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首页> 外文期刊>British journal of ophthalmology >An immune response after intraocular administration of an adenoviral vector containing a beta galactosidase reporter gene slows retinal degeneration in the rd mouse.
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An immune response after intraocular administration of an adenoviral vector containing a beta galactosidase reporter gene slows retinal degeneration in the rd mouse.

机译：眼内注射含有β半乳糖苷酶报道基因的腺病毒载体后，免疫反应会减慢rd小鼠的视网膜变性。

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BACKGROUND/AIMS: Retinal degenerations are a leading cause of blindness for which there are currently no effective treatments. This has stimulated interest in the investigation of gene therapy strategies for these diseases in a variety of animal models. A number of attempts have been made to prevent photoreceptor loss in the rd mouse model of retinal degeneration using adenoviral vectors containing either a copy of the missing functional gene or a gene encoding either a neurotrophic factor or an antiapoptotic factor. The authors have previously demonstrated that intraocular administration of an adenoviral vector containing a beta galactosidase gene (AV.LacZ) results in an immune response to viral gene products and beta galactosidase. Here the effect of the immune response on retinal degeneration is examined. METHODS: Juvenile rd mice were injected intravitreally with AV.LacZ and a proportion were depleted of either CD4+ or CD8+ T cells or both. Control animals were injected with PBS. The mice were sacrificed 10 and 20 days post-injection and their eyes embedded in paraffin wax and sectioned. RESULTS: 10 days after intravitreal injection of AV.LacZ, the outer nuclear layer contains an average of 2.5 rows compared with 1.5 in PBS injected animals (p<0.005). The protective effect of AV.LacZ is negated by immune suppression and does not extend beyond 20 days. CONCLUSION: An immune response to vector and transgene products is able to slow degeneration in the rd mouse. This phenomenon should be taken into account when analysing the degeneration in the rd mouse following gene transfer.
机译：背景/目的：视网膜变性是失明的主要原因，目前尚无有效的治疗方法。这激发了在各种动物模型中研究这些疾病的基因治疗策略的兴趣。已经进行了许多尝试，以使用含有缺失的功能基因的拷贝或编码神经营养因子或抗凋亡因子的基因的腺病毒载体，在视网膜变性的rd小鼠模型中防止光感受器丧失。作者先前已经证明，眼内施用含有β半乳糖苷酶基因（AV.LacZ）的腺病毒载体可导致对病毒基因产物和β半乳糖苷酶的免疫反应。在此检查了免疫应答对视网膜变性的影响。方法：向幼年rd小鼠玻璃体内注射AV.LacZ，并清除一部分CD4 +或CD8 + T细胞或两者。对照动物注射PBS。注射后10和20天处死小鼠，将其眼睛包埋在石蜡中并切成薄片。结果：玻璃体内注射AV.LacZ后10天，外核层平均包含2.5行，而PBS注射的动物为1.5行（p <0.005）。 AV.LacZ的保护作用被免疫抑制所抵消，并且不会持续超过20天。结论：对载体和转基因产物的免疫反应能够减慢rd小鼠的变性。分析基因转移后rd小鼠的变性时，应考虑到这种现象。

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