Transgenic mouse models of multiple sclerosis

被引：20

作者：

Scheikl, Tanja ^{[2
,3
]}

Pignolet, Beatrice ^{[2
,3
]}

Mars, Lennart T. ^{[2
,3
]}

Liblau, Roland S. ^{[1
,2
,3
]}

机构：

[1] CHU Purpan, Ctr Physiopathol Toulouse Purpan, INSERM U563, F-31024 Toulouse 3, France

[2] Inst Natl Sante & Rech Med, Unite 563, Toulouse, France

[3] Univ Toulouse 3, F-31062 Toulouse, France

来源：

CELLULAR AND MOLECULAR LIFE SCIENCES | 2010年 / 67卷 / 23期

关键词：

Transgenesis; Multiple sclerosis; EAE; CNS; T cells; Autoimmunity; CENTRAL-NERVOUS-SYSTEM; EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS; MYELIN BASIC-PROTEIN; CD8(+) T-CELLS; MONOCYTE CHEMOATTRACTANT PROTEIN-1; EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS; VIRUS-INDUCED DEMYELINATION; NECROSIS-FACTOR-ALPHA; MACROPHAGE INFLAMMATORY PROTEIN-1-ALPHA; MICE EXPRESSING INTERLEUKIN-6;

D O I：

10.1007/s00018-010-0481-9

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Multiple sclerosis (MS) is an inflammatory demyelinating disease affecting the central nervous system (CNS) and a frequent cause of neurological disability in young adults. Multifocal inflammatory lesions in the CNS white matter, demyelination, oligodendrocyte loss, axonal damage, as well as astrogliosis represent the histological hallmarks of the disease. These pathological features of MS can be mimicked, at least in part, using animal models. This review discusses the current concepts of the immune effector mechanisms driving CNS demyelination in murine models. It highlights the fundamental contribution of transgenesis in identifying the mediators and mechanisms involved in the pathophysiology of MS models.

引用

页码：4011 / 4034

页数：24

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