Moriuchi M, Moriuchi H
Laboratory of Immunoregulation, NIAID, National Institutes of Health, Bethesda, Maryland 20892 , USA.
J Biol Chem. 2001 Mar 23;276(12):8639-42. doi: 10.1074/jbc.M008391200. Epub 2000 Nov 8.
T cell activation can induce expression of CCR5, a major coreceptor for macrophage-tropic (R5) human immunodeficiency virus type 1 (HIV-1). Here we report that overexpression of the Oct-2 transcription factor and octamer coactivator BOB.1/OBF/OCA-B, both of which are induced in T cells following T cell receptor signaling, synergistically up-regulates CCR5 promoter activity via interaction with an octamer motif on the promoter. We also show that the octamer transcription factors can increase cell surface expression of CCR5 and fusogenicity of the cells with R5 HIV-1 Env. These results suggest that octamer transcription factors may play a critical role in the induction of CCR5 expression on, and thereby susceptibility to, R5 HIV-1 of T cells following antigenic stimulation.
T细胞活化可诱导CCR5的表达，CCR5是嗜巨噬细胞型（R5）1型人类免疫缺陷病毒（HIV-1）的主要共受体。在此我们报告，Oct-2转录因子和八聚体共激活因子BOB.1/OBF/OCA-B的过表达，这两者在T细胞受体信号传导后在T细胞中被诱导，通过与启动子上的八聚体基序相互作用协同上调CCR5启动子活性。我们还表明，八聚体转录因子可增加CCR5的细胞表面表达以及细胞与R5 HIV-1包膜蛋白的融合能力。这些结果表明，八聚体转录因子可能在抗原刺激后T细胞上CCR5表达的诱导以及因此对R5 HIV-1的易感性中起关键作用。
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