Experimental autoimmune myositis in the Lewis rat: lack of spontaneous T-cell apoptosis and therapeutic response to glucocorticosteroid application

被引:20
作者
Schneider, C
Matsumoto, Y
Kohyama, K
Toyka, KV
Hartung, HP
Gold, R
机构
[1] Univ Wurzburg, Dept Neurol, D-97080 Wurzburg, Germany
[2] Tokyo Metropolitan Inst Neurosci, Dept Neuropathol, Tokyo, Japan
关键词
polymyositis; methylprednisolone; therapy; apoptosis;
D O I
10.1016/S0165-5728(00)00254-X
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
Recently, it has been shown that inflammatory T-cells in human idiopathic myositis only very rarely undergo spontaneous apoptosis. The animal model of experimental autoimmune myositis (EAM) in the Lewis rat was chosen to investigate whether similar findings hold true in rat muscle and if glucocorticosteroids act by induction of T-cell apoptosis in inflammatory lesions. The rate of spontaneous T-cell apoptosis in rat EAM was low, even in muscle specimens with extensive inflammation. After intravenous glucocorticosteroid pulse therapy we found a dramatic increase in the rate of apoptotic T-cells in the inflamed muscles. Up to 50% of these apoptotic T-cells were CD8 positive apoptotic T-cells. T-cell apoptosis was significantly lower in similarly inflamed muscle specimens of the control group. We suggest that glucocorticosteroids induce apoptosis of endomysial T-cells in human idiopathic polymyositis. Glucocorticosteroid-induced apoptosis may be a candidate mechanism in the termination of inflammatory activity. (C) 2000 Elsevier Science B.V. All rights reserved.
引用
收藏
页码:83 / 87
页数:5
相关论文
共 14 条
[1]
Cytotoxic mechanisms in inflammatory myopathies - Co-expression of Fas and protective Bcl-2 in muscle fibres and inflammatory cells [J].
Behrens, L ;
Bender, A ;
Johnson, MA ;
Hohlfeld, R .
BRAIN, 1997, 120 :929-938
[2]
BOUMPAS DT, 1991, CLIN EXP RHEUMATOL, V9, P413
[3]
POLYMYOSITIS, DERMATOMYOSITIS, AND INCLUSION-BODY MYOSITIS [J].
DALAKAS, MC .
NEW ENGLAND JOURNAL OF MEDICINE, 1991, 325 (21) :1487-1498
[4]
Di Virgilio F, 1998, CELL DEATH DIFFER, V5, P191
[5]
Gene transfer into CD4+ T lymphocytes:: Green fluorescent protein-engineered, encephalitogenic T cells illuminate brain autoimmune responses [J].
Flügel, A ;
Willem, M ;
Berkowicz, T ;
Wekerle, H .
NATURE MEDICINE, 1999, 5 (07) :843-847
[6]
T-cell apoptosis in autoimmune diseases: termination of inflammation in the nervous system and other sites with specialized immune-defense mechanisms [J].
Gold, R ;
Hartung, HP ;
Lassmann, H .
TRENDS IN NEUROSCIENCES, 1997, 20 (09) :399-404
[7]
GOLD R, 1994, LAB INVEST, V71, P219
[8]
Goldstein R A., 1992, Inflammation: Basic Principles and Clinical Correlates, V2nd, P1061
[9]
HAYNES BF, 1992, CECIL TXB MED, P104
[10]
Myosin-induced autoimmune polymyositis in the rat [J].
Kojima, T ;
Tanuma, N ;
Aikawa, Y ;
Shin, T ;
Sasaki, A ;
Matsumoto, Y .
JOURNAL OF THE NEUROLOGICAL SCIENCES, 1997, 151 (02) :141-148