T-CELL RECEPTOR-V-BETA USAGE IN RHEUMATOID NODULES - MARKED OLIGOCLONALITY AMONG IL-2 EXPANDED LYMPHOCYTES

被引:10
作者
DEKEYSER, F [1 ]
VERBRUGGEN, G [1 ]
VEYS, EM [1 ]
CUVELIER, C [1 ]
MALFAIT, AM [1 ]
BENOIT, D [1 ]
ELEWAUT, D [1 ]
VERMEERSCH, J [1 ]
HEIRWEGH, A [1 ]
机构
[1] STATE UNIV GHENT HOSP, DEPT PATHOL, B-9000 GHENT, BELGIUM
来源
CLINICAL IMMUNOLOGY AND IMMUNOPATHOLOGY | 1993年 / 68卷 / 01期
关键词
D O I
10.1006/clin.1993.1090
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 [免疫学];
摘要
Rheumatoid arthritis is an autoimmune disease which is characterized by chronic polyarthritis and joint destruction as well as by extra-articular manifestations, typically including the appearance of rheumatoid nodules. Although the pathogenesis of the disease is unknown, substantial evidence suggests that it is T cell-mediated. In contrast to experimental models, the disease-mediating T cells in the human situation have never been isolated or identified. We expanded T lymphocytes from human rheumatoid nodules by IL-2 stimulation and observed a marked oligoclonality among these expanded lymphocytes. This tendency towards oligoclonality was not seen in IL-2-expanded lymphocytes from peripheral blood. We hypothesize that this oligoclonal expansion reflects a clonally restricted in situ preactivation of lymphocytes and that precisely these preactivated cells are involved in the pathogenesis of the rheumatic process. © 1993 Academic Press, Inc.
引用
收藏
页码:29 / 34
页数:6
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