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首页> 外文期刊>Molecular and Cellular Biology >Interleukin-1 synergy with phosphoinositide pathway agonists for induction of interleukin-2 gene expression: molecular basis of costimulation.
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Interleukin-1 synergy with phosphoinositide pathway agonists for induction of interleukin-2 gene expression: molecular basis of costimulation.

机译：白介素-1与磷酸肌醇途径激动剂的协同作用，诱导白介素2基因表达：共刺激的分子基础。

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The macrophage-derived cytokine interleukin-1 (IL-1) can provide a second signal with antigen to elicit production of interleukin-2 (IL-2) by helper T cells. The pathway(s) involved remains controversial, with protein kinase C and cyclic AMP (cAMP) invoked as possible second messengers. In the murine thymoma EL4.E1, IL-1 could synergize with the phosphoinositide pathway, because the cells made higher levels of IL-2 in the presence of IL-1 than could be induced by phorbol ester plus calcium ionophore alone. IL-1 is unlikely to act through a sustained increase in cAMP in these cells because it did not raise cAMP levels detectably and because IL-1 and forskolin had opposite effects on IL-2 gene expression. Inducible expression of a transfected reporter gene linked to a cloned fragment of the murine IL-2 gene promoter was initially increased by IL-1 costimulation, implying that IL-1 can increase the rate of transcription of IL-2. The minimal promoter elements required for iL-1 responsiveness were located within 321 bp of the IL-2 RNA cap site, and further upstream sequences to -2800 did not modify this response. IL-1 costimulation resulted in enhanced activity of both an inducible NF-kappa B-like factor and one of two distinct AP-1-like factors that bind to IL-2 regulatory sequences. Neither was induced, however, by IL-1 alone. Another AP-1-like factor and NFAT-1, while inducible in other cell types, were expressed constitutively in the EL4.E1 cells and were unaffected by IL-1. These results are discussed in terms of the combinatorial logic of IL-2 gene expression.
机译：巨噬细胞源性细胞因子白介素-1（IL-1）可以提供带有抗原的第二信号，以诱导辅助T细胞产生白介素-2（IL-2）。所涉及的途径仍存在争议，蛋白激酶C和环状AMP（cAMP）可能作为第二信使被调用。在鼠胸腺瘤EL4.E1中，IL-1可以与磷酸肌醇途径协同作用，因为在存在IL-1的情况下，细胞产生的IL-2水平要比佛波酯和钙离子载体单独诱导的水平高。 IL-1不太可能通过这些细胞中cAMP的持续增加而起作用，因为它没有检测到cAMP水平的升高，并且IL-1和福司可林对IL-2基因的表达有相反的作用。最初通过IL-1共刺激提高了与鼠IL-2基因启动子克隆片段连接的转染报告基因的诱导表达，这暗示IL-1可以提高IL-2的转录速率。 iL-1响应所需的最小启动子元件位于IL-2 RNA帽位点的321 bp之内，-2800的其他上游序列并未改变该响应。 IL-1共刺激导致可诱导的NF-κB样因子和与IL-2调控序列结合的两个不同AP-1样因子之一的活性增强。但是，单独用IL-1都不能诱导。另一个AP-1样因子和NFAT-1虽然可以在其他细胞类型中诱导，但在EL4.E1细胞中组成性表达，不受IL-1的影响。根据IL-2基因表达的组合逻辑讨论了这些结果。

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