pristane诱导的关节炎。一种自身免疫性疾病实验性小鼠模型的免疫学和遗传学特征。

Pristane-induced arthritis. The immunologic and genetic features of an experimental murine model of autoimmune disease.

作者信息

Wooley P H, Seibold J R, Whalen J D, Chapdelaine J M

机构信息

Department of Internal Medicine, Wayne State University Medical School, Detroit, MI 48201.

出版信息

Arthritis Rheum. 1989 Aug;32(8):1022-30. doi: 10.1002/anr.1780320812.

DOI:10.1002/anr.1780320812

PMID:2765002

Abstract

Pristane was injected intraperitoneally into mice of several strains, inducing an inflammatory seropositive arthritis in susceptible strains. The evolving histologic features included synovial hyperplasia, periostitis, and progressive marginal erosions. Multiple serologic immune abnormalities, including rheumatoid factor and anticollagen antibodies, also developed. Genetic analysis indicated that the major histocompatibility complex (H-2), C5 hemolytic complement (Hc), Newcastle disease virus-induced interferon (IF-1), and athymic (nu/nu) loci were involved in regulating susceptibility to pristane-induce arthritis. This experimental murine disease may provide a novel model of rheumatoid arthritis.

摘要

将 pristane 腹腔注射到多个品系的小鼠体内，在易感品系中诱发炎症性血清阳性关节炎。不断演变的组织学特征包括滑膜增生、骨膜炎和进行性边缘侵蚀。还出现了多种血清学免疫异常，包括类风湿因子和抗胶原蛋白抗体。基因分析表明，主要组织相容性复合体（H-2）、C5 溶血补体（Hc）、新城疫病毒诱导的干扰素（IF-1）和无胸腺（nu/nu）基因座参与调节对 pristane 诱导性关节炎的易感性。这种实验性小鼠疾病可能为类风湿性关节炎提供一种新模型。