| Characterization of the interaction between astrocytes and encephalitogenic lymphocytes during the development of experimental autoimmune encephalitomyelitis (EAE) in mice. | |
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MedLine Citation:
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PMID: 23121666 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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. |
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Authors:
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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:
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Type: Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Clinical and experimental immunology Volume: 170 ISSN: 1365-2249 ISO Abbreviation: Clin. Exp. Immunol. Publication Date: 2012 Dec |
Date Detail:
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Created Date: 2012-11-05 Completed Date: 2013-01-08 Revised Date: 2013-04-16 |
Medline Journal Info:
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Nlm Unique ID: 0057202 Medline TA: Clin Exp Immunol Country: England |
Other Details:
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Languages: eng Pagination: 254-65 Citation Subset: IM |
Copyright Information:
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© 2012 British Society for Immunology. |
Affiliation:
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Department of Neurobiology, Harbin Medical University Provincial Key Lab of Neurobiology, Harbin Medical University, Harbin, China. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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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:
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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 |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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