MICE LACKING THE C-REL PROTOONCOGENE EXHIBIT DEFECTS IN LYMPHOCYTE-PROLIFERATION, HUMORAL IMMUNITY, AND INTERLEUKIN-2 EXPRESSION
MICE LACKING THE C-REL PROTOONCOGENE EXHIBIT DEFECTS IN LYMPHOCYTE-PROLIFERATION, HUMORAL IMMUNITY, AND INTERLEUKIN-2 EXPRESSION
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DOI：
10.1101/gad.9.16.1965
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发表时间：
1995-08-15
影响因子：
10.5
通讯作者：
GERONDAKIS, S
中科院分区：
文献类型：
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作者：
KONTGEN, F;GRUMONT, RJ;GERONDAKIS, S
主要在造血细胞中表达的c-rel原癌基因编码NF-κ B样转录因子家族的亚基。在小鼠与失活的c-rel基因，而从所有造血谱系细胞的发展似乎正常，体液免疫受损，成熟的B和T细胞被发现是最有丝分裂刺激无反应。佛波酯和钙离子载体共刺激，在某些膜受体介导的信号相反，克服了T细胞增殖的缺陷，表明T细胞增殖发生的依赖性和非依赖性机制。外源性白细胞介素-2恢复T细胞而不是B细胞增殖的能力表明，Rel调节B和T细胞中对细胞分裂和免疫功能至关重要的不同基因的表达。
The c-rel proto-oncogene, which is expressed predominantly in hemopoietic cells encodes a subunit of the NF-kappa B-like family of transcription factors. In mice with an inactivated c-rel gene, whereas development of cells from all hemopoietic lineages appeared normal, humoral immunity was impaired and mature B and T cells were found to be unresponsive to most mitogenic stimuli. Phorbol ester and calcium ionophore costimulation, in contrast to certain membrane receptor-mediated signals, overcame the T cell-proliferative defect, demonstrating that T cell proliferation occurs by Rel-dependent and -independent mechanisms. The ability of exogenous interleukin-2 to restore T cell, but not B cell, proliferation indicates that Rel regulates the expression of different genes in B and T cells that are crucial for cell division and immune function.