Regulation of expression of the reovirus receptor on differentiated HL60 cells.
Regulation of expression of the reovirus receptor on differentiated HL60 cells.
复制标题
分化的 HL60 细胞上呼肠孤病毒受体表达的调节。
DOI：
10.1099/0022-1317-73-8-1961
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发表时间：
1992
期刊：
影响因子：
--
通讯作者：
Maratos-Flier,E
中科院分区：
文献类型：
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作者：
el-Ghorr,AA;Gordon,DA;George,K;Maratos-Flier,E
哺乳动物细胞上的呼肠孤病毒受体尚未完全表征，并且对该受体的性质存在争议。我们在这里报告，这种受体的表达依赖于人早幼粒细胞白血病细胞系（HL 60）的分化状态。在160 nm至1 nm的浓度范围内，佛波醇处理HL 60细胞24 h，导致这些细胞向单核细胞分化，并在荧光测定中丧失约80%的结合呼肠孤病毒的能力。这些细胞也失去了对T1和T3呼肠孤病毒感染的易感性。以1.25%（v/v）的浓度DMSO处理24小时导致向粒细胞分化。这伴随着呼肠孤病毒与这些细胞的结合增加约15%。经T1或T3呼肠孤病毒感染后，粒细胞产生的子代病毒滴度高于未经处理的HL 60细胞。当使用放射性标记的呼肠孤病毒测定病毒与HL 60细胞的结合时，注意到类似的差异。当小鼠L成纤维细胞用DMSO或佛波醇处理时，未检测到这些作用。ATCC衍生的鼠R1.1细胞不结合呼肠孤病毒。竞争数据表明，HL 60细胞上可能存在两种呼肠孤病毒受体，T1只能与一种受体结合，而T3可以与两种受体结合。我们的数据还表明，β-肾上腺素能受体不太可能作为呼肠孤病毒受体在HL 60细胞上发挥作用。
The reovirus receptor on mammalian cells has not been fully characterized and controversy exists over the nature of this receptor. We report here that the expression of this receptor is dependent on the differentiation status of a human promyelocytic leukaemia cell line (HL60). Phorbol treatment of HL60 cells for 24 h, at a concentration range of 160 nmdown to 1 nm, led to differentiation of these cells towards monocytes and a loss of approximately 80% of their ability to bind reovirus in a fluorescence assay. These cells also lost their susceptibility to T1 and T3 reovirus infection. DMSO treatment for 24 h at a concentration of 1.25% (v/v) led to differentiation towards granulocytes. This was accompanied by an increase of approximately 15% in binding of reovirus to these cells. After being infected by T1 or T3 reovirus, the granulocytes produced higher titres of progeny virus than did untreated HL60 cells. Similar differences were noted when virus binding to HL60 cells was assayed using radiolabelled reovirus. These effects were not detected when murine L fibroblasts were treated with DMSO or phorbol. ATCC-derived murine R1.1 cells did not bind reovirus. Competition data indicated that there may be two reovirus receptors on HL60 cells, and that T1 can bind to only one receptor whereas T3 can bind to both receptors. Our data also suggested that theβ-adrenergic receptor was unlikely to act as the reovirus receptor on HL60 cells.