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对内源性RNA肿瘤病毒的自身免疫:对病毒包膜抗原的体液免疫反应。

Autogenous immunity to endogenous RNA tumor virus: humoral immune response to virus envelope antigens.

作者信息

Hanna M G, Ihle J N, Lee J C

出版信息

Cancer Res. 1976 Feb;36(2 pt 2):608-14.

PMID:56222
Abstract

Autogenous immune sera from several strains of mice have been examined for type-, group-, or interspecies-specific reactivities against leukemia virus envelope antigens and virus-induced cell surface proteins. The natural antibody of these test sera react with gp69/71, gp43, and p15 structural components on murine leukemia viruses including AKR, Friend, Rauscher, Moloney, and xenotropic BALB:virus-2. Furthermore, comparable radioimmune titration curves are obtained when these viruses are used in radioimmune precipitation assays. Competition experiments, however, suggest that natural immune sera are predominantly type specific and only weakly cross-react with the Rauscher or Friend virus. Natural immune sera react with the virion envelope but not with the virus-induced cell surface antigen. With respect to the biological activity of autogenous immune sera, there appears to be an inconsistency between the spectrum of virus-precipitating antibody and virus-neutralizing antibody. Although normal mouse serum readily neutralizes xenotropic viruses (BALB:virus-2), only weak neutralization of the ecotropic viruses can be achieved in vitro. Although there is a lack of direct evidence to indicate that autogenous immunity to murine leukemia virus is involved in the control of virus-mediated neoplasia, several empirical correlations point in this direction.

摘要

已对来自数种小鼠品系的自身免疫血清进行检测,以确定其针对白血病病毒包膜抗原和病毒诱导的细胞表面蛋白的型特异性、组特异性或种间特异性反应性。这些检测血清中的天然抗体与包括AKR、Friend、Rauscher、Moloney和嗜异性BALB:virus - 2在内的鼠白血病病毒上的gp69/71、gp43和p15结构成分发生反应。此外,当这些病毒用于放射免疫沉淀试验时,可获得相当的放射免疫滴定曲线。然而,竞争实验表明,天然免疫血清主要是型特异性的,与Rauscher或Friend病毒仅发生微弱的交叉反应。天然免疫血清与病毒粒子包膜发生反应,但不与病毒诱导的细胞表面抗原发生反应。关于自身免疫血清的生物学活性,病毒沉淀抗体谱和病毒中和抗体谱之间似乎存在不一致。虽然正常小鼠血清能轻易中和嗜异性病毒(BALB:virus - 2),但在体外只能对亲嗜性病毒实现微弱的中和作用。尽管缺乏直接证据表明对鼠白血病病毒的自身免疫参与了病毒介导的肿瘤形成的控制,但一些经验性关联指向了这个方向。

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