Mechanism of experimental autoimmune encephalomyelitis in Lewis rats: recent insights from macrophages / 대한해부학회지
Anatomy & Cell Biology
; : 141-148, 2012.
Article
de En
| WPRIM
| ID: wpr-125844
Bibliothèque responsable:
WPRO
ABSTRACT
Experimental autoimmune encephalomyelitis (EAE) in Lewis rats is an acute monophasic paralytic central nervous system disease, in which most rats spontaneously recover from paralysis. EAE in Lewis rats is induced by encephalitogenic antigens, including myelin basic protein. EAE is mediated by CD4+ Th1 cells, which secrete pro-inflammatory mediators, and spontaneous recovery is mediated by regulatory T cells. Recently, it was established that classically activated macrophages (M1 phenotype) play an important role in the initiation of EAE, while alternatively activated macrophages (M2 phenotype) contribute to spontaneous recovery from rat EAE. This review will summarize the neuroimmunological aspects of active monophasic EAE, which manifests as neuroinflammation followed by neuroimmunomodulation and/or neuroprotection, with a focus on the role of alternatively activated macrophages.
Mots clés
Texte intégral:
1
Indice:
WPRIM
Sujet Principal:
Paralysie
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Neuro-immunomodulation
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Système nerveux central
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Lymphocytes T régulateurs
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Lymphocytes auxiliaires Th1
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Protéine basique de la myéline
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Encéphalomyélite auto-immune expérimentale
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Macrophages
Limites du sujet:
Animals
langue:
En
Texte intégral:
Anatomy & Cell Biology
Année:
2012
Type:
Article