移植物抗宿主病加速NZB/NZW F1小鼠的自身免疫反应。

Acceleration of autoimmunity in NZB/NZW F1 mice by graft-versus-host disease.

作者信息

Goldblum R, Pillarisetty R, Dauphinee M J, Talal N

出版信息

Clin Exp Immunol. 1975 Feb;19(2):377-85.

PMID:2403

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1538084/

Abstract

Chronic graft-versus-host (GVH) disease was induced in NZB/NZW F1 (B/W) hybrid female mice by the weekly injection of parental NZB spleen cells. Control mice received injections of syngeneic spleen cells only. The mice were assayed for antibodies to [3H]DNA and [3H]polyadenylic-polyuridylic acid by a cellulose ester filter radioimmunoassay, and for antibody to thymocytes by a cytotoxicity method. GVH disease accelerated the development of all three antibodies in B/W mice. In addition, sucrose density gradient ultracentrifugation of pooled sera suggested that an accelerated switch from 19S to 7S anti-DNA production may be an early effect of GVH. The mechanism of acceleration is discussed in terms of immunological and viral factors generated by the GVH reaction.

摘要

通过每周注射亲代新西兰黑鼠脾脏细胞，在新西兰黑鼠/新西兰白鼠F1（B/W）杂交雌性小鼠中诱发慢性移植物抗宿主（GVH）病。对照小鼠仅注射同基因脾脏细胞。通过纤维素酯滤膜放射免疫测定法检测小鼠针对[3H]DNA和[3H]聚腺苷酸-聚尿苷酸的抗体，并通过细胞毒性方法检测针对胸腺细胞的抗体。GVH病加速了B/W小鼠中所有这三种抗体的产生。此外，对合并血清进行蔗糖密度梯度超速离心表明，从19S抗DNA产生加速转换为7S抗DNA产生可能是GVH的早期效应。从GVH反应产生的免疫和病毒因素方面讨论了加速机制。

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