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Gm系统。抗Gm抗体:类风湿性关节炎中的特征;无需借助同种异型进行实验诱导;在单核细胞增多症中频繁出现。

The Gm system. Anti-Gm's: characteristics in rheumatoid arthritis; experimental induction without resort to allotype; frequent occurrence in mononucleosis.

作者信息

Grubb R

机构信息

Department of Medical Microbiology, University of Lund, Sweden.

出版信息

Scand J Rheumatol Suppl. 1988;75:227-32. doi: 10.3109/03009748809096768.

Abstract

UNLABELLED

Gm system: Some RFs specifically detect Mendelian markers of human Ig, originally proving that Ig production is gene controlled. The genetic marker systems of human Ig with 17 Gm, 2 Am, 3 Km and 1 Em markers are briefly described. Examples of the usefulness of the Gm system in medicine, immunology and molecular biology are mentioned.

CONCLUSIONS

  1. Some RFs have been essential tools in elucidating genetic control mechanisms in Ig production. 2. Knowledge of the Gm system is extensive. Anti-Gm's: High-titered anti-Gm's are common in R.A. The anti-allotypes in R.A. are markedly restricted as to their specificity. They are usually not directed against the individuals own Gm markers. Anti-human-immunoglobulins were observed in 12 of 18 sera from patients with mononucleosis. The majority of these anti-immunoglobulins were inhibitable by native human Ig and showed restricted specificity.

CONCLUSIONS

  1. There is a strong stimulus for production of particular anti-Gm's in a majority of R.A. cases. 2. Notions of an autoimmune origin for many anti-Gm's in R.A. are not in obvious agreement with experimental observations. 3. Anti-human-Ig's with restricted specificity are commonly induced in mononucleosis.
摘要

未标记

Gm系统:一些类风湿因子(RF)可特异性检测人类免疫球蛋白(Ig)的孟德尔标记,最初证明了Ig的产生受基因控制。简要描述了具有17个Gm、2个Am、3个Km和1个Em标记的人类Ig遗传标记系统。提及了Gm系统在医学、免疫学和分子生物学中的应用实例。

结论

  1. 一些RF是阐明Ig产生中基因控制机制的重要工具。2. 关于Gm系统的知识很广泛。抗Gm:高滴度抗Gm在类风湿关节炎(R.A.)中很常见。类风湿关节炎中的抗同种异型抗体在特异性方面明显受限。它们通常不针对个体自身的Gm标记。在18例单核细胞增多症患者的血清中,有12例检测到抗人免疫球蛋白。这些抗免疫球蛋白中的大多数可被天然人Ig抑制,并显示出受限的特异性。

结论

  1. 在大多数类风湿关节炎病例中,存在产生特定抗Gm的强烈刺激。2. 类风湿关节炎中许多抗Gm的自身免疫起源观点与实验观察结果并不明显一致。3. 单核细胞增多症中通常会诱导产生特异性受限的抗人Ig。

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