Lymphocytic choriomeningitis virus-induced immunodepression: inherent defect of B and T lymphocytes
Lymphocytic choriomeningitis virus-induced immunodepression: inherent defect of B and T lymphocytes
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淋巴细胞性脉络膜脑膜炎病毒引起的免疫抑制：B和T淋巴细胞的固有缺陷
DOI：
10.1128/jvi.64.9.4076-4083.1990
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发表时间：
1990
影响因子：
5.4
通讯作者：
Paolo Truffa
中科院分区：
文献类型：
--
作者：
M. Saron;B. Shidani;M. Nahori;JEAN;Paolo Truffa
淋巴细胞性脉络丛脑膜炎病毒（LCMV）感染小鼠后，可迅速诱导免疫抑制，表现为对脂多糖（LPS）和刀豆球蛋白A（ConA）的低淋巴细胞增殖反应。感染后7天，在细胞和分子水平上分析了对这些有丝分裂原无反应的机制。CD 8 + T细胞的选择性消除和共培养实验的结果表明，无反应性是由于抑制细胞。类似地，抑制因子如野牡丹素的作用被排除，因为抑制其产生的吲哚美辛并不逆转无反应性。ConA激活的巨噬细胞或T细胞分泌的不同细胞因子的分析表明，白细胞介素-1（IL-1），在T依赖性激活巨噬细胞的ConA，通常产生的细胞从LCMV感染的小鼠。相反，由活化的CD 4 + T细胞产生的IL-2是检测不到的。加入外源性IL-2并没有恢复增殖反应，虽然IL-2受体的p55-千道尔顿蛋白被ConA诱导的CD 4+细胞从LCMV感染的小鼠。我们的结果可以解释为：（i）LCMV感染小鼠的细胞对有丝分裂原无反应不是由于巨噬细胞产生IL-1的功能改变;（ii）CD 4+细胞被激活，因为IL-2受体的p55链被诱导;（iii）IL-2产生的缺乏不能解释T细胞无应答性，因为外源性IL-2的加入不能恢复增殖应答。两者合计，这些数据表明，T淋巴细胞无反应性应与T细胞活化和IL-2受体表达后的固有增殖缺陷有关。
Infection of mice with lymphocytic choriomeningitis virus (LCMV) produces a rapidly induced immuno-suppression manifested by low lymphocyte proliferation in response to lipopolysaccharide (LPS) and concanavalin A (ConA). Analysis of the mechanisms underlying the unresponsiveness to these mitogens was undertaken at the cellular and molecular levels 7 days after infection. The selective elimination of CD8+ T cells and the results of coculture experiments demonstrated that unresponsiveness was not due to suppressor cells. Similarly, the role of inhibitory factors such as prostaglandins was excluded, since indomethacin, which inhibits their production, did not reverse the unresponsiveness. Analysis of different cytokines secreted by ConA-activated macrophages or T cells revealed that interleukin-1 (IL-1), synthesized during the T-dependent activation of macrophages by ConA, was normally produced by cells from LCMV-infected mice. In contrast, IL-2, which is produced by activated CD4+ T cells, was undetectable. Addition of exogenous IL-2 did not restore the proliferative response, although the p55-kilodalton protein of the IL-2 receptor was induced by ConA on CD4+ cells from LCMV-infected mice. Our results can be interpreted as showing that (i) unresponsiveness to mitogens of cells from LCMV-infected mice is not due to altered functions of the macrophages with respect to IL-1 production; (ii) CD4+ cells are activated, since the p55 chain of the IL-2 receptor is induced; (iii) the lack of IL-2 production cannot explain T-cell unresponsiveness, since addition of exogenous IL-2 did not restore the proliferative response. Taken together, these data suggest that T-lymphocyte unresponsiveness should be related to an inherent proliferative defect subsequent to T-cell activation and IL-2 receptor expression.
影响因子：
56.9
作者：
SMITH, KA
通讯作者：
SMITH, KA
体内病毒感染期间 L3T4 和 Lyt-2 淋巴细胞中 IL-2 转录的激活。
DOI：
--
发表时间：
1989
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
Kasaian,MT;Biron,CA
通讯作者：
Biron,CA
病毒诱导的免疫抑制：机会性感染易感性的小鼠模型。
DOI：
10.1093/infdis/158.1.232
发表时间：
1988
期刊：
The Journal of infectious diseases
影响因子：
--
作者：
Wu-Hsieh,B;Howard,DH;Ahmed,R
通讯作者：
Ahmed,R