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rdf:type |
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lifeskim:mentions |
umls-concept:C0014063,
umls-concept:C0021467,
umls-concept:C0021469,
umls-concept:C0030956,
umls-concept:C0040690,
umls-concept:C0205369,
umls-concept:C0255732,
umls-concept:C0441712,
umls-concept:C0678889,
umls-concept:C1280500,
umls-concept:C1314939,
umls-concept:C1417683
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pubmed:issue |
1-2
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pubmed:dateCreated |
2000-8-25
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pubmed:abstractText |
Transforming growth factor (TGF)-beta exerts a counter-regulatory effect on interleukin (IL)-12-mediated immune modulation. The underlying mechanism is not fully understood. Here we demonstrate that the expression of IL-12Rbeta1 and IL-12Rbeta2 in MBP peptide Ac1-11-primed splenocytes is upregulated upon antigen stimulation. TGF-beta induces an unresponsiveness of these primed splenocytes to IL-12 signaling through a mechanism involved in inhibition of both IL-12Rbeta1 and beta2. The modulation of IL-12Rbeta1 and beta2 expression by Ac1-11 stimulation and TGF-beta is mainly involved in CD4+ population. These data indicate that both IL-12Rbeta1 and IL-12Rbeta2 expression are crucial during T cell activation. TGF-beta-induced inhibition of IL-12R expression will reduce cellular immune responses during IL-12-mediated autoimmune disease.
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pubmed:grant |
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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 |
http://linkedlifedata.com/resource/pubmed/chemical/Autoantigens,
http://linkedlifedata.com/resource/pubmed/chemical/Il12rb1 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Il12rb2 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Interferon-gamma,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-12,
http://linkedlifedata.com/resource/pubmed/chemical/Myelin Basic Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Peptide Fragments,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Interleukin,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Interleukin-12,
http://linkedlifedata.com/resource/pubmed/chemical/Transforming Growth Factor beta
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pubmed:status |
MEDLINE
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pubmed:month |
Aug
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pubmed:issn |
0165-5728
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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 |
108
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
53-63
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:10900337-Animals,
pubmed-meshheading:10900337-Autoantigens,
pubmed-meshheading:10900337-Autoimmune Diseases,
pubmed-meshheading:10900337-CD4-Positive T-Lymphocytes,
pubmed-meshheading:10900337-Cells, Cultured,
pubmed-meshheading:10900337-Female,
pubmed-meshheading:10900337-Gene Expression Regulation,
pubmed-meshheading:10900337-Interferon-gamma,
pubmed-meshheading:10900337-Interleukin-12,
pubmed-meshheading:10900337-Lymphocyte Activation,
pubmed-meshheading:10900337-Mice,
pubmed-meshheading:10900337-Mice, Inbred Strains,
pubmed-meshheading:10900337-Myelin Basic Proteins,
pubmed-meshheading:10900337-Peptide Fragments,
pubmed-meshheading:10900337-RNA, Messenger,
pubmed-meshheading:10900337-Receptors, Interleukin,
pubmed-meshheading:10900337-Receptors, Interleukin-12,
pubmed-meshheading:10900337-Spleen,
pubmed-meshheading:10900337-Transforming Growth Factor beta
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pubmed:year |
2000
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pubmed:articleTitle |
The suppressive effect of TGF-beta on IL-12-mediated immune modulation specific to a peptide Ac1-11 of myelin basic protein (MBP): a mechanism involved in inhibition of both IL-12 receptor beta1 and beta2.
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pubmed:affiliation |
Department of Neurology, University of Pennsylvania Medical Center, 3400 Spruce Street, Philadelphia, PA 19104, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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