Katsuki M, Kimura M, Ohta M, Otani H, Tanaka O, Yamamoto T, Nozawa-Kimura S, Yokoyama M, Nomura T, Habu S
Department of DNA Biology, School of Medicine, Tokai University, Isehara, Japan.
Int Immunol. 1989;1(2):214-8. doi: 10.1093/intimm/1.2.214.
We created transgenic mice with an intact human genomic interleukin-2 gene (gIL-2) or a mouse metallothionein-I promoter-human IL-2 chimeric gene (MTgIL-2). Nine (2 gIL-2 and 7 MTgIL-2 transgenics) out of 12 transgenic mice which were obtained independently had motor ataxic symptoms. All transgenic offspring of the symptomatic founders showed the same symptoms as their transgenic parents. Morphological examination demonstrated perivascular lymphocyte accumulation in the cerebellar meninx which was followed by increased cell infiltration of neutrophils and monocytes in the destructive cerebellum of all transgenic mice. These findings suggest that the lymphocyte infiltration in the cerebellum is caused by the specific effect of the exogenously introduced human IL-2 gene.
我们构建了带有完整人类基因组白细胞介素-2基因(gIL-2)或小鼠金属硫蛋白-I启动子-人类白细胞介素-2嵌合基因(MTgIL-2)的转基因小鼠。在独立获得的12只转基因小鼠中,有9只(2只gIL-2转基因小鼠和7只MTgIL-2转基因小鼠)出现运动性共济失调症状。有症状奠基者的所有转基因后代都表现出与其转基因亲本相同的症状。形态学检查显示,所有转基因小鼠的小脑软膜出现血管周围淋巴细胞聚集,随后在受损小脑中嗜中性粒细胞和单核细胞的细胞浸润增加。这些发现表明,小脑中的淋巴细胞浸润是由外源导入的人类IL-2基因的特定作用引起的。