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首页> 外文期刊>The Journal of Immunology: Official Journal of the American Association of Immunologists >Up-Regulation of Fas Ligand Expression by Human Cytomegalovirus Immediate-Early Gene Product 2: A Novel Mechanism in Cytomegalovirus-Induced Apotosis in Human Retina
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Up-Regulation of Fas Ligand Expression by Human Cytomegalovirus Immediate-Early Gene Product 2: A Novel Mechanism in Cytomegalovirus-Induced Apotosis in Human Retina

机译：Fas配体的表达由人类巨细胞病毒立即早期基因产品2的上调：巨细胞病毒诱导的人类视网膜细胞凋亡的新机制。

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摘要

Human CMV (HCMV) is an important pathogen that causes widespread diseases in immunocompromised individuals. Among the opportunistic HCMV infections, HCMV ritinitis is most common in transplant recipients and AIDS patients. It often leads to blindness if left untreated. The question as to how HCMV infection causes retinal pathogenesis remains unresolved. Here, we report that viral immediate-early gene product 2 (IE2), but not IE1, up-regulates the Fas ligand (FasL) expression in HCMV-infected human retinal pigment epithelium cells. Increased secretion of FasL from virally infected cells into cultured medium was observed upon HCMV infection. The capability of such cell-free meidium to induce apoptosis of Fas (CD95)-expressing Jurkat cells further implies that Fas-FasL interaction might mediate cell death in the lesion of HCMV retinitis. To support this idea, we observed augmented soluble FasL levels in vitreous from AIDS patients with HCMV retinitis as compared with that from AIDS patientw without HCMV infection. In addition, by in situ hybridization and immunohistochemistry, we detected enhanced signals of FasL, the existence of viral IE Ags and apoptotic cells at the same sites in the lesion of HCMV-infected retina. These results strongly suggest that IE2 induction of FasL expression in human retina might be an important event that takes place in the early stage of infection and finally leads to visual loss in individuals affiliated with HCMV retinitis.
机译：人CMV（HCMV）是一种重要的病原体，可在免疫受损的个体中引起广泛的疾病。在机会性HCMV感染中，HCMV鼻炎最常见于移植受者和AIDS患者。如果不及时治疗，通常会导致失明。关于HCMV感染如何引起视网膜发病的问题仍未解决。在这里，我们报告病毒立即早期基因产物2（IE2），而不是IE1，上调了HCMV感染的人类视网膜色素上皮细胞Fas配体（FasL）的表达。在HCMV感染后，观察到FasL从病毒感染细胞向培养基的分泌增加。这种无细胞的亚甲基能够诱导表达Fas（CD95）的Jurkat细胞凋亡的能力进一步暗示Fas-FasL相互作用可能介导HCMV视网膜炎病变中的细胞死亡。为了支持这一想法，我们观察到与未感染HCMV的AIDS患者相比，患有HCMV视网膜炎的AIDS患者玻璃体中可溶性FasL水平增加。此外，通过原位杂交和免疫组织化学，我们检测到增强的FasL信号，在HCMV感染的视网膜病变的相同部位存在病毒IE Ag和凋亡细胞。这些结果强烈表明，IE2诱导人视网膜FasL表达可能是在感染早期发生的重要事件，并最终导致与HCMV视网膜炎有关的个体发生视力丧失。

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