Natural killer cell activity in lymphocytic choriomeningitis virus-infected beta 2-microglobulin-deficient mice.
Natural killer cell activity in lymphocytic choriomeningitis virus-infected beta 2-microglobulin-deficient mice.
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淋巴细胞性脉络膜脑膜炎病毒感染的β2-微球蛋白缺陷小鼠中的自然杀伤细胞活性。
DOI：
10.1093/intimm/7.10.1545
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发表时间：
1995
影响因子：
4.4
通讯作者：
Quinn,DG
中科院分区：
文献类型：
--
作者：
Zajac,AJ;Muller,D;Pederson,K;Frelinger,JA;Quinn,DG
我们研究了淋巴细胞性脉络丛脑膜炎病毒（LCMV）感染的β2-微球蛋白缺陷（β 2 m −）小鼠中自然杀伤（NK）活性的诱导和作用。我们证明，LCMV感染在刺激β 2 m −的NK活性方面比聚肌苷酸：聚胞苷酸（poly I：C）更有效。此外，β 2 m −NK细胞对IL-12体外处理的反应较差。病毒诱导的NK细胞的靶特异性与先前报道的化学诱导的β 2 m-NK细胞的靶特异性相似。在这两种情况下，它们都可以溶解YAC-1肿瘤细胞，但不能杀死β 2 m −或β 2 m +T细胞母细胞。我们还发现，与正常小鼠相比，LCMV在β 2 m −小鼠中诱导NK和细胞毒性T淋巴细胞（CTL）活性的时间进程延迟。在β 2 m −中，NK和CTL活性分别在感染后第8天和第10天达到最大，而在B6小鼠中，NK和CTL活性分别在感染后第4天和第6-8天达到最大。正常小鼠在颅内感染LCMV后约7天死亡，而β2− m小鼠的病程延长，并以体重显著减轻为特征。我们表明，虽然在这些小鼠中的CD 4 +CTL反应密切参与介导的体重减轻，病毒诱导的NK细胞似乎没有发挥作用的疾病。
We have investigated the induction and role of natural killer (NK) activity in lymphocytic choriomeningitis virus (LCMV)-infected β2-microglobulin-deficient (β2m−) mice. We demonstrate that LCMV infection is more effective than polyinosinic:poiycytidylic acid (poly I:C) at stimulating NK activity in β2m−.In addition, β2m−NK cells respond poorly toin vitrotreatment with IL-12. The target specificity of the virally induced NK cells is similar to that previously reported for chemically induced β2m−NK cells. In both cases they can lyse YAC-1 tumor cells but are unable to kill β2m−orβ2m+T cell blasts. We have also found that the time course of induction of NK and cytotoxic T lymphocyte (CTL) activity by LCMV in β2m−mice is delayed compared with normal mice. Maximal NK and CTL activity is attained at day 8 and 10 post-infection respectively in β2m−compared with day 4 and 6—8 in B6 mice. Whereas normal mice die ˜7 days following intracranial infection with LCMV, the course of disease in β2−mmice is protracted and characterized by a marked loss of body weight. We show that although the CD4+CTL response in these mice is intimately involved in mediating weight loss, the virus-induced NK cells do not appear to play a role in the disease.