Imada K, Takaori-Kondo A, Akagi T, Shimotohno K, Sugamura K, Hattori T, Yamabe H, Okuma M, Uchiyama T
First Department of Internal Medicine, Kyoto University, Japan.
Blood. 1995 Sep 15;86(6):2350-7.
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.
成人T细胞白血病(ATL)的白血病发生及肿瘤细胞生长所涉及的机制仍不清楚。我们在使用严重联合免疫缺陷(SCID)小鼠的体内细胞增殖模型中检测了I型人类T细胞白血病病毒(HTLV-I)感染的细胞系的致瘤性。将11个HTLV-I感染的细胞系注射到SCID小鼠体内,我们发现其中4个能够在SCID小鼠体内增殖。4个可移植细胞系中的3个源自白血病细胞克隆,6个非白血病细胞来源的HTLV-I感染细胞系均不能在SCID小鼠体内植入。有趣的是,研究表明一些HTLV-I感染且依赖白细胞介素-2(IL-2)的细胞系能够成功植入SCID小鼠体内。在这些体内或体外生长的细胞系中均未检测到IL-2 mRNA的表达。在体内增殖的4个可移植细胞系中有3个未检测到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小鼠中没有致瘤潜力。这些数据表明:(1)非白血病细胞来源的HTLV-I感染细胞系没有足够的致白血病变化以在SCID小鼠中获得致瘤潜力;(2)IL-2自分泌机制不直接参与肿瘤细胞生长;(3)肿瘤细胞生长的维持不需要病毒基因表达;(4)tax基因的表达不足以支持体内肿瘤细胞生长。