The role of natural killer cells in the development of herpes simplex virus type 1 induced stromal keratitis in mice.
The role of natural killer cells in the development of herpes simplex virus type 1 induced stromal keratitis in mice.
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自然杀伤细胞在 1 型单纯疱疹病毒诱导的小鼠基质性角膜炎发展中的作用。
DOI：
10.1038/eye.1994.61
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发表时间：
1994
期刊：
影响因子：
--
通讯作者：
Foster,CS
中科院分区：
文献类型：
--
作者：
Tamesis,RR;Messmer,EM;Rice,BA;Dutt,JE;Foster,CS
自然杀伤(NK)细胞和获得性细胞介导的免疫效应细胞(迟发型超敏反应(DTH)和细胞毒性T淋巴细胞(CTL))在抵抗眼以外部位的肿瘤和病毒感染方面发挥着至关重要的作用。然而，对病毒感染的角膜产生强烈的细胞炎症反应，伴随着对角膜透明度的损害，具有明显的进化劣势，大量证据表明，在动物(如小鼠)中，在与单纯疱疹病毒接触后高度容易发生角膜炎症破坏的动物中，是动物的免疫/炎症反应导致了角膜损伤。我们研究了自然杀伤细胞在NK缺乏(C57BL/6J-bgj(米色))小鼠及其NK功能正常(C57BL/6J(黑色))近亲疱疹间质角膜炎(HSK)发生中的作用。米色(NK缺乏)小鼠对HSK的抵抗力与黑色小鼠一样。我们还研究了BALB/c IgH-1异基因小鼠NK细胞耗竭的影响。AL-20(IgH-L d)小鼠通常对坏死性单纯疱疹病毒高度易感。在体内，这些小鼠的NK细胞耗尽显著降低了这些动物单纯疱疹病毒性角膜炎的发生率和严重程度(p<；0.0005)。未经处理的C.AL-20小鼠的角膜含有T细胞、巨噬细胞和NK细胞。NK耗竭的C.AL-20小鼠角膜浸润物由T细胞和巨噬细胞组成，但没有NK细胞。这些数据表明，NK细胞参与了单纯疱疹病毒病小鼠模型的发展。
Natural killer (NK) cells and acquired cell-mediated immunity effector cells (delayed type hypersensitivity (DTH) and cytotoxic T lymphocytes (CTL)) have been reported to play a vital role in the defence of the host against tumour and viral infections in locations other than the eye. A vigorous cellular inflammatory response to viral infections of the cornea, however, with the attendant damage to the corneal clarity, has obvious evolutionary disadvantages, and a substantial body of evidence indicates that in animals (eg mice) which are highly suceptible to inflammatory destruction of the cornea following corneal encounter with herpes simplex virus, it is the animal's immunological/inflammatory response which is responsible for the corneal damage. We examined the role of natural killer cells in the development of herpes stromal keratitis (HSK) in NK-deficient (C57BL/6J-bgj (beige)) mice and their NK-competent (C57BL/6J (black)) relatives. The beige (NK-deficient) mice were just as resistant to HSK as were the black mice. We also studied the effects of NK cell depletion of BALB/c Igh-1 disparate congenic mice. C. AL-20 (Igh-l d) mice are ordinarily highly susceptible to necrotising HSK. In vivo NK-cell depletion in these mice significantly decreased the incidence and severity of HSK in these animals (p< 0.0005). Corneas from untreated C. AL-20 mice contained T cells, macrophages and NK cells. The corneal infiltrate from NK-depleted C. AL-20 mice consisted of T cells and macrophages but no NK cells. These data indicate that NK cells are participants in the development of HSK in the murine model of this disease.