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rdf:type |
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lifeskim:mentions |
umls-concept:C0013018,
umls-concept:C0017950,
umls-concept:C0039194,
umls-concept:C0205263,
umls-concept:C0851285,
umls-concept:C0856825,
umls-concept:C0946292,
umls-concept:C1167395,
umls-concept:C1883254,
umls-concept:C1948023,
umls-concept:C2350466
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pubmed:issue |
1
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pubmed:dateCreated |
2004-12-21
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pubmed:abstractText |
NKT cells are a unique immunoregulatory T cell population that produces large amounts of cytokines. We have investigated whether stimulation of host NKT cells could modulate acute graft-vs-host disease (GVHD) in mice. Injection of the synthetic NKT cell ligand alpha-galactosylceramide (alpha-GalCer) to recipient mice on day 0 following allogeneic bone marrow transplantation promoted Th2 polarization of donor T cells and a dramatic reduction of serum TNF-alpha, a critical mediator of GVHD. A single injection of alpha-GalCer to recipient mice significantly reduced morbidity and mortality of GVHD. However, the same treatment was unable to confer protection against GVHD in NKT cell-deficient CD1d knockout (CD1d(-/-)) or IL-4(-/-) recipient mice or when STAT6(-/-) mice were used as donors, indicating the critical role of host NKT cells, host production of IL-4, and Th2 cytokine responses mediated by donor T cells on the protective effects of alpha-GalCer against GVHD. Thus, stimulation of host NKT cells through administration of NKT ligand can regulate acute GVHD by inducing Th2 polarization of donor T cells via STAT6-dependent mechanisms and might represent a novel strategy for prevention of acute GVHD.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD1,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD1d,
http://linkedlifedata.com/resource/pubmed/chemical/Galactosylceramides,
http://linkedlifedata.com/resource/pubmed/chemical/Glycolipids,
http://linkedlifedata.com/resource/pubmed/chemical/STAT6 Transcription Factor,
http://linkedlifedata.com/resource/pubmed/chemical/Stat6 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Trans-Activators,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha,
http://linkedlifedata.com/resource/pubmed/chemical/alpha-galactosylceramide
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pubmed:status |
MEDLINE
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pubmed:month |
Jan
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pubmed:issn |
0022-1767
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
1
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pubmed:volume |
174
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
551-6
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:15611282-Animals,
pubmed-meshheading:15611282-Antigens, CD1,
pubmed-meshheading:15611282-Antigens, CD1d,
pubmed-meshheading:15611282-Bone Marrow Transplantation,
pubmed-meshheading:15611282-Enzyme-Linked Immunosorbent Assay,
pubmed-meshheading:15611282-Female,
pubmed-meshheading:15611282-Flow Cytometry,
pubmed-meshheading:15611282-Galactosylceramides,
pubmed-meshheading:15611282-Glycolipids,
pubmed-meshheading:15611282-Graft vs Host Disease,
pubmed-meshheading:15611282-Mice,
pubmed-meshheading:15611282-Mice, Knockout,
pubmed-meshheading:15611282-STAT6 Transcription Factor,
pubmed-meshheading:15611282-T-Lymphocyte Subsets,
pubmed-meshheading:15611282-T-Lymphocytes,
pubmed-meshheading:15611282-Th2 Cells,
pubmed-meshheading:15611282-Trans-Activators,
pubmed-meshheading:15611282-Tumor Necrosis Factor-alpha
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pubmed:year |
2005
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pubmed:articleTitle |
Stimulation of host NKT cells by synthetic glycolipid regulates acute graft-versus-host disease by inducing Th2 polarization of donor T cells.
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pubmed:affiliation |
Biopathological Science, Okayama University Graduate School of Medicine and Dentistry, Okayama, Japan.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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