Cytomegalovirus inhibits major histocompatibility class II expression on infected endothelial cells.

Cytomegalovirus inhibits major histocompatibility class II expression on infected endothelial cells.
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发表时间:
1994-04
期刊:
The American journal of pathology
影响因子:
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通讯作者:
Daniel D. Sedmak;Guglielmo Am;Deborah A. Knight;D. Birmingham;Emina H. Huang;W. Waldman
Daniel D. Sedmak;Guglielmo Am;Deborah A. Knight;D. Birmingham;Emina H. Huang;W. Waldman
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文献类型:
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作者:
Daniel D. Sedmak;Guglielmo Am;Deborah A. Knight;D. Birmingham;Emina H. Huang;W. Waldman

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持续性人巨细胞病毒(HCMV)感染是导致免疫功能低下个体显著发病率和死亡率的原因。原发性感染后HCMV可能持续存在的一种机制是通过抑制宿主细胞人类白细胞抗原(HLA)II类表达,从而逃避正常的抗病毒免疫监视。免疫荧光流式细胞术检测感染HCMV AD 169和EC增殖株VHL/E的人内皮细胞(EC)培养物,结果显示干扰素-γ(IFN-γ)诱导的HLA-DR表面表达显著降低。双标记免疫组织化学法测定,HCMV特异性抑制感染细胞表面和细胞质II类抗原的诱导。HCMV感染还抑制IFN-γ和肿瘤坏死因子-α上调HLA I类表达。北方印迹分析感染,IFN-γ处理的人脐静脉内皮细胞显示II类mRNA的情况下。HCMV的持续存在可能部分是由于其抑制感染细胞中HLA II类诱导的能力。
Persistent human cytomegalovirus (HCMV) infections are responsible for significant morbidity and mortality in immunocompromised individuals. One mechanism by which HCMV may develop persistence after primary infection is through inhibition of host cell human leukocyte antigen (HLA) class II expression with resultant escape from normal antiviral immune surveillance. Immunofluorescence flow cytometry of human endothelial cell (EC) cultures infected with HCMV AD169 and an EC propagated strain, VHL/E, showed a marked reduction in interferon-gamma (IFN-gamma)-induced surface expression of HLA-DR. This inhibition did not occur when EC were treated with ultraviolet-inactivated virus and IFN-gamma. HCMV, as determined by dual-labeling immunohistochemistry, inhibited induction of surface and cytoplasmic class II antigens specifically in infected cells. HCMV infection also inhibited IFN-gamma and tumor necrosis factor-alpha up-regulation of HLA class I expression. Northern blot analysis of infected, IFN-gamma-treated human umbilical vein endothelial cells revealed an absence of class II mRNA. Persistence of HCMV may result in part from its ability to inhibit HLA class II induction in infected cells.