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Protective effects of type I and type II interferons toward Rous sarcoma virus-induced tumors in chickens.

机译:I型和II型干扰素对劳斯肉瘤病毒诱导的鸡肿瘤的保护作用。

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Growth of tumors induced by Rous sarcoma virus (RSV) is controlled by alleles at the major histocompatibility complex locus in chickens, indicating that immunological host defense mechanisms play a major role. We show here that the resistance phenotype of CB regressor chickens can be partially reverted by treating the animals with a monoclonal antibody that neutralizes the major serotype of chicken type I interferon, ChIFN-alpha. Injection of recombinant ChIFN-alpha into susceptible CC progressor chickens resulted in a dose-dependent inhibition of RSV-induced tumor development. This treatment was not effective, however, in CC chickens challenged with a DNA construct expressing the v-src oncogene, suggesting that the beneficial effect of type I interferon in this system resulted from its intrinsic antiviral activity and probably not from indirect immunmodulatory effects. By contrast, recombinant chicken interferon-gamma strongly inhibited tumor growth when given to CC chickens that were challenged with the v-src oncogene, indicating that the two cytokines target different steps of tumor development. Copyright 1999 Academic Press.
机译:劳斯肉瘤病毒(RSV)诱导的肿瘤生长受鸡主要组织相容性复合体基因座的等位基因控制,表明免疫宿主防御机制起主要作用。我们在这里显示,通过用中和鸡I型干扰素的主要血清型ChIFN-α的单克隆抗体处理动物,可以部分还原CB消退鸡的抗性表型。重组ChIFN-α注入易感CC进步鸡中导致剂量依赖性抑制RSV诱导的肿瘤发展。然而,这种处理在用表达v-src癌基因的DNA构建体攻击的CC鸡中无效,这表明I型干扰素在该系统中的有益作用是其固有的抗病毒活性,可能不是间接的免疫调节作用。相比之下,重组鸡干扰素-γ给予被v-src致癌基因攻击的CC鸡时,可强烈抑制肿瘤生长,表明这两种细胞因子靶向不同的肿瘤发展步骤。版权所有1999,学术出版社。

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