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首页> 外文期刊>The Journal of Immunology: Official Journal of the American Association of Immunologists >Expression of Mig (Monokine Induced by Interferon-#gamma#)Is Important in T Lymphocyte Recruitment and Host Defense Following Viral Infection of the Central Nervous System
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Expression of Mig (Monokine Induced by Interferon-#gamma#)Is Important in T Lymphocyte Recruitment and Host Defense Following Viral Infection of the Central Nervous System

机译:Mig(干扰素-#γ#诱导的Monokine)的表达在病毒感染中枢神经系统后的T淋巴细胞募集和宿主防御中很重要。

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Induction of a Th1 immune response against viral infection of the CNS is important in contributing to viral clearance. The present tudies demonstrate a role for the T cell chemoattractant chemokine Mig (monokine induced by IFN-,,) in contributing to a Thl esponse against mouse hepatitis virus infection of the CNS. Analysis of the kinetics of Mig expression revealed mRNA transcript! Iresent at days 7 and 12 postinfection (p.i.) but not early (day 2) or late (day 35) in the infection. To determine functional ignificance, mouse hepatitis virus-infected mice were treated with anti-Mig antisera, and the severity of disease was evaluated. :uch treatment resulted in a marked increase in mortality that correlated with a> 3 log increase in viral burden within the brains s compared with control mice treated with normal rabbit serum. Anti-Mig-treated mice displayed a significant decrease (p < 1.005) in CD4+ and CDS+ T cell recruitment into the CNS as compared with normal rabbit serum-treated mice. In addition, ,nti-Mig treatment resulted in a significant decrease (p < 0.05) in levels of IFN-" and IFN-fJ that coincided with increased (p < 1.02) expression of the anti-inflammatory Th2 cytokine IL-10 within the CNS. Collectively, these data indicate that Mig is im. lortant in contributing to host defense by promoting a protective Th1 response against viral infection of the CNS.
机译:诱导抗CNS病毒感染的Th1免疫反应在促进病毒清除方面很重要。本研究证明了T细胞趋化因子趋化因子Mig(由IFN-γ诱导的单核细胞因子)在促成针对CNS的小鼠肝炎病毒感染的Th1反应中的作用。 Mig表达动力学的分析揭示了mRNA转录本!在感染后第7天和第12天(p.i.)出现,但在感染的早期(第2天)或晚期(第35天)不出现。为了确定功能的重要性,将小鼠肝炎病毒感染的小鼠用抗Mig抗血清进行治疗,并评估疾病的严重程度。 :与用正常兔血清治疗的对照组小鼠相比,许多治疗导致死亡率显着增加,其与大脑内病毒载量的增加> 3 log有关。与正常兔血清处理的小鼠相比,抗Mig处理的小鼠的CD4 +和CDS + T细胞募集到CNS的能力显着降低(p <1.005)。此外,nti-Mig治疗导致IFN-γ和IFN-fJ水平显着降低(p <0.05),与抗炎性Th2细胞因子IL-10的表达增加(p <1.02)相吻合。总体而言,这些数据表明,Mig通过促进针对CNS病毒感染的保护性Th1反应,在促进宿主防御中起着至关重要的作用。

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