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C型病毒致白血病机制。I. 体外淋巴细胞母细胞生成与病毒血症及白血病的相关性。

Mechanisms of C-type viral leukemogenesis. I. Correlation of in vitro lymphocyte blastogenesis to viremia and leukemia.

作者信息

Lee J C, Ihle J N

出版信息

J Immunol. 1979 Nov;123(5):2351-8.

PMID:90708
Abstract

Various inbred strains of mice respond immunologically to genetically transmitted ecotropic C-type viruses. Part of this response is T cell blastogenesis with type specificity for the viral envelope glycoprotein gp71. Of those nonviremic, nonleukemic strains, and F1 crosses examined, in which virus expression occurs early in life, gp71-specific blastogenic T cells were detected within the first 2 months of age and temporally preceded the development of a humoral immune response. However, in the viremic, highly leukemic strain of AKR mice, gp71-specific T cell blastogenesis in vitro was readily detectable throughout the preleukemic phase, the first 5 months of age. In appropriate F1 crosses and backcrosses, the persistent in vitro blastogenic response segregated with viremia and leukemia. These data suggest that in vivo T cell stimulation by endogenous viral gp71, caused by viremia, may contribute to virus-induced leukemogenesis in mice.

摘要

各种近交系小鼠对基因传递的亲嗜性C型病毒产生免疫反应。这种反应的一部分是T细胞母细胞化,对病毒包膜糖蛋白gp71具有类型特异性。在那些非病毒血症、非白血病的品系以及所检测的F1杂交后代中,病毒表达在生命早期出现,在2月龄内即可检测到gp71特异性母细胞化T细胞,且在时间上先于体液免疫反应的发展。然而,在病毒血症高、白血病高发的AKR小鼠品系中,在白血病前期(即出生后的前5个月),体外很容易检测到gp71特异性T细胞母细胞化。在合适的F1杂交和回交中,持续的体外母细胞化反应与病毒血症和白血病相关。这些数据表明,病毒血症引起的内源性病毒gp71在体内对T细胞的刺激可能在小鼠病毒诱导的白血病发生过程中起作用。

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