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Transgenic Bcl-3 slows T cell proliferation

机译:转基因Bcl-3减慢T细胞增殖

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摘要

Immunological adjuvants, such as bacterial LPS, increase the mRNA levels of the IkB-related NF-κB transcriptional transactivator, Bcl-3, in activated T cells. Adjuvants also increase the life expectancy of activated T cells, as does over-expression of Bcl-3, suggesting that Bcl-3 is part of the pathway whereby adjuvants affect T cell lifespans. However, previous reports, confirmed here, show that adjuvants also increase the life expectancies of Bcl-3-deficient T cells, making Bcl-3’s role and effects in adjuvant-induced survival uncertain. To investigate the functions of Bcl-3 further, here we confirm the adjuvant-induced expression of Bcl-3 mRNA and show Bcl-3 induction at the protein level. Bcl-3 was expressed in mice via a transgene driven by the human CD2 promoter. Like other protective events, over-expression of Bcl-3 slows T cell activation very early in T cell responses to antigen, both in vitro and in vivo. This property was intrinsic to the T cells over-expressing the Bcl-3 and did not require Bcl-3 expression by other cells such as antigen-presenting cells.
机译:免疫佐剂,例如细菌LPS,会增加活化T细胞中IkB相关NF-κB转录反式激活子Bcl-3的mRNA水平。佐剂也能增加活化T细胞的预期寿命,Bcl-3的过表达也是如此,这表明Bcl-3是佐剂影响T细胞寿命的途径的一部分。但是,以前的报道在这里得到证实,显示佐剂还可以增加Bcl-3缺陷T细胞的预期寿命,从而使Bcl-3在佐剂诱导的存活中的作用和影响不确定。为了进一步研究Bcl-3的功能,在这里我们证实了佐剂诱导的Bcl-3 mRNA表达,并在蛋白水平上显示了Bcl-3诱导。 Bcl-3通过人类CD2启动子驱动的转基因在小鼠中表达。像其他保护事件一样,在体外和体内,Bcl-3的过度表达都会在T细胞对抗原的应答中非常早地减慢T细胞活化。此特性是过表达Bcl-3的T细胞固有的,不需要其他细胞(如抗原呈递细胞)表达Bcl-3。

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