Expression of alpha/beta interferons (IFN-alpha/beta) and their relationship to IFN-alpha/beta-induced genes in lymphocytic choriomeningitis.
Expression of alpha/beta interferons (IFN-alpha/beta) and their relationship to IFN-alpha/beta-induced genes in lymphocytic choriomeningitis.
复制标题
淋巴细胞性脉络膜脑膜炎中α/β干扰素（IFN-α/β）的表达及其与IFN-α/β诱导基因的关系。
DOI：
10.1128/jvi.68.11.7358-7366.1994
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发表时间：
1994
影响因子：
5.4
通讯作者：
Campbell,IL
中科院分区：
文献类型：
--
作者：
Sandberg,K;Eloranta,ML;Campbell,IL
在淋巴细胞性脉络丛脑膜炎（LCM）的发展过程中监测α干扰素（IFN-α）、IFN-β和IFN-α/β诱导基因的表达，以评估这些抗病毒细胞因子是否在中枢神经系统（CNS）中存在有限的影响。在LCM病毒感染小鼠的血液中，在感染后3天存在高水平的IFN-α（83 +/- 42 U/ml），而在任何时间点均未检测到IFN-β（< 1.0 U/ml）。在感染后第1天和第3天，脾脏中含有高水平的IFN-α和IFN-β mRNA，而在大脑中没有IFN-α mRNA，仅检测到低水平的IFN-β mRNA。原位杂交显示，在脾脏边缘区以及颈淋巴结的被膜下窦和外皮质中存在表达IFN-alpha mRNA的细胞。脑内2 '，5'-寡腺苷酸合成酶（2 '，5'-OAS）mRNA的表达紧随IFN-β mRNA的表达，而外周中的2 '，5'-OAS mRNA与系统性IFN-α相关。IFN-α表达细胞在脾脏和淋巴结中靠近T细胞和B细胞区室的定位与这些细胞因子在免疫调节中的作用一致。此外，IFN-α的缺乏和IFN-β在脑中的相对低水平和延迟表达表明CNS是病毒复制特别脆弱的器官。对于某些LCM病毒株，早期抗病毒IFN-α/β活性的缺乏和脑中病毒的优先生长可能导致CNS的靶向T细胞炎症，导致动物死亡。
Expression of alpha interferon (IFN-alpha)-, IFN-beta-, and IFN-alpha/beta-induced genes was monitored during the development of lymphocytic choriomeningitis (LCM) to assess whether a restricted influence of these antiviral cytokines could be found in the central nervous system (CNS). High levels of IFN-alpha (83 +/- 42 U/ml) were present in the blood of LCM virus-infected mice 3 days postinfection, whereas IFN-beta was not detected (< 1.0 U/ml) at any time point. Spleens contained high levels of IFN-alpha and IFN-beta mRNAs at days 1 and 3 postinfection, whereas no IFN-alpha mRNA and only low levels of IFN-beta mRNA were detected in brains. In situ hybridization showed IFN-alpha mRNA-expressing cells in the marginal zones of the spleen and in the subcapsular sinus and outer cortex of cervical lymph nodes. The expression of 2',5'-oligoadenylate synthetase (2',5'-OAS) mRNA followed the expression of IFN-beta mRNA in the brain, whereas 2',5'-OAS mRNA in the periphery was associated with systemic IFN-alpha. The localization of IFN-alpha-expressing cells in the spleen and lymph nodes in proximity to T- and B-cell compartments is consistent with a role for these cytokines in immune regulation. Furthermore, the absence of IFN-alpha and the relatively low level and delayed expression of IFN-beta in the brain suggest that the CNS is an especially vulnerable organ for virus replication. With certain strains of LCM virus, the absence of early antiviral IFN-alpha/beta activity and preferential virus growth in the brain might lead to targeted T-cell inflammation of the CNS, resulting in death of the animal.