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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Inhibition of human T cell leukemia virus type 2 replication by the suppressive action of class II transactivator and nuclear factor Y
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Inhibition of human T cell leukemia virus type 2 replication by the suppressive action of class II transactivator and nuclear factor Y

机译：通过II类反式激活因子和核因子Y的抑制作用抑制人2型T细胞白血病病毒的复制

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摘要

The master regulator of MHC-II gene transcription, class II transactivator (CIITA), acts as a potent inhibitor of human T cell leukemia virus type 2 (HTLV-2) replication by blocking the activity of the viral Tax-2 transactivator. Here, we show that this inhibitory effect takes place at the nuclear level and maps to the N-terminal 1-321 region of CIITA, where we identified a minimal domain, from positions 64-144, that is strictly required to suppress Tax-2 function. Furthermore, we show that Tax-2 specifically cooperates with cAMP response element binding protein-binding protein (CBP) and p300, but not with p300/CBP-associated factor, to enhance transcription from the viral promoter. This finding represents a unique difference with respect to Tax-1, which uses all three coactivators to transactivate the human T cell leukemia virus type 1 LTR. Direct sequestering of CBP or p300 is not the primary mechanism by which CIITA causes suppression of Tax-2. Interestingly, we found that the transcription factor nuclear factor Y, which interacts with CIITA to increase transcription of MHC-II genes, exerts a negative regulatory action on the Tax-2-mediated HTLV-2 LTR transactivation. Thus, CIITA may inhibit Tax-2 function, at least in part, through nuclear factor Y. These findings demonstrate the dual defensive role of CIITA against pathogens: it increases the antigen-presenting function for viral determinants and suppresses HTLV-2 replication in infected cells.
机译：MHC-II基因转录的主调节剂II类反式激活因子（CIITA）通过阻断病毒Tax-2反式激活因子的活性，成为2型人T细胞白血病病毒（HTLV-2）复制的有效抑制剂。在这里，我们显示了这种抑制作用发生在核水平，并映射到CIITA的N末端1-321区，我们从64-144位确定了一个最小域，该域是抑制Tax-2的严格要求功能。此外，我们显示，Tax-2与cAMP反应元件结合蛋白结合蛋白（CBP）和p300特别协同，但与p300 / CBP相关因子不协同，以增强从病毒启动子的转录。这一发现代表了与Tax-1的独特区别，后者使用所有三种共激活因子来激活人类T细胞白血病病毒1型LTR。直接隔离CBP或p300并不是CIITA抑制Tax-2的主要机制。有趣的是，我们发现与CIITA相互作用以增加MHC-II基因转录的转录因子核因子Y对Tax-2介导的HTLV-2 LTR反式激活具有负调控作用。因此，CIITA可能至少部分地通过核因子Y抑制了Tax-2功能。这些发现证明CIITA对病原体具有双重防御作用：它增加了病毒决定簇的抗原呈递功能，并抑制了感染者中HTLV-2的复制。细胞。

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