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Induction of endogenous retroviral gene product (SU) as an acute-phase protein by IL-6 in murine hepatocytes.

机译:IL-6在鼠肝细胞中诱导内源性逆转录病毒基因产物(SU)作为急性期蛋白。

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摘要

The effect of Lps locus and IL-6 on the production of SU (previously termed gp70), a mouse endogenous retroviral gene product, was studied. Back-cross studies using the progeny between (NZB x C3H/HeJ)F1 and C3H/HeJ mice indicate that the basal level of SU is not associated with the Lps locus on chromosome 4. Lipopolysaccharide (LPS) mitogen response-negative mice did not show the enhancement of serum SU production after LPS injection. Spleen cells from LPS-mitogen response-positive but not from negative mice showed increase of IL-6 synthesis in the presence of LPS. Since IL-6 may be involved in the production of serum SU, we tested the effect of IL-6 in a primary hepatocyte culture system. SU production was clearly enhanced in the presence of recombinant IL-6, indicating that IL-6 induced by LPS can enhance the expression of retroviral genome.
机译:研究了Lps基因座和IL-6对小鼠内源性逆转录病毒基因产物SU(以前称为gp70)产生的影响。使用(NZB x C3H / HeJ)F1和C3H / HeJ小鼠之间的后代进行回交研究表明,SU的基础水平与4号染色体上的Lps基因位点无关。脂多糖(LPS)促细胞分裂反应阴性的小鼠没有显示注射LPS后血清SU产生的增强。来自LPS-促细胞分裂剂反应阳性但不来自阴性小鼠的脾细胞在LPS存在下显示IL-6合成增加。由于IL-6可能参与血清SU的产生,因此我们在原代肝细胞培养系统中测试了IL-6的作用。在重组IL-6的存在下,SU的产生明显增强,表明LPS诱导的IL-6可以增强逆转录病毒基因组的表达。

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