Viral Immunology Center, Department of Biology, Georgia State University, Atlanta, GA, United States; Department of Ophthalmology, Emory University School of Medicine, Atlanta, GA, United States.
Viral Immunology Center, Department of Biology, Georgia State University, Atlanta, GA, United States; Department of Ophthalmology, Emory University School of Medicine, Atlanta, GA, United States.
Cytokine. 2017 Sep;97:38-41. doi: 10.1016/j.cyto.2017.05.021. Epub 2017 May 28.
AIDS-related human cytomegalovirus retinitis remains a leading cause of blindness worldwide. We compared two C57BL/6 mouse models of experimental murine cytomegalovirus (MCMV) retinitis for intraocular expression of suppressors of cytokine signaling (SOCS)1 and SOCS3, host proteins that are inducible negative feedback regulators of cytokine signaling. These mouse models differed in method of immune suppression, one by retrovirus-induced immune suppression (MAIDS) and the other by corticosteroid-induced immune suppression. Following subretinal injection of MCMV to induce retinitis, intraocular SOCS1 and SOCS3 were only mildly stimulated, and often without significance, within MCMV-infected eyes during the progression of MCMV retinitis in corticosteroid-immunosuppressed mice, contrary to MCMV-infected eyes of mice with MAIDS that showed significant high stimulation of SOCS1 and SOCS3 expression in agreement with previous findings. Frequency and severity of retinitis as well as amounts of intraocular infectious MCMV in corticosteroid-immunosuppressed mice were also unexpectedly lower than values previously reported for MAIDS animals during MCMV retinitis. These data reveal a major difference between two mouse models of experimental MCMV retinitis and suggest a possible link between the amplitude of SOCS1 and SOCS3 stimulation and severity of disease in these models.
艾滋病相关的人巨细胞病毒视网膜炎仍然是全球范围内导致失明的主要原因。我们比较了两种用于实验性小鼠巨细胞病毒 (MCMV) 视网膜炎的 C57BL/6 小鼠模型,以比较细胞因子信号转导抑制因子 (SOCS)1 和 SOCS3 的眼内表达,SOCS1 和 SOCS3 是细胞因子信号转导的诱导性负反馈调节剂。这两种小鼠模型的免疫抑制方法不同,一种是通过逆转录病毒诱导的免疫抑制 (MAIDS),另一种是通过皮质类固醇诱导的免疫抑制。在通过视网膜下注射 MCMV 诱导视网膜炎后,在皮质类固醇免疫抑制小鼠的 MCMV 视网膜炎进展过程中,眼内 SOCS1 和 SOCS3 的刺激程度仅轻度且通常无统计学意义,与 MAIDS 小鼠的 MCMV 感染眼不同,后者表现出 SOCS1 和 SOCS3 表达的显著高刺激,这与之前的发现一致。皮质类固醇免疫抑制小鼠的视网膜炎的频率和严重程度以及眼内传染性 MCMV 的量也出乎意料地低于 MAIDS 动物在 MCMV 视网膜炎期间的报道值。这些数据揭示了两种实验性 MCMV 视网膜炎小鼠模型之间的主要差异,并提示这些模型中 SOCS1 和 SOCS3 刺激的幅度与疾病严重程度之间可能存在联系。