INDUCTION OF INTERLEUKIN-2 RECEPTOR GENE-EXPRESSION BY P40X ENCODED BY HUMAN T-CELL LEUKEMIA-VIRUS TYPE-1
INDUCTION OF INTERLEUKIN-2 RECEPTOR GENE-EXPRESSION BY P40X ENCODED BY HUMAN T-CELL LEUKEMIA-VIRUS TYPE-1
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DOI：
10.1002/j.1460-2075.1986.tb04583.x
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发表时间：
1986-11-01
期刊：
影响因子：
11.4
通讯作者：
YOSHIDA, M
中科院分区：
文献类型：
--
作者：
INOUE, J;SEIKI, M;YOSHIDA, M
人T细胞白血病病毒1型(HTLV-1)是成人T细胞白血病(ATL)的病原体。HTLV-1的Px序列编码的病毒产物p40x是长端重复序列的反式转录激活因子，被怀疑参与了白血病的发生，激活了细胞基因。表达于ATL白血病细胞的IL-2及其受体(IL-2)在两种T细胞系Jurkat和HSB-2中被瞬时诱导，而在其他人T和B细胞系中则不能。Px表达诱导IL-2R的细胞类型特异性与植物血凝素/佛波酯激活的细胞类型特异性相同，提示需要某些特定的细胞因子或一定的细胞分化状态。IL-2和IL-2R在基因水平上也能被诱导。PMTPX突变体对p40x、p27x-III和p21x-III的开放阅读框失活的转基因结果表明，p40x本身就足以诱导诱导细胞产生IL-2R。HTLV-1 p40x对IL-2R的这种诱导可能有助于HTLV-1感染细胞在ATL发育的早期优先增殖，最终增加可能的恶性转化靶细胞的数量。
Human T-cell leukemia virus type 1 (HTLV-1) is an etiologic agent of adult T-cell leukemia (ATL). A viral product, p40x, encoded by the pX sequence of HTLV-1 is a trans-acting transcriptional activator of the long terminal repeat (LTR) and has been suspected of involvement in leukemogenesis, activating the cellular genes. The cellular interleukin-2 (IL-2) and its receptor (IL-2), the latter of which is expressed on ATL leukemic cells, were shown to be transiently induced by transfection of plasmid pMTPX expressing pX in two T-cell lines, Jurkat and HSB-2, but not in other human T- or B-cell lines. The cell type specificity of IL-2R induction by pX expression was the same as that by phytohaemagglutinin/phorbol ester activation, indicating the requirement for some specific cellular factors or a certain state of cellular differentiation. Induction of IL-2 and IL-2R at mRNA level was also demonstrated in transfected cells. Transfections with mutants of pMTPX in which the open reading frames for p40x, p27x-III and p21x-III were inactivated indicated that p40x alone was sufficient for induction of the IL-2R in inducible cells. This induction of the IL-2R by p40x of HTLV-1 may contribute to preferential proliferation of HTLV-1 infected cells at an early stage of ATL development and eventually increase the number of putative target cells for malignant transformation.