Source:http://linkedlifedata.com/resource/pubmed/id/17917039
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1-3
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pubmed:dateCreated |
2007-10-5
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pubmed:abstractText |
If Th1 or Th2 polarization could be artificially manipulated, effective immune responses would be generated depending on nature of the targets. In this study we attempted to regulate CD40 expressions on dendritic cells (DCs) in order to modify the T cell response. It was found that reducing agents selectively inhibited surface expression of CD40 on DCs. This finding may provide a new strategy of DC-mediated modulation of the Th1/Th2 balance. It was also shown that NKT-produced Th1/Th2 cytokine balance was under control of negative feedback loop through DCs. Th1 cytokine-pretreated DCs mainly induced Th2 cytokine production, whereas Th2 cytokine-pretreated DCs induced Th1 cytokine production by alpha-galactosylceramide-stimulated NKT cells. The negative feedback regulation system could be applicable to therapeutics of various diseases based on immunological disorders.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:issn |
0257-277X
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
38
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
319-32
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:17917039-Animals,
pubmed-meshheading:17917039-Antigens, CD40,
pubmed-meshheading:17917039-Cell Communication,
pubmed-meshheading:17917039-Cytokines,
pubmed-meshheading:17917039-Dendritic Cells,
pubmed-meshheading:17917039-Feedback, Physiological,
pubmed-meshheading:17917039-Galactosylceramides,
pubmed-meshheading:17917039-Killer Cells, Natural,
pubmed-meshheading:17917039-Mice,
pubmed-meshheading:17917039-Th1 Cells,
pubmed-meshheading:17917039-Th2 Cells
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pubmed:year |
2007
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pubmed:articleTitle |
Th1 or Th2 balance regulated by interaction between dendritic cells and NKT cells.
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pubmed:affiliation |
Division of Immunobiology, Institute for Genetic Medicine, Hokkaido University, Kita-15, Nishi-7, Sapporo, 060-0815, Japan. kazunori@igm.hokudai.ac.jp
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pubmed:publicationType |
Journal Article,
Review,
Research Support, Non-U.S. Gov't
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