双嗜性鼠白血病病毒SMX-1对AKR白血病发生的抑制作用。
Inhibition of AKR leukemogenesis by SMX-1, a dualtropic murine leukemia virus.
作者信息
Stockert E, O'Donnell P V, Obata Y, Old L J
出版信息
Proc Natl Acad Sci U S A. 1980 Jun;77(6):3720-4. doi: 10.1073/pnas.77.6.3720.
Intrathymic injection of SMX-1, a dualtropic murine leukemia virus (MuLV) originally derived from Moloney murine leukemia virus stocks, protects AKR mice from developing MuLV-accelerated leukemia and spontaneous leukemia. Thymuses of SMX-1-injected mice show no change in weight, morphology, or thymocyte size, and quantitative expression of Thy-1 and Lyt-2 differentiation antigens is identical to control mice. The amplified thymic expression of MuLV-related antigens that occurs spontaneously in 6-month-old preleukemic AKR mice or that can be induced in young AKR mice by leukemogenic AKR dualtropic MuLV is prevented by SMX-1. It appears unlikely that the protective effect of SMX-1 is explicable in terms of cross-immunogenicity with transforming MuLV or transformed cells. As SMX-1 persists for long periods after intrathymic injection and does not alter levels of thymic ecotropic MuLV, SMX-1 may interfere with the generation, spread, or leukemogenicity of dualtropic MuLV that form de novo in AKR thymus during the late preleukemic phase. SMX-1 provides a way to probe the events leading to cell transformation in AKR mice.
向胸腺内注射SMX-1（一种最初源自莫洛尼氏鼠白血病病毒株的双嗜性鼠白血病病毒（MuLV））可保护AKR小鼠不发生MuLV加速白血病和自发性白血病。注射SMX-1的小鼠的胸腺在重量、形态或胸腺细胞大小方面均无变化，Thy-1和Lyt-2分化抗原的定量表达与对照小鼠相同。SMX-1可阻止在6个月大的白血病前期AKR小鼠中自发出现的或可由致白血病的AKR双嗜性MuLV在年轻AKR小鼠中诱导产生的MuLV相关抗原在胸腺中的表达增强。SMX-1的保护作用似乎不太可能用与转化型MuLV或转化细胞的交叉免疫原性来解释。由于SMX-1在胸腺内注射后可长期存在且不改变胸腺嗜亲性MuLV的水平，因此SMX-1可能会干扰在白血病前期晚期在AKR胸腺中重新形成的双嗜性MuLV的产生、传播或致白血病性。SMX-1为探究导致AKR小鼠细胞转化的事件提供了一种方法。
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