Staeheli P, Haller O, Boll W, Lindenmann J, Weissmann C
Cell. 1986 Jan 17;44(1):147-58. doi: 10.1016/0092-8674(86)90493-9.
Mx+ mice are much more resistant to influenza virus than Mx- strains. The resistance is mediated by interferon (IFN) alpha/beta. After IFN treatment, Mx+ but not Mx- cells accumulate Mx protein and become specifically resistant to orthomyxoviruses. cDNA encoding Mx protein was cloned and sequenced. Southern analyses indicate that Mx- alleles derive from their Mx+ counterpart by deletions. IFN-treated Mx+ cells contained a 3.5 kb Mx mRNA, while Mx- cells showed only traces of shorter Mx RNA. Mx- cells transformed with Mx cDNA expressed Mx protein constitutively to varying extents; resistance of individual cells to influenza virus correlated with Mx protein expression. Thus, specific resistance to influenza virus in vivo may be attributed to Mx protein expression and is independent of other IFN-mediated effects.
Mx+小鼠比Mx-品系对流感病毒的抵抗力强得多。这种抵抗力由α/β干扰素(IFN)介导。IFN处理后,Mx+细胞而非Mx-细胞积累Mx蛋白,并对正粘病毒产生特异性抗性。编码Mx蛋白的cDNA被克隆并测序。Southern分析表明,Mx-等位基因是通过缺失从其Mx+对应物衍生而来的。IFN处理的Mx+细胞含有3.5 kb的Mx mRNA,而Mx-细胞仅显示出较短Mx RNA的痕迹。用Mx cDNA转化的Mx-细胞在不同程度上组成性表达Mx蛋白;单个细胞对流感病毒的抗性与Mx蛋白表达相关。因此,体内对流感病毒的特异性抗性可能归因于Mx蛋白的表达,且独立于其他IFN介导的效应。