Journal
JOURNAL OF IMMUNOLOGY
Volume 185, Issue 12, Pages 7646-7653Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1000930
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Funding
- FWO
- Belgian Charcot Foundation
- Interuniversity Attraction Poles program [IAP6/18]
- Belgian Foundation against Cancer
- Instituut voor de Aanmoediging van Innovatie door Wetenschap en Technologie in Vlaanderen
- Centrum voor Gezwelziekten
- Ghent University
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Apoptosis of oligodendrocytes (ODCs), the myelin-producing glial cells in the CNS, plays a central role in demyelinating diseases such as multiple sclerosis and experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis. To investigate the mechanism behind ODC apoptosis in EAE, we made use of conditional knockout mice lacking the adaptor protein FADD specifically in ODCs (FADD(ODC-KO)). FADD mediates apoptosis by coupling death receptors with downstream caspase activation. In line with this, ODCs from FADD(ODC-KO) mice were completely resistant to death receptor-induced apoptosis in vitro. In the EAE model, FADD(ODC-KO) mice followed an ameliorated clinical disease course in comparison with control littermates. Lymphocyte and macrophage infiltration into the spinal cord parenchyma was significantly reduced, as was the extent of demyelination and proinflammatory gene expression. Collectively, our data show that FADD is critical for ODC apoptosis and the development of autoimmune demyelinating disease. The Journal of Immunology, 2010, 185: 7646-7653.
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