在缺乏穿孔素、Fas和γ干扰素的情况下，CD8 + T细胞对小鼠轮状病毒具有免疫作用的证据。
Evidence for CD8+ T-cell immunity to murine rotavirus in the absence of perforin, fas, and gamma interferon.
作者信息
Franco M A, Tin C, Rott L S, VanCott J L, McGhee J R, Greenberg H B
机构信息
Department of Medicine, Stanford University School of Medicine, California 94305, USA.
出版信息
J Virol. 1997 Jan;71(1):479-86. doi: 10.1128/JVI.71.1.479-486.1997.
We recently showed that class I-restricted CD8+ T cells mediate clearance of primary rotavirus infection in mice: JHD knockout (JHD -/-) (B-cell-deficient) mice depleted of CD8+ T cells become chronically infected with murine rotavirus, and beta2 microglobulin knockout (beta2m -/-) mice have delayed but complete clearance of primary rotavirus infection. In the present work we have analyzed the mechanism used by CD8+ T cells to clear rotavirus infection. We first determined that perforin knockout (perforin -/-) mice and lpr (fas-deficient) mice clear rotavirus infection with the same kinetics as control mice. When perforin -/- or perforin +/+ mice were depleted of CD8+ T cells by administration of an anti-CD8 monoclonal antibody, they showed a delay of 1 to 2 days in the clearance of rotavirus infection compared to the clearance time for untreated control mice, indicating that CD8+ T cells in both groups of mice participate in the resolution of primary rotavirus infection. In addition, passively transferred CD8+ T cells from rotavirus-infected perforin +/+ and perforin -/- mice were able to mediate viral clearance in Rag 2 knockout (Rag 2 -/-) mice chronically infected with rotavirus with similar kinetics, suggesting that CD8+ T cells from perforin -/- mice are as efficient as CD8+ T cells from perforin +/+ mice in clearing a rotavirus infection. Gamma interferon (IFN-gamma) was also shown to be unnecessary for the antirotavirus effect of CD8+ T cells: IFN-gamma knockout (IFN-gamma -/-) mice and JHD -/-, perforin -/-, and perforin +/+ mice depleted of IFN-gamma by administration of an anti-IFN-gamma monoclonal antibody cleared rotavirus infection with the same kinetics as those for control mice. Hence, CD8+ T cells have an antirotaviral effect that is not mediated by perforin and appears to be independent of fas and the release of IFN-gamma.
我们最近发现，I类分子限制性CD8⁺ T细胞介导小鼠原发性轮状病毒感染的清除：缺失CD8⁺ T细胞的JHD基因敲除（JHD⁻/⁻）（B细胞缺陷）小鼠会被鼠轮状病毒慢性感染，而β2微球蛋白基因敲除（β2m⁻/⁻）小鼠对原发性轮状病毒感染的清除有所延迟，但最终可以完全清除。在本研究中，我们分析了CD8⁺ T细胞清除轮状病毒感染所采用的机制。我们首先确定，穿孔素基因敲除（perforin⁻/⁻）小鼠和lpr（Fas缺陷）小鼠清除轮状病毒感染的动力学与对照小鼠相同。当通过给予抗CD8单克隆抗体使perforin⁻/⁻或perforin⁺/⁺小鼠的CD8⁺ T细胞耗竭时，与未处理的对照小鼠相比，它们清除轮状病毒感染的时间延迟了1至2天，这表明两组小鼠中的CD8⁺ T细胞都参与了原发性轮状病毒感染的消退过程。此外，从感染轮状病毒的perforin⁺/⁺和perforin⁻/⁻小鼠被动转移的CD8⁺ T细胞，能够以相似的动力学介导慢性感染轮状病毒的Rag 2基因敲除（Rag 2⁻/⁻）小鼠体内的病毒清除，这表明perforin⁻/⁻小鼠的CD8⁺ T细胞在清除轮状病毒感染方面与perforin⁺/⁺小鼠的CD8⁺ T细胞一样有效。γ干扰素（IFN-γ）对于CD8⁺ T细胞的抗轮状病毒作用也并非必需：IFN-γ基因敲除（IFN-γ⁻/⁻）小鼠以及通过给予抗IFN-γ单克隆抗体使IFN-γ耗竭的JHD⁻/⁻、perforin⁻/⁻和perforin⁺/⁺小鼠，清除轮状病毒感染的动力学与对照小鼠相同。因此，CD8⁺ T细胞具有一种抗轮状病毒的作用，该作用不是由穿孔素介导的，并且似乎独立于Fas和IFN-γ的释放。
Zotero 插件