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bcl‐2 Regulation in Normal Resting Lymphocytes and Lymphoblasts

机译:正常静息淋巴细胞和淋巴细胞中的bcl-2调节

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摘要

Expression of the bcl‐2 protein and bcl‐2 mRNA at the individual cell level was semiquantitatively examined in normal quiescent peripheral blood lymphocytes and pokeweed mitogen‐ or concanavalin A and interleukin‐2‐induced lymphoblasts in vitro by microscopic fluorometry using immunofluorescence and fluorescein‐labeled in situ hybridization. Approximately 90% of normal quiescent T and B lymphocytes expressed bcl‐2 protein at a level which was compatible with that of bcl‐2 mRNA. On the contrary, most mitogen‐induced lymphoblasts showed a posttranscriptional suppression of bcl‐2 protein expression. However, bcl‐2 protein was not downregulated by the posttranscriptional suppression in all lymphocytes activated in vitro, but approximately 15% of the lymphoblasts still expressed bcl‐2 protein at a higher level than nontransformed quiescent small lymphocytes; thus bcl‐2 protein expression in lymphoblasts showed a distinct bimodal pattern. Furthermore, it was supposed that lymphoblasts with no detectable bcl‐2 protein might fall into apoptosis but the remainder, expressing high levels of bcl‐2 protein, could escape apoptosis. Thus, the bcl‐2 gene may play an important role as a regulator of apoptosis in the human immune system.
机译:使用免疫荧光和荧光素荧光显微镜检测体外正常静息外周血淋巴细胞和商陆有丝分裂原或伴刀豆球蛋白A或白细胞介素2诱导的淋巴母细胞中bcl-2蛋白和bcl-2 mRNA在单个细胞水平的表达。标记的原位杂交。大约90%的正常静态T和B淋巴细胞表达bcl-2蛋白的水平与bcl-2 mRNA的水平相适应。相反,大多数丝裂原诱导的淋巴母细胞在转录后抑制bcl-2蛋白表达。然而,在体外激活的所有淋巴细胞中,转录后抑制均未下调bcl-2蛋白,但约15%的淋巴母细胞仍比未转化的静态小淋巴细胞表达bcl-2蛋白的水平更高。因此,淋巴母细胞中bcl-2蛋白的表达表现出独特的双峰模式。此外,据认为没有可检测到的bcl-2蛋白的淋巴母细胞可能会进入凋亡状态,而其余表达高水平的bcl-2蛋白的细胞能够逃脱凋亡。因此,bcl-2基因可能在人类免疫系统中作为凋亡调节剂发挥重要作用。

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