Interleukin 3 dependent retrovirus induced lymphomas: loss of the ability to terminally differentiate in response to differentiation factors.
Interleukin 3 dependent retrovirus induced lymphomas: loss of the ability to terminally differentiate in response to differentiation factors.
复制标题
白细胞介素 3 依赖性逆转录病毒诱导的淋巴瘤：响应分化因子而丧失终末分化能力。
DOI：
10.1007/978-3-642-69860-6_16
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发表时间：
1984
影响因子：
--
通讯作者：
Holmes,KL
中科院分区：
文献类型：
--
作者：
Ihle,JN;Morse3rd,HC;Keller,J;Holmes,KL
小鼠逆转录病毒诱导淋巴瘤的机制在很大程度上还不清楚。已经定义了一些要求，这些要求起着至关重要的作用。在Moloney白血病病毒(MoLV)诱导的白血病中，一个潜在的成分是免疫反应(Lee和Ihle，1981；Lee和Ihle，1981)。据推测，这是由于需要产生适当的靶细胞群，这是通过病毒抗原诱导抗原特异性辅助T细胞产生几种淋巴因子来实现的。这些淋巴因子随后会诱导多种细胞类型的增殖和分化。由于急性病毒血症和抗原特异性辅助性T细胞的存在，细胞增殖到T细胞来源的淋巴因子的频率比对照组小鼠高50-200倍。正是从这种扩大的人口中，淋巴瘤最终出现(Pepersack等人，1980年)。
The mechanisms by which murine retroviruses induce lymphomas are largely unknown. A number of requirements have been defined which play an essential role. In Moloney leukemia virus (MoLV) induced leukemia, one potential component is an immune response (Lee and Ihle, 1981; Lee and Ihle, 1981). This has been speculated to be due to a requirement to generate an appropriate target cell population, which is accomplished by viral antigen-induced production of several lymphokines by antigen-specific helper T cells. These lymphokines subsequently induce the proliferation and differentiation of a variety of cell types. As a consequence of the acute viremia and the presence of antigen-specific helper T cells, the frequency of cells proliferating to T cell-derived lymphokines is 50- to 200-fold higher than in control mice. It is from this expanded population that the lymphomas ultimately arise (Pepersack et al., 1980).