AUTOANTIBODIES TO HUMAN STRESS PROTEINS - A SURVEY OF VARIOUS RHEUMATIC AND OTHER INFLAMMATORY DISEASES

被引:105
|
作者
JARJOUR, WN
JEFFRIES, BD
DAVIS, JS
WELCH, WJ
MIMURA, T
WINFIELD, JB
机构
[1] UNIV N CAROLINA, THURSTON ARTHRIT RES CTR,DIV RHEUMATOL & IMMUNOL, 932 FLOB 231H,CB 7280, CHAPEL HILL, NC 27599 USA
[2] UNIV N CAROLINA, DIV GASTROENTEROL, CHAPEL HILL, NC 27514 USA
[3] UNIV CALIF SAN FRANCISCO, LUNG BIOL RES CTR, SAN FRANCISCO, CA 94143 USA
[4] UNIV VIRGINIA, DIV RHEUMATOL, CHARLOTTESVILLE, VA 22903 USA
来源
ARTHRITIS AND RHEUMATISM | 1991年 / 34卷 / 09期
关键词
D O I
10.1002/art.1780340909
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Unselected sera from patients with various rheumatic, inflammatory bowel, and autoimmune skin diseases (n = 268) were examined against human cell lysate by immunoblotting procedures, to determine the prevalence of autoantibodies to stress proteins (heat-shock proteins) hsp60 (homolog of Escherichia coli groEL and mycobacterial 65K antigens), hsp73, and hsp90. Using standard, sensitive and specific assay conditions, IgG and IgM autoantibodies to these stress proteins were not demonstrable, or were detected infrequently, in sera from control subjects (n = 36) and from patients with rheumatoid arthritis, Sjogren's syndrome, ankylosing spondylitis, Reiter's syndrome, systemic lupus erythematosus, and systemic sclerosis. Autoantibodies to hsp60 were relatively more common (greater-than-or-equal-to 20% of sera) in patients with mixed connective tissue disease, polymyositis/dermatomyositis, psoriatic arthritis, inflammatory bowel disease, epidermolysis bullosa acquisita, and bullous pemphigoid. Anti-hsp73 autoantibodies were detected in 20% or more of the sera from patients with Lyme disease and ulcerative colitis. Taken together, these data extend the spectrum of autoimmune and inflammatory diseases in which humoral anti-stress protein autoreactivity develops. However, the paucity of humoral autoreactivity to stress proteins in patients with systemic lupus erythematosus and rheumatoid arthritis argues against a direct role of anti-stress protein autoantibodies in the pathogenesis of these disorders.
引用
收藏
页码:1133 / 1138
页数:6
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