TERMINAL COMPLEMENT COMPLEXES AND C1/C1 INHIBITOR COMPLEXES IN RHEUMATOID-ARTHRITIS AND OTHER ARTHRITIC CONDITIONS

被引:0
|
作者
OLEESKY, DA
DANIELS, RH
WILLIAMS, BD
AMOS, N
MORGAN, BP
机构
[1] UNIV HOSP WALES,DEPT MED BIOCHEM,CARDIFF,WALES
[2] UNIV HOSP WALES,DEPT RHEUMATOL,CARDIFF,WALES
[3] UNIV COLL CARDIFF,CARDIFF CF4 4XN,S GLAM,WALES
来源
CLINICAL AND EXPERIMENTAL IMMUNOLOGY | 1991年 / 84卷 / 02期
基金
英国惠康基金;
关键词
COMPLEMENT; TERMINAL COMPLEMENT COMPLEX; C1/C1 INHIBITOR COMPLEX; RHEUMATOID ARTHRITIS;
D O I
暂无
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Terminal complement complex (TCC) and Clr-Cls-Cl inhibitor complex (Cl/Cl INH) concentrations were measured in plasma and synovial fluid from patients with arthritis and related to other measures of disease activity. Both TCC and Cl/Cl INH concentrations were significantly increased in patients with rheumatoid arthritis (RA) compared with patients with osteoarthritis (plasma and synovial fluid, P < 0.05) and normal subjects (plasma only, P < 0.001). In the patients with RA, there was no correlation between plasma or synovial fluid TCC concentrations and IgM rheumatoid factor, immune complex or Cl/Cl INH levels. However, in 10 patients with seronegative RA, Cl/Cl INH and immune complex levels correlated significantly in synovial fluid (r = 0.69, P < 0.05) although not in plasma (r = 0.52). Plasma and synovial fluid TCC and Cl/Cl INH concentrations did not differ in rheumatoid patients with severe compared with mild joint disease (categorized by the Ritchie score). These results confirm a role for complement activation in RA but suggest that several mechanisms are involved in its pathogenesis.
引用
收藏
页码:250 / 255
页数:6
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