Source:http://linkedlifedata.com/resource/pubmed/id/15153463
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rdf:type | |
lifeskim:mentions |
umls-concept:C0021756,
umls-concept:C0039194,
umls-concept:C0152060,
umls-concept:C0205154,
umls-concept:C0542341,
umls-concept:C1306235,
umls-concept:C1332714,
umls-concept:C1334114,
umls-concept:C1514873,
umls-concept:C1533691,
umls-concept:C1546857,
umls-concept:C1556066,
umls-concept:C1619636,
umls-concept:C1879547,
umls-concept:C2003905
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pubmed:issue |
11
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pubmed:dateCreated |
2004-5-21
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pubmed:abstractText |
CD4(+)CD25(+) T cells are potent immunoregulatory cells that suppress TCR-induced proliferation of CD4 and CD8 T cells in vitro by a cell contact-dependent mechanism. Addition of IL-2 or anti-CD28 abrogates CD4(+)CD25(+)-mediated suppression of proliferation and has been assumed to "break suppression." We examined IL-2 mRNA by quantitative PCR in cocultures of mouse CD4(+)CD25(+) and CD4(+)CD25(-) T cells. Although IL-2 gene transcription was inhibited in the presence or absence of exogenous IL-2, the addition of anti-CD28 stimulated endogenous IL-2 production. Surprisingly, transcription of IL-2 mRNA was also restored in the cocultures in the presence of anti-IL-2. These results are most compatible with a model in which CD4(+)CD25(+) T cells do not suppress the initial activation of CD4(+)CD25(-) T cells, but mediate their suppressive effects following production of IL-2 by the responder cells resulting in both the expansion of the CD4(+)CD25(+) T cells and the induction of their suppressor function.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD28,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD4,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-2,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Interleukin-2
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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 | |
pubmed:issnType |
Print
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pubmed:day |
1
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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 |
6519-23
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pubmed:dateRevised |
2005-11-17
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pubmed:meshHeading |
pubmed-meshheading:15153463-Animals,
pubmed-meshheading:15153463-Antigens, CD28,
pubmed-meshheading:15153463-Antigens, CD4,
pubmed-meshheading:15153463-Female,
pubmed-meshheading:15153463-Interleukin-2,
pubmed-meshheading:15153463-Lymphocyte Activation,
pubmed-meshheading:15153463-Mice,
pubmed-meshheading:15153463-Mice, Inbred BALB C,
pubmed-meshheading:15153463-RNA, Messenger,
pubmed-meshheading:15153463-Receptors, Interleukin-2,
pubmed-meshheading:15153463-T-Lymphocytes, Regulatory
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pubmed:year |
2004
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pubmed:articleTitle |
Cutting edge: IL-2 is critically required for the in vitro activation of CD4+CD25+ T cell suppressor function.
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pubmed:affiliation |
Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA. athornton@niaid.nih.gov
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pubmed:publicationType |
Journal Article
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