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小鼠主要组织相容性复合体(H-2)对弗瑞德白血病病毒诱导的免疫抑制的影响。

Influence of the murine MHC (H-2) on Friend leukemia virus-induced immunosuppression.

作者信息

Morrison R P, Nishio J, Chesebro B

出版信息

J Exp Med. 1986 Feb 1;163(2):301-14. doi: 10.1084/jem.163.2.301.

Abstract

Friend murine leukemia virus complex (FV)-induced immunosuppression was studied by assaying splenic anti-SRBC PFC responses and plasma antibody titers in mice at various times after FV inoculation. Genes located within the H-2 complex were found to influence resistance to FV-induced immunosuppression. Near normal responses were observed in mice having the H-2a/b or H-2b/b genotype, whereas mice having the H-2a/a genotype were suppressed. This H-2 effect was observed not only in mice having heterozygous C57BL/10 X A background genes, including Rfv-3r/s, but also was apparent in mice having homozygous A-strain background genes, including Rfv-3s/s. Therefore, the Rfv-3 gene did not appear to convey resistance to FV-induced immunosuppression. The suppression in susceptible H-2a/a mice was characterized by a partial suppression of the IgM response and a profound suppression of both the primary and secondary IgG responses. Neither splenomegaly nor viremia alone appeared to be sufficient for the induction or maintenance of the immunosuppression. The mechanism of suppression was unclear, but both B lymphocyte and T lymphocyte functions appeared to be altered.

摘要

通过检测接种Friend鼠白血病病毒复合物(FV)后不同时间点小鼠的脾脏抗绵羊红细胞空斑形成细胞(PFC)反应和血浆抗体滴度,研究了FV诱导的免疫抑制作用。发现位于H-2复合物内的基因会影响对FV诱导的免疫抑制的抵抗力。具有H-2a/b或H-2b/b基因型的小鼠表现出接近正常的反应,而具有H-2a/a基因型的小鼠则受到抑制。这种H-2效应不仅在具有杂合C57BL/10×A背景基因(包括Rfv-3r/s)的小鼠中观察到,在具有纯合A系背景基因(包括Rfv-3s/s)的小鼠中也很明显。因此,Rfv-3基因似乎并未赋予对FV诱导的免疫抑制的抵抗力。易感的H-2a/a小鼠的抑制表现为IgM反应部分受到抑制,初次和二次IgG反应均受到严重抑制。单独的脾肿大或病毒血症似乎都不足以诱导或维持免疫抑制。抑制机制尚不清楚,但B淋巴细胞和T淋巴细胞的功能似乎都发生了改变。

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Immunity to retroviral infection: the Friend virus model.对逆转录病毒感染的免疫:弗瑞德病毒模型
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