Document Detail


Current views on the roles of Th1 and Th17 cells in experimental autoimmune encephalomyelitis.
MedLine Citation:
PMID:  20107924     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Multiple sclerosis (MS) and its animal model, experimental autoimmune encephalomyelitis (EAE), are autoimmune demyelinating diseases of the central nervous system (CNS). Interferon-gamma-producing Th1 and interleukin-17-producing Th17 CD4(+) T helper (Th) cells mediate disease pathogenesis in EAE and likely in MS as well. However, the relative contribution of each Th subset to autoimmune processes in the CNS remains unclear. Emerging data suggest that both Th1 and Th17 cells contribute to CNS autoimmunity, albeit through different mechanisms. A better understanding of the roles that Th1 and Th17 cells play in autoimmune inflammation will be helpful in developing new therapeutic approaches. In this review, we discuss recent findings on the roles of Th1 and Th17 cells in the pathogenesis of EAE.
Authors:
Mohamed El-behi; Abdolmohamad Rostami; Bogoljub Ciric
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Publication Detail:
Type:  Journal Article; Review     Date:  2010-01-27
Journal Detail:
Title:  Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology     Volume:  5     ISSN:  1557-1904     ISO Abbreviation:  J Neuroimmune Pharmacol     Publication Date:  2010 Jun 
Date Detail:
Created Date:  2010-05-10     Completed Date:  2010-08-03     Revised Date:  2011-07-28    
Medline Journal Info:
Nlm Unique ID:  101256586     Medline TA:  J Neuroimmune Pharmacol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  189-97     Citation Subset:  IM    
Affiliation:
Department of Neurology, Thomas Jefferson University, Ste. 300 JHN, 900 Walnut Street, Philadelphia, PA 19107, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
CD4-Positive T-Lymphocytes / metabolism,  physiology*
Encephalomyelitis, Autoimmune, Experimental / immunology*
Humans
Interleukin-17 / biosynthesis,  physiology*
Interleukin-23 / physiology
Receptors, Chemokine / physiology
Th1 Cells / metabolism,  physiology*
Grant Support
ID/Acronym/Agency:
R01 NS046782-05A2/NS/NINDS NIH HHS
Chemical
Reg. No./Substance:
0/Interleukin-17; 0/Interleukin-23; 0/Receptors, Chemokine
Comments/Corrections

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