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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
6
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pubmed:dateCreated |
2003-9-8
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pubmed:abstractText |
Notch receptors signal through a highly conserved pathway to influence cell fate decisions. Notch1 is required for T lineage commitment; however, a role for Notch signaling has not been clearly defined for the peripheral T cell response. Notch gene expression is induced, and Notch1 is activated in primary CD4(+) T cells following specific peptide-Ag stimulation. Notch activity contributes to the peripheral T cell response, as inhibition of endogenous Notch activation decreases the proliferation of activated T cells in a manner associated with the diminished production of IL-2 and the expression of the high affinity IL-2R (CD25). Conversely, forced expression of a constitutively active Notch1 in primary T cells results in increased surface expression of CD25, and renders these cells more sensitive to both cognate Ag and IL-2, as measured by cell division. These data suggest an important role for Notch signaling during CD4(+) T cell responses, which operates through augmenting a positive feedback loop involving IL-2 and its high affinity receptor.
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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 |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Adjuvants, Immunologic,
http://linkedlifedata.com/resource/pubmed/chemical/Growth Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-2,
http://linkedlifedata.com/resource/pubmed/chemical/Membrane Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Notch1 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Receptor, Notch1,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Cell Surface,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Interleukin-2,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Notch,
http://linkedlifedata.com/resource/pubmed/chemical/Transcription Factors
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pubmed:status |
MEDLINE
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pubmed:month |
Sep
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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 |
171
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
2896-903
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:12960312-Adjuvants, Immunologic,
pubmed-meshheading:12960312-Animals,
pubmed-meshheading:12960312-CD4-Positive T-Lymphocytes,
pubmed-meshheading:12960312-Cell Division,
pubmed-meshheading:12960312-Cell Membrane,
pubmed-meshheading:12960312-Cells, Cultured,
pubmed-meshheading:12960312-Down-Regulation,
pubmed-meshheading:12960312-Growth Inhibitors,
pubmed-meshheading:12960312-Interleukin-2,
pubmed-meshheading:12960312-Intracellular Fluid,
pubmed-meshheading:12960312-Lymphocyte Activation,
pubmed-meshheading:12960312-Membrane Proteins,
pubmed-meshheading:12960312-Mice,
pubmed-meshheading:12960312-Mice, Inbred BALB C,
pubmed-meshheading:12960312-Mice, Transgenic,
pubmed-meshheading:12960312-Receptor, Notch1,
pubmed-meshheading:12960312-Receptors, Cell Surface,
pubmed-meshheading:12960312-Receptors, Interleukin-2,
pubmed-meshheading:12960312-Receptors, Notch,
pubmed-meshheading:12960312-Retroviridae,
pubmed-meshheading:12960312-Signal Transduction,
pubmed-meshheading:12960312-Transcription Factors,
pubmed-meshheading:12960312-Transduction, Genetic,
pubmed-meshheading:12960312-Up-Regulation
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pubmed:year |
2003
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pubmed:articleTitle |
Notch signaling augments T cell responsiveness by enhancing CD25 expression.
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pubmed:affiliation |
Departments of Medicine, Institute for Medicine and Engineering, The Abramson Family Cancer Research Institute, University of Pennsylvania Medical Center, 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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