Human T-cell leukemia virus type I induces adult T-cell leukemia: from clinical aspects to molecular mechanisms.
Human T-cell leukemia virus type I induces adult T-cell leukemia: from clinical aspects to molecular mechanisms.
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DOI：
10.1177/107327480701400206
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发表时间：
2007-04
期刊：
影响因子：
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通讯作者：
Jun-ichirou Yasunaga;M. Matsuoka
中科院分区：
文献类型：
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作者：
Jun-ichirou Yasunaga;M. Matsuoka
人类T细胞白血病病毒I型（HTLV-I）是成人T细胞白血病（ATL）、HTLV-I相关的脊髓病/热带痉挛性下肢轻瘫和HTLV-I相关的葡萄膜炎的致病病毒。ATL是一种CD 4阳性T淋巴细胞的肿瘤性疾病，其特征在于具有多节段核的多形性肿瘤细胞，称为“花细胞”。“白血病发生的机制尚未完全阐明。方法对HTLV-I和ATL的病毒学、临床和免疫学特征进行综述，并对ATL的致瘤机制和治疗进展进行总结。结果病毒基因、遗传学和表观遗传学改变以及宿主免疫系统等多种因素可能参与ATL的白血病发生。其中，病毒基因、Tax和HBZ被认为起着重要作用。侵袭型ATL的预后仍然很差，无论加强化疗。异基因干细胞移植治疗ATL的有效性最近已有报道。结论虽然ATL致白血病的确切机制尚不清楚，但最近的进展为HTLV-I致肿瘤提供了重要线索。未来的研究应集中在新的治疗策略，包括预防，在白血病发生机制的证据的基础上组成。
BACKGROUND Human T-cell leukemia virus type I (HTLV-I) is a causative virus of adult T-cell leukemia (ATL), HTLV-I-associated myelopathy/tropical spastic paraparesis, and HTLV-I-associated uveitis. ATL is a neoplastic disease of CD4-positive T lymphocytes that is characterized by pleomorphic tumor cells with hypersegmented nuclei, termed "flower cells." The mechanisms of leukemogenesis have not been fully clarified. METHODS The authors reviewed the virological, clinical, and immunological features of HTLV-I and ATL and summarized recent findings on the oncogenic mechanisms of ATL and therapeutic advances. RESULTS Multiple factors, such as viral genes, genetic and epigenetic alterations, and the host immune system, may be implicated in the leukemogenesis of ATL. Among them, viral genes, tax, and HBZ have been thought to play important roles. The prognosis of aggressive-type ATL remains poor, regardless of intensive chemotherapy. Effectiveness of allogeneic stem cell transplantation for ATL has been recently reported. CONCLUSIONS Although the precise mechanism of leukemogenesis of ATL remains unclear, recent progress provides important clues in oncogenesis by HTLV-I. Future research should focus on the composition of novel therapeutic strategies, including prevention, based on the evidence in the leukemogenic mechanisms.