Grawunder U, Rolink A, Melchers F
Basel Institute for Immunology, Switzerland.
Int Immunol. 1995 Dec;7(12):1915-25. doi: 10.1093/intimm/7.12.1915.
B cell development in RAG-2-deficient (RAG-2T) mice is impeded at an early stage, due to the inability of these animals to rearrange their endogenous ig gene loci. Expression of an E mu-bcl-2 transgene in these mice did not change this phenotype. However, stromal cell/IL-7-reactive B cell progenitors (pro-B cells) were found in fetal live and bone marrow of RAG-2T and RAG-2T/E mu-bcl-2 transgenic mice in numbers comparable to normal mice. Like cells from normal mice they are c-kit+, surrogate L chain+ and CD25-, and can proliferate in vitro for long periods of time. Upon IL-7 deprivation, they can be induced to differentiate into c-kit-, surrogate L chain- and CD25+ cells that are no longer clonable on stromal cells and IL-7. Furthermore, sterile transcription from the kappa L chain gene loci is induced. The latter was also observed with pro-B cells directly isolated ex vivo from the bone marrow of RAG-2-deficient animals. The results suggest that progenitor B cell differentiation can occur in cells from V(D)J recombinase-deficient mice to the stage where kL chain gene rearrangements would normally be initiated. It further indicates that some molecular programs of early B cell differentiation can take place in the absence of Ig gene rearrangements.
由于RAG-2缺陷(RAG-2T)小鼠无法重排其内源免疫球蛋白(ig)基因座,其B细胞发育在早期阶段就受到阻碍。在这些小鼠中表达Eμ-bcl-2转基因并未改变这种表型。然而,在RAG-2T和RAG-2T/Eμ-bcl-2转基因小鼠的胎肝和骨髓中发现了基质细胞/IL-7反应性B细胞祖细胞(前B细胞),其数量与正常小鼠相当。与正常小鼠的细胞一样,它们c-kit阳性、替代轻链阳性且CD25阴性,并且能在体外长时间增殖。在缺乏IL-7的情况下,它们可被诱导分化为c-kit阴性、替代轻链阴性和CD25阳性的细胞,这些细胞在基质细胞和IL-7上不再具有克隆能力。此外,κ轻链基因座的无菌转录被诱导。从RAG-2缺陷动物骨髓中直接离体分离的前B细胞也观察到了后者。结果表明,祖B细胞分化可在V(D)J重组酶缺陷小鼠的细胞中发生至正常情况下κ轻链基因重排起始的阶段。这进一步表明,早期B细胞分化的一些分子程序可在无Ig基因重排的情况下发生。