Source:http://linkedlifedata.com/resource/pubmed/id/11548979
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
4
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pubmed:dateCreated |
2001-9-10
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pubmed:abstractText |
Glatiromer acetate (GA) is an approved treatment for multiple sclerosis (MS). The proposed mechanism of action is the induction of GA-specific T cells characterized by protective anti-inflammatory Th2 response. We tested this hypothesis in 11 MS patients treated with GA from 1-19 months. Interferon-gamma and IL-5 (markers of Th1 and Th2 responses respectively) were assayed by ELISA in GA-specific T-cell lines (TCL) supernatants. Th1/Th2 bias was defined based on the ratio of IFN-gamma/IL-5 secretion. Fifty-eight pre-treatment and 75 on-treatment GA-specific TCL were generated. On-treatment mean IL-5 levels in GA-TCL increased significantly, whereas those for IFN-gamma were markedly reduced. Consequently, the ratio of IFN-gamma IL-5 also shifted in favor of a Th2 response. The percentage of GA-TCL classified as Th1 was decreased, whereas those classified as Th2 increased on-treatment as compared to pre-treatment. Some GA-specific TCL, (approximately 25%) generated during treatment secreted predominantly IL-5 in response to MBP and the immunodominant MBP peptide 83-99, indicating that these crossreactive antigens can act as partial agonists for GA-reactive TCL. These results strongly suggest that the mechanism of action of GA in MS involves the induction of crossreactive GA-specific T cells with a predominant Th2 cytokine profile.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Cytokines,
http://linkedlifedata.com/resource/pubmed/chemical/Immunosuppressive Agents,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-5,
http://linkedlifedata.com/resource/pubmed/chemical/Myelin Basic Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Peptides,
http://linkedlifedata.com/resource/pubmed/chemical/copolymer 1
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pubmed:status |
MEDLINE
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pubmed:month |
Aug
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pubmed:issn |
1352-4585
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
7
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
209-19
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:11548979-Cell Line,
pubmed-meshheading:11548979-Cross Reactions,
pubmed-meshheading:11548979-Cytokines,
pubmed-meshheading:11548979-Enzyme-Linked Immunosorbent Assay,
pubmed-meshheading:11548979-Humans,
pubmed-meshheading:11548979-Immunosuppressive Agents,
pubmed-meshheading:11548979-Interleukin-5,
pubmed-meshheading:11548979-Multiple Sclerosis,
pubmed-meshheading:11548979-Myelin Basic Proteins,
pubmed-meshheading:11548979-Peptides,
pubmed-meshheading:11548979-Regression Analysis,
pubmed-meshheading:11548979-T-Lymphocytes,
pubmed-meshheading:11548979-Th2 Cells
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pubmed:year |
2001
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pubmed:articleTitle |
Glatiramer acetate induces a Th2-biased response and crossreactivity with myelin basic protein in patients with MS.
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pubmed:affiliation |
University of Maryland School of Medicine, Baltimore 21201, USA.
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pubmed:publicationType |
Journal Article,
Clinical Trial,
Research Support, U.S. Gov't, P.H.S.,
Research Support, U.S. Gov't, Non-P.H.S.,
Controlled Clinical Trial,
Research Support, Non-U.S. Gov't
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