Document Detail


Characterization of the interaction between astrocytes and encephalitogenic lymphocytes during the development of experimental autoimmune encephalitomyelitis (EAE) in mice.
MedLine Citation:
PMID:  23121666     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The nature of pathogenic mechanisms associated with the development of multiple sclerosis (MS) have long been debated. However, limited research was conducted to define the interplay between infiltrating lymphocytes and resident cells of the central nervous system (CNS). Data presented in this report describe a novel role for astrocyte-mediated alterations to myelin oligodendrocyte glycoprotein (MOG)(35-55) -specific lymphocyte responses, elicited during the development of experimental autoimmune encephalitomyelitis (EAE). In-vitro studies demonstrated that astrocytes inhibited the proliferation and interferon (IFN)-γ, interleukin (IL)-4, IL-17 and transforming growth factor (TGF)-β secretion levels of MOG(35-55) -specific lymphocytes, an effect that could be ameliorated by astrocyte IL-27 neutralization. However, when astrocytes were pretreated with IFN-γ, they could promote the proliferation and secretion levels of MOG(35-55) -specific lymphocytes, coinciding with apparent expression of major histocompatibility complex (MHC)-II on astrocytes themselves. Quantitative polymerase chain reaction (qPCR) demonstrated that production of IL-27 in the spinal cord was at its highest during the initial phases. Conversely, production of IFN-γ in the spinal cord was highest during the peak phase. Quantitative analysis of MHC-II expression in the spinal cord showed that there was a positive correlation between MHC-II expression and IFN-γ production. In addition, astrocyte MHC-II expression levels correlated positively with IFN-γ production in the spinal cord. These findings suggested that astrocytes might function as both inhibitors and promoters of EAE. Astrocytes prevented MOG(35-55) -specific lymphocyte function by secreting IL-27 during the initial phases of EAE. Then, in the presence of higher IFN-γ levels in the spinal cord, astrocytes were converted into antigen-presenting cells. This conversion might promote the progression of pathological damage and result in a peak of EAE severity.
Authors:
J F Yang; H Q Tao; Y M Liu; X X Zhan; Y Liu; X Y Wang; J H Wang; L L Mu; L L Yang; Z M Gao; Q F Kong; G Y Wang; J H Han; B Sun; H L Li
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Clinical and experimental immunology     Volume:  170     ISSN:  1365-2249     ISO Abbreviation:  Clin. Exp. Immunol.     Publication Date:  2012 Dec 
Date Detail:
Created Date:  2012-11-05     Completed Date:  2013-01-08     Revised Date:  2013-12-04    
Medline Journal Info:
Nlm Unique ID:  0057202     Medline TA:  Clin Exp Immunol     Country:  England    
Other Details:
Languages:  eng     Pagination:  254-65     Citation Subset:  IM    
Copyright Information:
© 2012 British Society for Immunology.
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MeSH Terms
Descriptor/Qualifier:
Animals
Astrocytes / drug effects,  immunology*,  metabolism
Cell Communication / immunology*
Coculture Techniques
Cytokines / biosynthesis
Disease Models, Animal
Encephalomyelitis, Autoimmune, Experimental / genetics,  immunology*
Epitopes / immunology
Female
Gene Expression Regulation / drug effects
Genes, MHC Class II
Interferon-gamma / genetics,  immunology,  pharmacology
Interleukins / biosynthesis,  genetics
Lymphocyte Activation / drug effects,  immunology
Lymphocytes / drug effects,  immunology*,  metabolism
Mice
Mice, Inbred C57BL
Myelin-Oligodendrocyte Glycoprotein / adverse effects,  immunology
Peptide Fragments / adverse effects,  immunology
Spinal Cord / immunology,  metabolism
Chemical
Reg. No./Substance:
0/Cytokines; 0/Epitopes; 0/Il27 protein, mouse; 0/Interleukins; 0/Myelin-Oligodendrocyte Glycoprotein; 0/Peptide Fragments; 0/myelin oligodendrocyte glycoprotein (35-55); 82115-62-6/Interferon-gamma
Comments/Corrections

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