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首页> 外文期刊>Cytokine >Interleukin-27 expression following infection with the murine gammaherpesvirus 68.
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Interleukin-27 expression following infection with the murine gammaherpesvirus 68.

机译：鼠γ疱疹病毒感染后白介素27的表达68。

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摘要

IL-27 is a heterodimeric cytokine composed of p28 and Epstein Barr virus induced gene 3 (Ebi3) protein subunits. In the present study, we questioned whether murine gammaherpesvirus 68 (HV-68) could induce expression of Ebi3, p28, and IL-27 in this mouse model of an EBV-like infection. Cultured macrophages and dendritic cells exposed to HV-68 upregulated p28 mRNA expression and increased secretion of the p28 and IL-27 (p28+Ebi3) proteins. B220(+) and CD11b(+) cells also upregulated p28 mRNA expression following in vivo infection with this virus. Surprisingly, no significant increases in p28 or IL-27 protein production were observed in vivo during the acute or mononucleosis phases of the disease. The possibility that HV-68-induced upregulation of p28 mRNA expression primed cells for IL-27 secretion was suggested by the ability of a TLR4 agonist to augment cytokine production. When cultured macrophages and dendritic cells were exposed to virus plus a suboptimal dose of LPS, increased levels of p28 protein expression were observed. More importantly, when latently infected mice were challenged with a sublethal dose of LPS, augmented p28 and IL-27 protein production occurred. Using a model of sepsis, mice latently infected with HV-68 had exaggerated p28 protein production when compared to mice that were singularly infected or subjected to cecal ligation and puncture. Taken together, these studies define expression of HV-68 induced IL-27, and suggest that mice latently infected with this gammaherpesvirus will have exaggerated responses when confronted with other stimuli capable of inducing this member of the IL-12 family of cytokines.
机译：IL-27是由p28和爱泼斯坦巴尔病毒诱导的基因3（Ebi3）蛋白亚基组成的异二聚体细胞因子。在本研究中，我们质疑鼠伽马疱疹病毒68（HV-68）是否可以在这种EBV样感染的小鼠模型中诱导Ebi3，p28和IL-27的表达。暴露于HV-68的培养巨噬细胞和树突状细胞上调了p28 mRNA表达，并增加了p28和IL-27（p28 + Ebi3）蛋白的分泌。在体内感染该病毒后，B220（+）和CD11b（+）细胞也上调了p28 mRNA的表达。令人惊讶地，在该疾病的急性或单核细胞增多症阶段，在体内未观察到p28或IL-27蛋白产量的显着增加。 TLR4激动剂增加细胞因子产生的能力提示了HV-68诱导的p28 mRNA表达上调引发细胞分泌IL-27的可能性。当将培养的巨噬细胞和树突状细胞暴露于病毒以及次适量的LPS时，观察到p28蛋白表达水平增加。更重要的是，当用亚致死剂量的LPS攻击潜伏感染的小鼠时，p28和IL-27蛋白的产生会增加。使用脓毒症模型，与单独感染或盲肠结扎和穿刺的小鼠相比，潜在感染HV-68的小鼠p28蛋白产生过大。综上所述，这些研究确定了HV-68诱导的IL-27的表达，并表明潜伏地感染这种伽马疱疹病毒的小鼠在面对其他能够诱导这种IL-12家族细胞因子成员的刺激时，会具有夸大的反应。

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