Hasegawa Hideki, Sawa Hirofumi, Lewis Martha J, Orba Yasuko, Sheehy Noreen, Yamamoto Yoshie, Ichinohe Takeshi, Tsunetsugu-Yokota Yasuko, Katano Harutaka, Takahashi Hidehiro, Matsuda Junichiro, Sata Tetsutaro, Kurata Takeshi, Nagashima Kazuo, Hall William W
Department of Pathology, National Institute of Infectious Diseases, 4-7-1 Gakuen, Musashimurayama-shi, Tokyo 208-0011, Japan.
Nat Med. 2006 Apr;12(4):466-72. doi: 10.1038/nm1389. Epub 2006 Mar 19.
Adult T-cell leukemia-lymphoma (ATLL) is a group of T-cell malignancies caused by infection with human T-lymphotropic virus type I (HTLV-I). Although the pathogenesis of ATLL remains incompletely understood, the viral regulatory protein Tax is centrally involved in cellular transformation. Here we describe the generation of HTLV-I Tax transgenic mice using the Lck proximal promoter to restrict transgene expression to developing thymocytes. After prolonged latency periods, transgenic mice developed diffuse large-cell lymphomas and leukemia with clinical, pathological and immunological features characteristic of acute ATLL. Transgenic mice were functionally immunocompromised and they developed opportunistic infections. Fulminant disease also developed rapidly in SCID mice after engraftment of lymphomatous cells from transgenic mice. Flow cytometry showed that the cells were CD4(-) and CD8(-), but CD44(+), CD25(+) and cytoplasmic CD3(+). This phenotype is indicative of a thymus-derived pre-T-cell phenotype, and disease development was associated with the constitutive activation of NF-kappaB. Our model accurately reproduces human disease and will provide a tool for analysis of the molecular events in transformation and for the development of new therapeutics.
成人T细胞白血病-淋巴瘤(ATLL)是一组由I型人类嗜T淋巴细胞病毒(HTLV-I)感染引起的T细胞恶性肿瘤。尽管ATLL的发病机制仍未完全明确,但病毒调节蛋白Tax在细胞转化过程中起着核心作用。在此,我们描述了利用Lck近端启动子将转基因表达限制在发育中的胸腺细胞中来生成HTLV-I Tax转基因小鼠的过程。经过较长的潜伏期后,转基因小鼠发展出具有急性ATLL临床、病理和免疫学特征的弥漫性大细胞淋巴瘤和白血病。转基因小鼠在功能上存在免疫缺陷,并出现机会性感染。将转基因小鼠的淋巴瘤细胞移植到SCID小鼠体内后,暴发性疾病也迅速发展。流式细胞术显示,这些细胞为CD4(-)和CD8(-),但CD44(+)、CD25(+)且细胞质CD3(+)。这种表型表明是胸腺来源的前T细胞表型,并且疾病的发展与NF-κB的组成性激活有关。我们的模型准确地再现了人类疾病,将为分析转化过程中的分子事件以及开发新的治疗方法提供一个工具。