Glucocorticoid-Induced Apoptosis in Animal Models of Multiple Sclerosis

被引:8
|
作者
Herold, Marco J. [1 ]
Reichardt, Holger M. [2 ]
机构
[1] Walter & Eliza Hall Inst Med Res, Melbourne, Australia
[2] Univ Gottingen, Sch Med, Inst Cellular & Mol Immunol, D-37073 Gottingen, Germany
基金
澳大利亚国家健康与医学研究理事会;
关键词
glucocorticoids; experimental autoimmune encephalomyelitis; apoptosis; neuroinflammation; EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS; EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS; T-CELL DEATH; ACUTE LYMPHOBLASTIC-LEUKEMIA; CENTRAL-NERVOUS-SYSTEM; BCL-2 PROTEIN FAMILY; IMMUNE-SYSTEM; ACID SPHINGOMYELINASE; BH3-ONLY PROTEINS; RECEPTOR GENE;
D O I
10.1615/CritRevImmunol.2013007415
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Glucocorticoids (GCs) are highly potent anti-inflammatory and immunosuppressive agents. They exert influence on many cell types of the immune system and impact a plethora of processes such as cytokine production, leukocyte differentiation, migration and adhesion, apoptosis induction, and changes in morphology Those that axe most relevant for the modulation of neuroinflammatory diseases, however, are still under debate. In this review, we will elaborate on how GCs impact inflammatory responses in general and revisit the ambivalent role that apoptosis plays in animal models of multiple sclerosis. Furthermore, we will discuss arguments that speak in favor or against an essential function of GC-induced apoptosis in neuroinflammation. We anticipate that a better knowledge of the mechanisms that GCs employ will eventually find its way into clinical practice for the future benefit of afflicted patients.
引用
收藏
页码:183 / 202
页数:20
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