Are T cells in rheumatoid synovium aggressors or bystanders?

被引:41
作者
Miossec, P [1 ]
机构
[1] Hop Edouard Herriot, Dept Immunol, Clin Immunol Unit, F-69437 Lyon 03, France
[2] Hop Edouard Herriot, Dept Rheumatol, F-69437 Lyon 03, France
关键词
D O I
10.1097/00002281-200005000-00004
中图分类号
R5 [内科学];
学科分类号
1002 [临床医学]; 100201 [内科学];
摘要
T cells have been directly associated with rheumatoid arthritis (RA) because they represent the largest cell population infiltrating the synovium, Their direct contribution to disease and joint destruction has been more difficult to demonstrate. Locally, they interact with other blood-derived and resident cells. Some T cells may contribute to disease through the secretion of cytokines, Indeed, interleukin-17, a T-cell-specific cytokine, is produced by RA synovium and acts as a bone and cartilage destructive factor. In addition, it increases the production of proinflammatory cytokines by monocytes and further enhances their effects on matrix destruction, Once considered bystanders in RA, T cells can now be classified as aggressors through their direct and indirect contribution to destruction. In particular, a subset of Th1 T cells can aggravate the proinflammatory and destructive pattern associated with monocyte activation. Manipulation of this subset may control the destructive pattern, Such a result can be achieved when a switch can be induced from a destructive pattern to a protective one leading to repair. Curr Opin Rheumatol 2000, 12:181-185 (C) 2000 Lippincott Williams & Wilkins, Inc.
引用
收藏
页码:181 / 185
页数:5
相关论文
共 33 条
[1]
Aarvak T, 1999, SCAND J IMMUNOL, V50, P1
[2]
Aarvak T, 1999, J IMMUNOL, V162, P1246
[3]
CTLA4Ig-mediated blockade of T-cell costimulation in patients with psoriasis vulgaris [J].
Abrams, JR ;
Lebwohl, MG ;
Guzzo, CA ;
Jegasothy, BV ;
Goldfarb, MT ;
Goffe, BS ;
Menter, A ;
Lowe, NJ ;
Krueger, G ;
Brown, MJ ;
Weiner, RS ;
Birkhofer, MJ ;
Warner, GL ;
Berry, KK ;
Linsley, PS ;
Krueger, JG ;
Ochs, HD ;
Kelley, SL ;
Kang, SW .
JOURNAL OF CLINICAL INVESTIGATION, 1999, 103 (09) :1243-1252
[4]
Asselin S, 1998, CLIN EXP IMMUNOL, V114, P284
[5]
Awane M, 1999, J IMMUNOL, V162, P5337
[6]
Burger D, 1998, ARTHRITIS RHEUM, V41, P1748, DOI 10.1002/1529-0131(199810)41:10<1748::AID-ART7>3.3.CO
[7]
2-V
[8]
Chabaud M, 1999, ARTHRITIS RHEUM-US, V42, P963, DOI 10.1002/1529-0131(199905)42:5<963::AID-ANR15>3.0.CO
[9]
2-E
[10]
Chabaud M, 1998, J IMMUNOL, V161, P409