Maraskovsky E, Peschon J J, McKenna H, Teepe M, Strasser A
Department of Immunobiology, Immunex Corp., Seattle, WA 98101, USA.
Int Immunol. 1998 Sep;10(9):1367-75. doi: 10.1093/intimm/10.9.1367.
IL-7 receptor-deficient (IL-7R(-/-)) mice are lymphopenic as a result of defective cell production at early steps in both B and T lymphopoiesis. In the bone marrow, there is an incomplete block in B cell development at the transition from the pro-B to the pre-B cell stage. As a consequence, peripheral lymphoid organs of IL-7R(-/-) mice contain abnormally low numbers of mature surface (s) Ig-expressing B cells and this is accompanied by a relative increase in immature sIg- B cells. Transgenic expression of the anti-apoptotic protein Bcl-2 in IL-7R(-/-) mice rescues the defect in T cell development and in mature T cell function. The present report shows that constitutive expression of Bcl-2 is incapable of rescuing B lymphopoiesis in IL-7R(-/-) mice but can enhance survival of those mature B cells which escape the developmental arrest. Thus the essential role of IL-7R signaling in B lymphoid cells cannot be replaced by Bcl-2, indicating that in B lymphopoiesis IL-7R signaling is necessary for promoting cell division and/or for inhibiting a Bcl-2-insensitive pathway to apoptosis.
白细胞介素-7受体缺陷（IL-7R(-/-)）小鼠由于B淋巴细胞生成和T淋巴细胞生成早期阶段的细胞生成缺陷而出现淋巴细胞减少。在骨髓中，B细胞从祖B细胞向前B细胞阶段过渡时发育存在不完全阻滞。因此，IL-7R(-/-)小鼠的外周淋巴器官中表达成熟表面（s）Ig的B细胞数量异常低，同时未成熟sIg - B细胞相对增加。在IL-7R(-/-)小鼠中抗凋亡蛋白Bcl-2的转基因表达挽救了T细胞发育和成熟T细胞功能的缺陷。本报告表明，Bcl-2的组成型表达无法挽救IL-7R(-/-)小鼠中的B淋巴细胞生成，但可以提高那些逃脱发育阻滞的成熟B细胞的存活率。因此，IL-7R信号在B淋巴细胞中的重要作用不能被Bcl-2替代，这表明在B淋巴细胞生成中，IL-7R信号对于促进细胞分裂和/或抑制对Bcl-2不敏感的凋亡途径是必需的。
