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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
12
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pubmed:dateCreated |
2004-6-9
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pubmed:abstractText |
The glucocorticoid-induced TNF receptor (GITR), which is a member of the TNF receptor family, is expressed preferentially at high levels on CD25+CD4+ regulatory T cells and plays a key role in the peripheral tolerance that is mediated by these cells. GITR is also expressed on conventional CD4+ and CD8+ T cells, and its expression is enhanced rapidly after activation. In this report we show that the GITR provides a potent costimulatory signal to both CD25+ and CD25- CD4+ T cells. GITR-mediated stimulation induced by anti-GITR mAb DTA-1 or GITR ligand transfectants efficiently augmented the proliferation of both CD25-CD4+ and CD25+CD4+ T cells under the limited dose of anti-CD3 stimulation. The augmentation of T cell activation was further confirmed by the enhanced cell cycle progression; early induction of the activation Ags, CD69 and CD25; cytokine production, such as IL-2, IFN-gamma, IL-4, and IL-10; anti-CD3-induced redirected cytotoxicity; and intracellular signaling, assessed by translocation of NF-kappaB components. GITR costimulation showed a potent ability to produce high amounts of IL-10, which resulted in counter-regulation of the enhanced proliferative responses. Our results highlight evidence that GITR acts as a potent and unique costimulator for an early CD4+ T cell activation.
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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, CD,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD3,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, Differentiation...,
http://linkedlifedata.com/resource/pubmed/chemical/CD69 antigen,
http://linkedlifedata.com/resource/pubmed/chemical/Cytokines,
http://linkedlifedata.com/resource/pubmed/chemical/Glucocorticoid-Induced...,
http://linkedlifedata.com/resource/pubmed/chemical/Lectins, C-Type,
http://linkedlifedata.com/resource/pubmed/chemical/NF-kappa B,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Interleukin-2,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Nerve Growth Factor,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Tumor Necrosis Factor,
http://linkedlifedata.com/resource/pubmed/chemical/Tnfrsf18 protein, mouse
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pubmed:status |
MEDLINE
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pubmed:month |
Jun
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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 |
15
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pubmed:volume |
172
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
7306-14
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pubmed:dateRevised |
2011-11-17
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pubmed:meshHeading |
pubmed-meshheading:15187106-Animals,
pubmed-meshheading:15187106-Antigens, CD,
pubmed-meshheading:15187106-Antigens, CD3,
pubmed-meshheading:15187106-Antigens, Differentiation, T-Lymphocyte,
pubmed-meshheading:15187106-CD4-Positive T-Lymphocytes,
pubmed-meshheading:15187106-Cell Division,
pubmed-meshheading:15187106-Cell Line, Tumor,
pubmed-meshheading:15187106-Cytokines,
pubmed-meshheading:15187106-Female,
pubmed-meshheading:15187106-Glucocorticoid-Induced TNFR-Related Protein,
pubmed-meshheading:15187106-Lectins, C-Type,
pubmed-meshheading:15187106-Lymphocyte Activation,
pubmed-meshheading:15187106-Mice,
pubmed-meshheading:15187106-Mice, Inbred BALB C,
pubmed-meshheading:15187106-NF-kappa B,
pubmed-meshheading:15187106-Receptors, Interleukin-2,
pubmed-meshheading:15187106-Receptors, Nerve Growth Factor,
pubmed-meshheading:15187106-Receptors, Tumor Necrosis Factor,
pubmed-meshheading:15187106-Signal Transduction,
pubmed-meshheading:15187106-Spleen
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pubmed:year |
2004
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pubmed:articleTitle |
Costimulation via glucocorticoid-induced TNF receptor in both conventional and CD25+ regulatory CD4+ T cells.
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pubmed:affiliation |
Department of Molecular Immunology, Graduate School, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo 113-8549, Japan.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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