INTERLEUKIN-1 ENHANCES THE DEVELOPMENT OF SPONTANEOUS ARTHRITIS IN MRL/IPR MICE

被引:34
作者
HOM, JT
COLE, H
BENDELE, AM
机构
[1] Department of Connective Tissue and Monoclonal Antibody Research, Lilly Research Laboratories, Indianapolis
来源
CLINICAL IMMUNOLOGY AND IMMUNOPATHOLOGY | 1990年 / 55卷 / 01期
关键词
D O I
10.1016/0090-1229(90)90072-X
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
We previously reported that treatments with human recombinant interleukin-1β (rIL-1β) in DBA 1 mice which were suboptimally immunized with native chick type II collagen (NcII) markedly accelerated the onset of collagen-induced arthritis (CIA). In the present study, we further characterized this IL-1-mediated enhancement of murine arthritis by examining the in vivo effects of rIL-1β in another arthritis model, namely, the spontaneous arthritis of the MRL lpr mouse strain. The results of these studies demonstrated that IL-1 treatments also enhanced the onset and progression of the spontaneous arthritic disease in MRL lpr mice. A substantial proportion of the IL-1-treated MRL lpr mice that were between 3 and 3.5 months of age exhibited swelling in either the hind or front paws. Moreover, histopathologic studies demonstrated the presence of striking alterations within the various joints of these IL-1-treated MRL lpr mice. Such abnormalities were not detected in the non-IL-1-treated, age-matched MRL lpr mice. Therefore, as in the experimentally induced disease of CIA, IL-1 may also be capable of contributing to the pathogenesis of the spontaneous arthritis of MRL lpr mice. © 1990.
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页码:109 / 119
页数:11
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