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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
24
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pubmed:dateCreated |
2003-12-3
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pubmed:abstractText |
The ability of a remedy to modulate the pathological process in the target organ is crucial for its therapeutic activity. Glatiramer acetate (GA, Copaxone, Copolymer 1), a drug approved for the treatment of multiple sclerosis, induces regulatory T helper 2/3 cells that penetrate the CNS. Here we investigated whether these GA-specific T cells can function as suppressor cells with therapeutic potential in the target organ by in situ expression of T helper 2/3 cytokines and neurotrophic factors. GA-specific cells and their in situ expression were detected on the level of whole-brain tissue by using a two-stage double-labeling system: (i) labeling of the GA-specific T cells, followed by their adoptive transfer, and (ii) detection of the secreted factors in the brain by immunohistological methods. GA-specific T cells in the CNS demonstrated intense expression of the brain-derived neurotrophic factor and of two antiinflammatory cytokines, IL-10 and transforming growth factor beta. No expression of the inflammatory cytokine IFN-gamma was observed. This pattern of expression was manifested in brains of normal and experimental autoimmune encephalomyelitis-induced mice to which GA-specific cells were adoptively transferred, but not in control mice. Furthermore, infiltration of GA-induced cells to the brain resulted in bystander expression of IL-10 and transforming growth factor beta by resident astrocytes and microglia. The ability of infiltrating GA-specific cells to express antiinflammatory cytokines and neurotrophic factor in the organ in which the pathological processes occur correlates directly with the therapeutic activity of GA in experimental autoimmune encephalomyelitis/multiple sclerosis.
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/14614135,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14614135-10571670,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14614135-10719355,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14614135-10749576,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14614135-10861010,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14614135-11027347,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14614135-11371357,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14614135-11834594,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14614135-11921201,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14614135-12020957,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14614135-12390966,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14614135-12791309,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14614135-1527389,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14614135-7570017,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14614135-7880387,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14614135-9009184,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14614135-9119972,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14614135-9212104,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14614135-9380718,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14614135-9394808,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14614135-9846830
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Nov
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pubmed:issn |
0027-8424
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
25
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pubmed:volume |
100
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
14157-62
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:14614135-Adoptive Transfer,
pubmed-meshheading:14614135-Animals,
pubmed-meshheading:14614135-Brain,
pubmed-meshheading:14614135-Brain-Derived Neurotrophic Factor,
pubmed-meshheading:14614135-Cytokines,
pubmed-meshheading:14614135-Encephalomyelitis, Autoimmune, Experimental,
pubmed-meshheading:14614135-Female,
pubmed-meshheading:14614135-Humans,
pubmed-meshheading:14614135-Immunohistochemistry,
pubmed-meshheading:14614135-Immunosuppressive Agents,
pubmed-meshheading:14614135-Interferon-gamma,
pubmed-meshheading:14614135-Interleukin-10,
pubmed-meshheading:14614135-Mice,
pubmed-meshheading:14614135-Mice, Inbred BALB C,
pubmed-meshheading:14614135-Multiple Sclerosis,
pubmed-meshheading:14614135-Peptides,
pubmed-meshheading:14614135-T-Lymphocyte Subsets,
pubmed-meshheading:14614135-T-Lymphocytes, Helper-Inducer,
pubmed-meshheading:14614135-Th2 Cells,
pubmed-meshheading:14614135-Transforming Growth Factor beta
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pubmed:year |
2003
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pubmed:articleTitle |
Glatiramer acetate-specific T cells in the brain express T helper 2/3 cytokines and brain-derived neurotrophic factor in situ.
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pubmed:affiliation |
Department of Immunology, The Weizmann Institute, Rehovot 76100, Israel.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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