TUMORIGENICITY OF HUMAN T-CELL LEUKEMIA-VIRUS TYPE I-INFECTED CELL-LINES IN SEVERE COMBINED IMMUNODEFICIENT MICE AND CHARACTERIZATION OF THE CELLS PROLIFERATING IN-VIVO
TUMORIGENICITY OF HUMAN T-CELL LEUKEMIA-VIRUS TYPE I-INFECTED CELL-LINES IN SEVERE COMBINED IMMUNODEFICIENT MICE AND CHARACTERIZATION OF THE CELLS PROLIFERATING IN-VIVO
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DOI：
10.1182/blood.v86.6.2350.bloodjournal8662350
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发表时间：
1995-09-15
期刊：
影响因子：
20.3
通讯作者：
UCHIYAMA, T
中科院分区：
文献类型：
--
作者：
IMADA, K;TAKAORIKONDO, A;UCHIYAMA, T
成人T细胞白血病（ATL）的发病机制和肿瘤细胞生长的机制尚不清楚。我们用严重联合免疫缺陷（SCID）小鼠体内细胞增殖模型研究了人T细胞白血病病毒I型（HTLV-I）感染细胞系的致瘤性。将11株HTLV-I感染的细胞系注射到SCID小鼠中，我们发现其中4株能够在SCID小鼠中增殖。4个可移植细胞系中有3个来自白血病细胞克隆，6个非白血病细胞来源的HTLV-1感染细胞系中有6个不能在SCID小鼠中移植。有趣的是，一些HTLV-I感染的和白细胞介素-2（IL-2）依赖的细胞系可以成功地移植到SCID小鼠中。这些细胞株在体内和体外生长时均未检测到IL-2 mRNA的表达。在体内增殖的4种可移植细胞系中，有3种未检测到HTLV-I病毒产物。通过导入HTLV I的tax基因而永生化的外周血T细胞在SCID小鼠中没有致瘤性。这些结果提示：（1）HTLV-Ⅰ感染的非白血病细胞系并不具有足够的致白血病性改变以获得在SCID小鼠中的致瘤性潜能;（2）IL-2自分泌机制并不直接参与肿瘤细胞的生长;（3）肿瘤细胞的生长不需要病毒基因的表达;（4）tax基因的表达不足以促进肿瘤细胞的体内生长。(C)1995年，美国血液学会。
The mechanism involved in leukemogenesis and neoplastic cell growth of adult T-cell leukemia (ATL) still remains unclear, We examined the tumorigenicity of human T-cell leukemia virus type I (HTLV-I)-infected cell lines in an in vivo cell proliferation model using severe combined immunodeficient (SCID) mice. Eleven HTLV-I-infected cell lines were injected into SCID mice and we found that 4 of them were capable of proliferating in SCID mice. Three of four transplantable cell lines are derived from the leukemic cell clone and 6 of 6 HTLV-I-infected cell lines of nonleukemic cell origin could not engraft in SCID mice. Interestingly, it was shown that some HTLV-I-infected and interleukin-2 (IL-2)-dependent cell lines could successfully engraft in SCID mice. The expression of IL-2 mRNA was not detected in these cell lines growing either in vivo or in vitro. HTLV-I viral products were not detected in 3 of 4 transplantable cell lines proliferating in vivo. Peripheral blood T cells immortalized by introduction of tax gene of HTLV I were found to have no tumorigenic potential in SCID mice. These data suggest that (1) HTLV-I-infected cell lines of nonleukemic cell origin do not have enough leukemogenic changes to acquire the tumorigenic potential in SCID mice; (2) the IL-2 autocrine mechanism is not directly involved in the tumor cell growth; (3) viral gene expression is not needed for the maintenance of neoplastic cell growth; and (4) the expression of tax gene is not sufficient for the neoplastic cell growth in vivo. (C) 1995 by The American Society of Hematology.