Involvement of natural killer cells in the pathogenesis of murine cytomegalovirus interstitial pneumonitis and the immune response to infection.
Involvement of natural killer cells in the pathogenesis of murine cytomegalovirus interstitial pneumonitis and the immune response to infection.
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自然杀伤细胞参与鼠巨细胞病毒间质性肺炎的发病机制和对感染的免疫反应。
DOI：
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发表时间：
1982
影响因子：
3.8
通讯作者：
N. Kirmani
中科院分区：
文献类型：
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作者：
G. Quinnan,;J. Manischewitz;N. Kirmani
本实验观察了小鼠巨细胞病毒（MCMV）感染后自然杀伤（NK）细胞应答的意义。在初步证明感染后3至6天之间发生的NK细胞应答与研究的其他小鼠品系相比相对较高后，选择该品系进行研究。氢化可的松治疗对抑制这种反应的剂量-反应效应被发现。氢化可的松的剂量，皮下给予连续两天，这被发现显着抑制NK细胞反应，没有影响血清干扰素或抗体水平的发展，或脾细胞毒性T细胞活性的条件下研究。然而，这种治疗对NK细胞反应的抑制伴随着体内脾脏和肺部病毒复制的增强，以及小鼠对致命感染的易感性的增加。MCMV间质性肺炎的组织学特征和肺淋巴细胞研究在感染后4天，发现有增加的NK细胞活性。发现用氢化可的松治疗小鼠可抑制肺炎的大体和组织学证据的发展。这些发现表明，NK细胞参与MCMV间质性肺炎的发病机制，并可能在感染早期发挥作用，以限制病毒复制的程度。
The significance of the natural killer (NK) cell response to murine cytomegalovirus (MCMV) infection was evaluated in C3H/HeN mice. This strain was selected for study after preliminary demonstration that the NK cell response, occurring between 3 and 6 days post-infection was relatively high in comparison to other mouse strains studied. A dose-response effect of hydrocortisone treatment on suppression of this response was found. A dose of hydrocortisone, given subcutaneously on two successive days, which was found to markedly inhibit the NK cell response, had no effect on development of serum interferon or antibody levels, or spleen cytotoxic T cell activity under the conditions studied. Suppression of the NK cell response by this treatment, however, was accompanied by enhanced spleen and pulmonary virus replication in vivo and increased susceptibility of mice to lethal infection. MCMV interstitial pneumonitis was characterized histologically and lung lymphocytes studied at 4 days post-infection were found to have increased NK cell activity. Treatment of mice with hydrocortisone was found to inhibit development of gross and histological evidence of pneumonitis. These findings indicate that NK cells are involved in the pathogenesis of MCMV interstitial pneumonitis and may function early in infection to restrict the extent of virus replication.