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对淋巴白血病病毒在抗白血病的C57BL/6小鼠中由Friend复合体引起的免疫抑制作用中所起作用的分析。

An analysis of the role of lymphatic leukemia virus in the immunodepression exerted by Friend complex in leukaemia-resistant C57BL/6 mice.

作者信息

Bendinelli M, Campa M, Toniolo A, Garzelli C

出版信息

J Gen Virol. 1978 May;39(2):243-51. doi: 10.1099/0022-1317-39-2-243.

Abstract

Leukaemia-resistant C57BL/6 mice inoculated with the Friend complex (FLC) present a transient but definite depression of the ability to develop IgM and IgG antibody-producing cells to sheep red cells (SRC). In this paper it is shown that this immunodepression cannot be attributed solely to the lymphatic leukaemia virus (LLV) component of FLC which is immunodepressive in susceptible mice. This conclusion was reached by investigating the immunological reactivity of C57BL/6 mice following inoculation with two isolates of LLV. Circumstantial evidence obtained by examining the replication of FLC and LLV, the antibody response to E. coli lipopolysaccharide (LPS) and the ability of syngeneic macrophages administered together with the antigen to restore the response to SRC points to the same conclusion. There were also indications that the low sensitivity to depression by viruses of the Friend complex exhibited by the anti-LPS antibody response is due to the mitogenic activity of this antigen.

摘要

接种了弗瑞德复合体(FLC)的抗白血病C57BL/6小鼠,其产生针对绵羊红细胞(SRC)的IgM和IgG抗体产生细胞的能力出现短暂但明确的下降。本文表明,这种免疫抑制不能仅仅归因于FLC中的淋巴白血病病毒(LLV)成分,该成分在易感小鼠中具有免疫抑制作用。通过研究接种两种LLV分离株后C57BL/6小鼠的免疫反应性得出了这一结论。通过检查FLC和LLV的复制、对大肠杆菌脂多糖(LPS)的抗体反应以及与抗原一起给予的同基因巨噬细胞恢复对SRC反应的能力所获得的间接证据也指向了相同的结论。也有迹象表明,抗LPS抗体反应所表现出的对弗瑞德复合体病毒抑制的低敏感性是由于该抗原的促有丝分裂活性。

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