人T细胞白血病病毒I型的反式作用转录激活因子Tax诱导T细胞上OX40（gp34的一种受体）的表达。
Induction of OX40, a receptor of gp34, on T cells by trans-acting transcriptional activator, Tax, of human T-cell leukemia virus type I.
作者信息
Higashimura N, Takasawa N, Tanaka Y, Nakamura M, Sugamura K
机构信息
Department of Microbiology, Tohoku University School of Medicine, Sendai.
出版信息
Jpn J Cancer Res. 1996 Mar;87(3):227-31. doi: 10.1111/j.1349-7006.1996.tb00210.x.
Abstract
gp34, which we had identified as a target molecule of the trans-activation by Tax of human T-cell leukemia virus type I (HTLV-I), has been found to bind OX40, a member of the tumor necrosis factor receptor family, resulting in growth stimulation of activated T cells. We here demonstrate that not only gp34 (OX40L), but also OX40 can be transcriptionally activated by Tax. Three Tax-producing human T-cell lines carrying the HTLV-I genome expressed OX40 on their surfaces. Furthermore, Tax-induced transcriptional activation of OX40 was shown in Tax-inducible JPX-9 cells. These results demonstrate that both OX40 and its ligand (gp34) are constitutively expressed on the surfaces of Tax-expressing T lymphocytes, suggesting that the OX40L/OX40 system contributes to growth stimulation of the virus-infected T cells.
摘要
gp34是我们已确定的人类I型T细胞白血病病毒（HTLV-I）Tax蛋白反式激活作用的一个靶分子，现已发现它能与肿瘤坏死因子受体家族成员OX40结合，从而刺激活化T细胞的生长。我们在此证明，不仅gp34（OX40L），而且OX40也能被Tax转录激活。三个携带HTLV-I基因组的产生Tax蛋白的人T细胞系在其表面表达OX40。此外，在Tax诱导型JPX-9细胞中也显示出Tax诱导的OX40转录激活。这些结果表明，OX40及其配体（gp34）在表达Tax蛋白的T淋巴细胞表面组成性表达，提示OX40L/OX40系统有助于病毒感染的T细胞的生长刺激。
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