Suppr超能文献

兔κ链b基因座抑制性免疫球蛋白同种异型自身抗体反应的克隆性和特异性的证明。

Demonstration of the clonality and specificity of an auto-antibody response to a suppressed immunoglobulin allotype of the rabbit kappa chain b locus.

作者信息

Hole N, Catty D, Appleby P, Catty J

出版信息

Immunol Lett. 1985;11(1):19-28. doi: 10.1016/0165-2478(85)90138-5.

Abstract

A regulatory idiotypic network is proposed to control allotype expression in normal rabbits. We have used suppression of the kappa chain b6 allotype in an attempt to restrict the number of regulatory idiotypes involved in an induced auto anti-allotype response. These auto anti-b6 antibodies were examined by an agarose imprint immuno-fixation IEF technique using iodinated allotype-bearing IgG. All totally b6-suppressed rabbits produced a clonally complex response which was generally spectrotypically unique - thus contradicting previous claims of a dominant common idiotypic pattern. The compensating light chains thus have available as many regulatory V genes as does the kappa 1 light chain. However, the b6/b6 homozygotes breaking b6 suppression produce an auto anti-b6 antibody which does not interact with their "escaping" molecules and which is clonally restricted. We propose a regulatory mechanism limiting the V genes utilised to produce the autoantibody, the latter then allowing only molecules bearing non-interactive allotopes to "escape" suppression.

摘要

有人提出一种调节性独特型网络来控制正常兔子的同种异型表达。我们通过抑制κ链b6同种异型,试图限制参与诱导的自身抗同种异型反应的调节性独特型数量。使用碘化的携带同种异型的IgG,通过琼脂糖印记免疫固定IEF技术检测这些自身抗b6抗体。所有完全被b6抑制的兔子都产生了克隆复杂的反应,这种反应通常在光谱类型上是独特的——因此与先前关于占主导地位的共同独特型模式的说法相矛盾。因此,补偿性轻链可利用的调节性V基因与κ1轻链一样多。然而,打破b6抑制的b6/b6纯合子产生一种自身抗b6抗体,该抗体不与其“逃脱”的分子相互作用,并且在克隆上受到限制。我们提出一种调节机制,限制用于产生自身抗体的V基因,后者随后只允许携带非相互作用同种异型表位的分子“逃脱”抑制。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验