In this article, we studied the production of the chemokine CXCL9, also termed Mig (monokine induced by gamma interferon) by cultured SJL/J mouse astrocytes infected with the BeAn strain of Theiler's murine encephalomyelitis virus (TMEV). This picornavirus induces demyelination in the SJL/J genetically susceptible strain of mice through an immune process mediated by CD4+ Th1 T cells. Those cells were chemoattracted by chemokines inside the central nervous system (CNS) after blood-brain barrier (BBB) disruption.cRNAs from TMEV- and mock-infected astrocytes cells were hybridized to the Affymetrix murine genome U74v2 DNA microarray. Hybridization data analysis revealed the upregulation of six sequences potentially coding for Mig. We confirmed post infection Mig mRNA increase by quantitative (qPCR) and RT-PCR. The presence of Mig in the supernatants of infected astrocytes was quantified using a specific ELISA. Secreted Mig was biologically active, inducing chemoattraction of mouse activated CD4+ T lymphocytes. Conversely, attracting activity on CD3+ resting T cells that can be attributed to chemokines as CXCL12/SDF-1α could not be demonstrated in these supernatants. No overinduction of the gene coding for this chemokine was assessed by DNA hybridization either. Both recombinant IFN-γ and TNF-α inflammatory cytokines were also strong inducers of Mig in SJL/J astrocyte cultures.

中文翻译：

---

泰勒氏鼠脑脊髓炎病毒感染星形胶质细胞诱导趋化因子的表达，这些趋化因子吸引活化的而不是静止的T淋巴细胞。

在本文中，我们研究了由Theiler鼠脑脊髓炎病毒BeAn株感染的培养SJL / J小鼠星形胶质细胞产生趋化因子CXCL9（也称为Mig（γ干扰素诱导的单核细胞因子））的过程。这种小核糖核酸病毒通过CD4 + Th1 T细胞介导的免疫过程在小鼠的SJL / J基因易感株中诱导脱髓鞘。血脑屏障（BBB）破坏后，这些细胞被中枢神经系统（CNS）内的趋化因子趋化。来自TMEV和模拟感染的星形胶质细胞的cRNA与Affymetrix鼠基因组U74v2 DNA微阵列杂交。杂交数据分析显示可能编码Mig的六个序列的上调。我们通过定量（qPCR）和RT-PCR证实了感染后Mig mRNA的增加。使用特异性ELISA定量感染的星形胶质细胞上清液中Mig的存在。分泌的Mig具有生物活性，可诱导小鼠活化的CD4 + T淋巴细胞的化学吸引。相反，在这些上清液中未证明可归因于趋化因子CXCL12 /SDF-1α的CD3 +静止T细胞上的吸引活性。通过DNA杂交也未评估编码该趋化因子的基因的过度诱导。在SJL / J星形胶质细胞培养物中，重组IFN-γ和TNF-α炎性细胞因子也是Mig的强诱导剂。在这些上清液中未证明可将趋化因子归因于趋化因子而在CD3 +静止T细胞上具有吸引活性。通过DNA杂交也未评估编码该趋化因子的基因的过度诱导。在SJL / J星形胶质细胞培养物中，重组IFN-γ和TNF-α炎性细胞因子也是Mig的强诱导剂。在这些上清液中未证明可将趋化因子归因于趋化因子而在CD3 +静止T细胞上产生吸引活性。通过DNA杂交也未评估编码该趋化因子的基因的过度诱导。在SJL / J星形胶质细胞培养物中，重组IFN-γ和TNF-α炎性细胞因子也是Mig的强诱导剂。