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淋巴细胞性脉络丛脑膜炎病毒感染小鼠的伴刀豆球蛋白A激活脾细胞导致细胞因子基因表达改变。

Altered cytokine genes expression by conA-activated spleen cells from mice infected by lymphocytic choriomeningitis virus.

作者信息

Colle J H, Saron M F, Truffa-Bachi P

机构信息

Unité d'Immunophysiologie Moléculaire, Institut Pasteur, Paris, France.

出版信息

Immunol Lett. 1993 Mar;35(3):247-53. doi: 10.1016/0165-2478(93)90190-d.

Abstract

The intravenous injection of mice with lymphocytic choriomeningitis virus (LCMV) induces a rapid and long-lasting immunodeficiency. T lymphocytes from 7-day-infected mice do not proliferate in vitro in response to ConA stimulation, do not produce IL-2 but display high affinity IL-2 receptors on their membrane. The non-coordinated regulation of these genes suggested that other cytokine-encoding genes may also be affected in their regulation. We have thus analyzed the expression of the genes encoding different cytokines transcribed during spleen cell activation by ConA. The genes encoding T lymphocyte-derived cytokines can be classified in three groups: the genes expressed similarly by normal and LCMV-cells (the p55 and the p75 chains of the IL-2 receptor [1]), the genes under expressed in LCMV-cells (IL-2, IL-3, IL-4 and IL-5) and the genes over expressed by these cells (GM-CSF and IFN-gamma). These results show that the viral infection has provoked a profound alteration of the overall regulation of the genetic program that follows T lymphocyte activation. Since T cell activation depends strictly on accessory cell-derived cytokines, we measured the level of transcription of IL-1, IL-6 and TNF-alpha; and our data show that the expression of these genes is equivalent in normal cells and in cells from LCMV-infected mice.

摘要

给小鼠静脉注射淋巴细胞性脉络丛脑膜炎病毒(LCMV)会引发快速且持久的免疫缺陷。来自感染7天的小鼠的T淋巴细胞在体外对刀豆蛋白A(ConA)刺激无增殖反应,不产生白细胞介素-2(IL-2),但其细胞膜上显示有高亲和力的IL-2受体。这些基因的不协调调节表明其他细胞因子编码基因的调节也可能受到影响。因此,我们分析了在ConA刺激脾细胞活化过程中转录的不同细胞因子编码基因的表达情况。编码T淋巴细胞衍生细胞因子的基因可分为三组:正常细胞和LCMV感染细胞中表达相似的基因(IL-2受体的p55和p75链[1])、LCMV感染细胞中表达不足的基因(IL-2、IL-3、IL-4和IL-5)以及这些细胞中过度表达的基因(粒细胞-巨噬细胞集落刺激因子(GM-CSF)和干扰素-γ(IFN-γ))。这些结果表明,病毒感染引发了T淋巴细胞活化后遗传程序整体调节的深刻改变。由于T细胞活化严格依赖于辅助细胞衍生的细胞因子,我们测量了IL-1、IL-6和肿瘤坏死因子-α(TNF-α)的转录水平;我们的数据表明,这些基因在正常细胞和LCMV感染小鼠的细胞中的表达相当。

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