Herpes simplex virus-specific memory CD8+ T cells are selectively activated and retained in latently infected sensory ganglia

Herpes simplex virus-specific memory CD8+ T cells are selectively activated and retained in latently infected sensory ganglia
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DOI:
10.1016/s1074-7613(03)00112-2
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发表时间:
2003-05-01
期刊:
影响因子:
32.4
通讯作者:
Hendricks, RL
Hendricks, RL
中科院分区:
医学1区
文献类型:
--
作者:
Khanna, KM;Bonneau, RH;Hendricks, RL

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该研究挑战了单纯疱疹病毒1型(HSV-1)潜伏期代表一种被宿主免疫系统忽略的沉默感染的概念,并提示抗原导向的记忆CD8(+) T细胞保留。特异性免疫显性gB(498-505) HSV-1表位的CD8(+) T细胞选择性保留在潜伏感染的三叉神经节的眼支中,在那里它们获得并维持激活表型和产生ifn - γ的能力。部分CD8(+) T细胞与神经元连接处呈现TCR极化。gB(498-505)肽特异性CD8(+) T细胞克隆可在体外三叉神经节培养中阻断HSV-1的潜伏期再激活。我们得出结论,CD8+ T细胞在潜伏感染的感觉神经元中提供HSV-1基因表达的主动监测。
This study challenges the concept that herpes simplex virus type 1 (HSV-1) latency represents a silent infection that is ignored by the host immune system, and suggests antigen-directed retention of memory CD8(+) T cells. CD8(+) T cells specific for the immunodominant gB(498-505) HSV-1 epitope are selectively retained in the ophthalmic branch of the latently infected trigeminal ganglion, where they acquire and maintain an activation phenotype and the capacity to produce IFN-gamma. Some CD8(+) T cells showed TCR polarization to junctions with neurons. A gB(498-505) peptide-specific CD8(+) T cell clone can block HSV-1 reactivation from latency in ex vivo trigeminal ganglion cultures. We conclude that CD8+ T cells provide active surveillance of HSV-1 gene expression in latently infected sensory neurons.