Lymphocytic choriomeningitis virus-induced immune dysfunction: induction of and recovery from T-cell anergy in acutely infected mice.
Lymphocytic choriomeningitis virus-induced immune dysfunction: induction of and recovery from T-cell anergy in acutely infected mice.
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淋巴细胞脉络膜脑膜炎病毒引起的免疫功能障碍:急性感染小鼠 T 细胞无反应性的诱导和恢复。
DOI:
10.1128/jvi.68.12.8477-8480.1994
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发表时间:
1994
影响因子:
5.4
通讯作者:
Southern,PJ
中科院分区:
文献类型:
--
作者:
Butz,EA;Southern,PJ
Acute infection of immunocompetent mice by lymphocytic choriomeningitis virus induces a potent cytotoxic T-lymphocyte response that eliminates infectious virus. Concurrently and paradoxically, there is a general suppression of lymphocyte responses to mitogens and to other infectious agents. Splenocytes from infected mice released significant amounts of gamma interferon in response to mitogenic stimulation in vitro, but neither interleukin 2 nor interleukin 4 was similarly elevated relative to the amounts released by control cells. Early T-cell receptor-proximal signaling events were found to be intact, confirming that the cells were viable and had received the mitogenic stimuli in an appropriate manner. Acutely infected adult thymectomized mice regained concanavalin A responsiveness in parallel with euthymic mice, if T cells were left unmanipulated for several weeks after clearance of virus from the mice. Therefore, although acute lymphocytic choriomeningitis virus infection has the effect of disrupting proliferation when the T-cell receptor is ligated, this state is only temporary. In contrast, T cells from persistently infected adult mice reveal long-lasting alterations in concanavalin A responsiveness.