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白细胞介素22是Tmevp3的一个候选基因,Tmevp3是一个控制泰勒氏病毒引起的神经疾病的基因座。

Interleukin 22 is a candidate gene for Tmevp3, a locus controlling Theiler's virus-induced neurological diseases.

作者信息

Levillayer F, Mas M, Levi-Acobas F, Brahic M, Bureau J F

机构信息

Unité des Virus Lents, URA CNRS1930, Institut Pasteur, 75724 Paris Cedex 15, France.

出版信息

Genetics. 2007 Jul;176(3):1835-44. doi: 10.1534/genetics.107.073536. Epub 2007 May 4.

Abstract

After intracerebral inoculation, Theiler's virus induces in its natural host, the mouse, an acute encephalomyelitis followed, in susceptible animals, by chronic inflammation and primary demyelination. Susceptibility to demyelination among strains of laboratory mice is explained by the capacity of the immune system to control viral load during persistence. Also, differences of susceptibility to viral load between the susceptible SJL strain and the resistant B10.S strain are mainly due to two loci, Tmevp2 and Tmevp3, located close to the Ifng locus on chromosome 10. In this article, we show that the Tmevp3 locus controls both mortality during the acute encephalomyelitis and viral load during persistence. Most probably, two genes located in the Tmevp3 interval control these two different phenotypes with efficiencies that depend on the age of the mouse at inoculation. Il22, a member of the IL-10 cytokine family, is a candidate gene for the control of mortality during the acute encephalomyelitis.

摘要

脑内接种后,泰勒病毒在其天然宿主小鼠中引发急性脑脊髓炎,在易感动物中随后出现慢性炎症和原发性脱髓鞘。实验小鼠品系间对脱髓鞘的易感性可通过免疫系统在病毒持续存在期间控制病毒载量的能力来解释。此外,易感的SJL品系和抗性的B10.S品系对病毒载量的易感性差异主要归因于位于10号染色体上靠近Ifng基因座的两个基因座Tmevp2和Tmevp3。在本文中,我们表明Tmevp3基因座既控制急性脑脊髓炎期间的死亡率,也控制病毒持续存在期间的病毒载量。很可能位于Tmevp3区间的两个基因控制这两种不同的表型,其效率取决于接种时小鼠的年龄。Il22是IL-10细胞因子家族的成员,是控制急性脑脊髓炎期间死亡率的候选基因。

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