the absence of significant cell death or cell growth. Receptor editing in non-Tg B cells was also documented in cultures treated with anti-immunoglobulin. These results provide direct evidence for the ability of BCR ligation to stimulate immunoglobulin light chain gene rearrangements in immature B cells.
利用来自免疫球蛋白(Ig)转基因(Tg)和非Tg小鼠的骨髓B细胞,在体外分析了BCR交联刺激受体编辑的能力。在培养的Ig-Tg细胞中,BCR连接诱导受体编辑,这可通过RAG基因表达上调、轻链基因DNA重排以及先前表达κ链的细胞中λ轻链蛋白的表达来衡量。在所使用的培养条件下,BCR连接在大多数未成熟IgM+IgD-骨髓B细胞中诱导轻链重排,且无明显细胞死亡或细胞生长。在用抗免疫球蛋白处理的培养物中也记录到了非Tg B细胞中的受体编辑。这些结果为BCR连接刺激未成熟B细胞中免疫球蛋白轻链基因重排的能力提供了直接证据。