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表达人白细胞介素4受体生长阴性突变体的BA/F3细胞依赖白细胞介素4的增殖通过强制表达Bcl-2得以恢复。

IL-4-dependent proliferation of BA/F3 cells expressing a growth-negative mutant of the human IL-4 receptor is restored by enforced expression of Bcl-2.

作者信息

Chung J, Deutsch H H, Kalthoff F S

机构信息

Department of Immunodermatology, Sandoz Research Institute, Vienna, Austria.

出版信息

J Leukoc Biol. 1996 Apr;59(4):586-90. doi: 10.1002/jlb.59.4.586.

Abstract

We have studied the regulation of growth and apoptosis in murine BA/F3 cells stably expressing cytoplasmic deletion mutants of the human interleukin-4 receptor (hIL-4R). Previously, we showed that BA/F3 cell transfectants expressing a cytoplasmic deletion mutant of the hIL-4R that lacks the region between Thr(462) and Ala(580), referred to as delta R3, fails to proliferate in the presence of hIL-4. Here we report that supertransfection of delta R3-expressing cells with a constitutively active murine bcl-2 gene results in prolonged survival of the delta R3/bel-2 double transfectants in the absence of cytokines. More importantly, however, the constitutive expression of Bcl-2 restored their capacity to grow permanently with hIL-4. This may provide an explanation for the discrepancy with previous reports showing growth mediation by hIL-4R truncated at position 367.

摘要

我们研究了稳定表达人白细胞介素-4受体(hIL-4R)胞质缺失突变体的小鼠BA/F3细胞中生长和凋亡的调控。此前,我们发现,表达hIL-4R胞质缺失突变体(缺失Thr(462)和Ala(580)之间区域,称为δR3)的BA/F3细胞转染子在hIL-4存在的情况下无法增殖。在此我们报告,用组成型活性小鼠bcl-2基因对表达δR3的细胞进行超转染,可使δR3/bcl-2双转染子在无细胞因子的情况下延长存活时间。然而,更重要的是,Bcl-2的组成型表达恢复了它们在hIL-4存在下永久生长的能力。这可能解释了与之前报道的在367位截断的hIL-4R介导生长之间的差异。

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