Altered Kinetics of CD4+T Cell Proliferation and Interferon-γ Production in the Absence of CD8+T Lymphocytes in Virus-Infected β2-Microglobulin-Deficient Mice
Altered Kinetics of CD4+T Cell Proliferation and Interferon-γ Production in the Absence of CD8+T Lymphocytes in Virus-Infected β2-Microglobulin-Deficient Mice
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病毒感染的 β2-微球蛋白缺陷小鼠中缺乏 CD8+T 淋巴细胞时 CD4+T 细胞增殖和干扰素-γ 产生的动力学改变
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发表时间：
1996
期刊：
影响因子：
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通讯作者：
D. Muller
中科院分区：
文献类型：
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作者：
A. Víkingsson;K. Pederson;D. Muller
CD8 + T细胞是控制正常小鼠病毒感染的细胞毒性T细胞活性的主要介质。CD8 + T细胞也参与调节其他免疫细胞的活性。我们通过比较表达正常CD8 + T细胞反应的小鼠和CD8 + T细胞缺陷β2微球蛋白“敲除”小鼠的免疫反应，研究了CD8 + T细胞对CD4 + T细胞可能的调节作用。在正常小鼠中，感染淋巴细胞性脉络丛脑膜炎病毒（LCMV）导致双相T细胞免疫反应。首先，CD8 + T细胞增殖并产生干扰素-γ (IFN-γ)，然后2至4天后，CD4 + T细胞增殖并产生IFN-γ。在β2微球蛋白缺陷小鼠LCMV感染期间未检测到CD8 + T细胞活性。然而，在β2-微球蛋白缺陷小鼠中，CD4 + T细胞扩增被夸大，并且比正常小鼠早2天发生。此外，CD4 + T细胞具有大量的细胞毒活性，这在正常小鼠的CD4 + T细胞群中没有观察到。然而，β2微球蛋白缺陷小鼠的CD4 + T细胞IFN-γ产生滞后于增殖反应，导致与正常小鼠相比，整体T细胞IFN-γ产生相对延迟。综上所述，这些数据表明，在LCMV的原发性免疫应答中，CD8 + T细胞激活的高峰时间点比CD4 + T细胞激活的高峰时间点更早，CD8 + T细胞可能抑制CD4 + T细胞的增殖和CD4 + T细胞毒性活性的发展。
Abstract CD8 + T cells are the major mediators of cytotoxic T cell activity controlling viral infections in normal mice. CD8 + T cells have also been implicated in regulating the activity of other immune cells. We have examined the possible regulatory role of CD8 + T cells on CD4 + T cells by comparing immune responses in mice expressing normal CD8 + T cell responses and in CD8 + T cell-deficient β2-microglobulin “knockout” mice. In normal mice, infection with lymphocytic choriomeningitis virus (LCMV) results in a biphasic T cell immune response. First, CD8 + T cells proliferate and produce interferon-γ (IFN-γ), and then 2 to 4 days later CD4 + T cells proliferate and produce IFN-γ. CD8 + T cell activity is not detected during LCMV infection in β2-microglobulin-deficient mice. However, in β2-microglobulin-deficient mice the CD4 + T cell expansion is exaggerated and occurs 2 days earlier than observed in normal mice. Furthermore, the CD4 + T cells have substantial cytotoxic activity, which is not observed in the CD4 + T cell population in normal mice. However, CD4 + T cell IFN-γ production in β2-microglobulin-deficient mice lags behind the proliferative response, resulting in a relative delay in overall T cell IFN-γ production compared to normal mice. Taken together, these data suggest that CD8 + T cell activation peaks at an earlier time point than CD4 + T cell activation during the primary immune response to LCMV and that CD8 + T cells may inhibit CD4 + T cell proliferation and the development of CD4 + T cell cytotoxic activity.