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围产期存在抗原(对氨基苯胂酸)或抗μ抗体导致A/J小鼠中反复出现的独特型(CRIA)丧失。

The perinatal presence of antigen (p-azophenylarsonate) or anti-mu antibodies lead to the loss of the recurrent idiotype (CRIA) in A/J mice.

作者信息

Ryelandt M, De Wit D, Baz A, Vansanten G, Denis O, Huetz F, Nisol F, Macedo-Soares F, Barcy S, Brait M

机构信息

Laboratoire de Physiologie Animale, Université Libre de Bruxelles, Rhode-saint-Genèse, Belgium.

出版信息

Int Immunol. 1995 Apr;7(4):645-52. doi: 10.1093/intimm/7.4.645.

Abstract

The immune response of A/J mice against p-azophenylarsonate (Ars)-keyhole limpet hemocyanin (KLH) is characterized by the dominance, late in primary and during the secondary, of a recurrent idiotype called CRIA, encoded by a canonical combination of Ig gene segments. In this study, A/J mice were given Ars coupled to deaggregated human gamma globulins (dHGG) within 24 h after delivery. The offsprings from these mice were then exposed as adults to Ars-KLH. These animals developed an unusual immune response. The level of anti-Ars antibodies was nearly normal but a dramatic shift in repertoire was observed: the cross-reactive idiotype which is the hallmark of the anti-Ars response in A/J mice was completely absent. The idiotype could be recovered by injection of anti-idiotypic antibodies alone, with no need of lipopolysaccharide coupling. Therefore the presence of antigen at birth can lead to a strong perturbation of idiotype selection. Similar results were obtained with neonatal treatment using anti-IgM antibodies. After recovery of suppression, A/J mice can mount an anti-arsonate response of normal level but devoid of the dominant idiotype.

摘要

A/J小鼠针对对氨基苯砷酸(Ars)-钥孔戚血蓝蛋白(KLH)的免疫反应的特征是,在初次免疫后期以及再次免疫期间,一种名为CRIA的复发独特型占主导地位,该独特型由Ig基因片段的典型组合编码。在本研究中,在分娩后24小时内给A/J小鼠注射与去聚合人γ球蛋白(dHGG)偶联的Ars。然后将这些小鼠的后代成年后暴露于Ars-KLH。这些动物产生了异常的免疫反应。抗Ars抗体水平接近正常,但观察到抗体库发生了显著变化:作为A/J小鼠抗Ars反应标志的交叉反应独特型完全缺失。仅通过注射抗独特型抗体就可以恢复该独特型,无需脂多糖偶联。因此,出生时抗原的存在可导致独特型选择的强烈扰动。使用抗IgM抗体进行新生儿治疗也获得了类似结果。抑制作用恢复后,A/J小鼠可以产生正常水平但缺乏主导独特型的抗砷酸盐反应。

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