Molecular triggers of neuroinflammation in mouse models of demyelinating diseases

被引：16

作者：

Barrette, Benoit ^{[1
]}

Nave, Klaus-Armin ^{[1
]}

Edgar, Julia M. ^{[1
,2
]}

机构：

[1] Max Planck Inst Expt Med, Dept Neurogenet, Hermann Rein Str 3, D-37075 Gottingen, Germany

[2] Univ Glasgow, Coll Med Vet & Life Sci, Inst Infect Immun & Inflammat, Appl Neurobiol Grp, Glasgow G12 8TA, Lanark, Scotland

来源：

BIOLOGICAL CHEMISTRY | 2013年 / 394卷 / 12期

关键词：

leukodystrophy; microglia/macrophages; myelin; neuroinflammation; neuropathy; T cells; MYELIN DEGENERATION; PROTEOLIPID PROTEIN; INFLAMMATORY RESPONSES; AXONOPATHIC CHANGES; DEFICIENT MICE; AXONAL DAMAGE; IMMUNE CELLS; GENE-THERAPY; SYSTEM; CNS;

D O I：

10.1515/hsz-2013-0219

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：

Myelinating cells wrap axons with multi-layered myelin sheaths for rapid impulse propagation. Dysfunctions of oligodendrocytes or Schwann cells are often associated with neuroinflammation, as observed in animal models of leukodystrophies and peripheral neuropathies, respectively. The neuroinflammatory response modulates the pathological changes, including demyelination and axonal injury, but also remyelination and repair. Here we discuss different immune mechanisms as well as factors released or exposed by myelinating glia in disease conditions. The spectrum of inflammatory mediators varies with different myelin disorders and has a major impact on the beneficial or detrimental role of immune cells in keeping nervous system integrity.

引用

页码：1571 / 1581

页数：11

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