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用334C(一种诱导小鼠淋巴白血病的病毒)接种小鼠后的免疫抑制。

Immunosuppression in mice after inoculation with 334C, a murine lymphatic leukemia-inducing virus.

作者信息

Schenk P J, Buffett R F

出版信息

J Natl Cancer Inst. 1977 Mar;58(3):665-71. doi: 10.1093/jnci/58.3.665.

DOI:10.1093/jnci/58.3.665
PMID:190412
Abstract

334C murine leukemia virus, which induces a high incidence of lymphatic leukemias (80-90%) in susceptible mice following a long latency period, was found to cause a severe in vivo suppression of direct plaque-forming cells from the spleen, following antigenic stimulation with sheep red blood cells. Neonatally infected inbred BALB/c and outbred Ha/ICR Swiss mice, which develop a sustained viremia, were highly susceptible to the immunosuppressive effect of this virus as early as 1 week after virus infection, long before any detectable histologic evidence of leukemia development. Ha/ICR Swiss mice, which are highly resistant to the leukemogenic potential of this virus following infection in adult life, were highly resistant to its immunosuppressive action; only a moderate and transient suppression, without viremia, occurred 2 weeks after virus infection. In marked contrast, BALB/c mice were highly susceptible to the immunosuppressive action of 334C murine leukemia virus following infection in adult life; a severe and sustained suppression was observed as early as 1 week after virus infection and was followed by a sustained viremia, beginning at 2 weeks, with a 55-60% incidence of leukemia observed over a period of 1 year. Infectious virus was essential to produce theimmunosuppressive effect; heat-inactivated (56 degrees C/30 min) and attenuated (4 degrees C/4 1/2 mo) virus preparations were ineffective. The plaque-forming response of spleen cells from lethally irradiated syngeneic adult BALB/c mice was markedly suppressed following reconstitution with thymus-dependent (T) or thymus-independent (B) cells from the thymus and bone marrow, respectively, of virus-infected mice, in combination with each other, or with the appropriate cell populations from normal mice.

摘要

334C小鼠白血病病毒在潜伏期较长后可诱导易感小鼠发生高发性淋巴白血病(80-90%),经绵羊红细胞抗原刺激后,发现该病毒可在体内严重抑制脾脏直接形成空斑细胞。新生期感染近交系BALB/c和远交系Ha/ICR瑞士小鼠会出现持续性病毒血症,早在病毒感染后1周,远在白血病发展出现任何可检测到的组织学证据之前,它们就对该病毒的免疫抑制作用高度敏感。成年后感染该病毒的Ha/ICR瑞士小鼠对其致白血病潜力具有高度抗性,对其免疫抑制作用也具有高度抗性;病毒感染2周后仅出现中度短暂抑制,无病毒血症。与之形成鲜明对比的是,成年后感染的BALB/c小鼠对334C小鼠白血病病毒的免疫抑制作用高度敏感;早在病毒感染后1周就观察到严重且持续的抑制,随后从2周开始出现持续性病毒血症,在1年期间白血病发病率为55-60%。感染性病毒对于产生免疫抑制作用至关重要;热灭活(56℃/30分钟)和减毒(4℃/4.5个月)病毒制剂无效。用来自病毒感染小鼠胸腺和骨髓的依赖胸腺(T)或非依赖胸腺(B)细胞、相互组合或与正常小鼠的适当细胞群体重建后,致死性照射的同基因成年BALB/c小鼠脾脏细胞的空斑形成反应受到明显抑制。

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Immunosuppression in mice after inoculation with 334C, a murine lymphatic leukemia-inducing virus.用334C(一种诱导小鼠淋巴白血病的病毒)接种小鼠后的免疫抑制。
J Natl Cancer Inst. 1977 Mar;58(3):665-71. doi: 10.1093/jnci/58.3.665.
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Expression of antigens coded in murine leukemia viruses on thymocytes of allogeneic donor origin in AKR mice following syngeneic or allogeneic bone marrow transplantation.同基因或异基因骨髓移植后,AKR小鼠中源自异基因供体的胸腺细胞上鼠白血病病毒编码抗原的表达。
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Differences in pathogenicity among cloned sublines of a murine leukemia virus.一种鼠白血病病毒克隆亚系之间致病性的差异。
J Virol. 1979 Apr;30(1):232-40. doi: 10.1128/JVI.30.1.232-240.1979.