Mechanism of experimental autoimmune encephalomyelitis in Lewis rats: recent insights from macrophages.
10.5115/acb.2012.45.3.141
- Author:
Taekyun SHIN
1
;
Meejung AHN
;
Yoh MATSUMOTO
Author Information
1. Department of Veterinary Anatomy, Veterinary Medical Research Institute, College of Veterinary Medicine, Jeju National University, Jeju, Korea. shint@jejunu.ac.kr
- Publication Type:Review
- Keywords:
Experimental autoimmune encephalomyelitis;
Lewis rats;
Macrophages;
Neuroimmunomodulation;
Regulatory T lymphocytes
- MeSH:
Animals;
Central Nervous System;
Encephalomyelitis, Autoimmune, Experimental;
Macrophages;
Myelin Basic Protein;
Neuroimmunomodulation;
Paralysis;
Rats;
T-Lymphocytes, Regulatory;
Th1 Cells
- From:Anatomy & Cell Biology
2012;45(3):141-148
- CountryRepublic of Korea
- Language:English
-
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.
