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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
5
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pubmed:dateCreated |
2009-2-9
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pubmed:abstractText |
T cell responses are determined by the environment in which antigen is encountered. In the absence of proper costimulation, anergizing stimuli induce the activation of a specific program of gene expression. Proteins encoded by these genes impose a state of functional unresponsiveness in anergic T cells through the activation of different mechanisms that include dampening of the T cell receptor signaling and direct inhibition of cytokine expression. Anergy can be reversed by stimulating T cells in the presence of interleukin (IL-)2. Signaling through the IL-2 receptor has been shown to activate mTOR, which plays an important role in the integration of signals that determine the fate of T cells. The mechanisms underlying the IL-2-dependent regulation of T cell tolerance are still not fully elucidated. In this study we show that IL-2 receptor signaling mediated through JAK3 and mTOR inhibits the expression of anergy-inducing genes independently of any effect on cell cycle progression. Interestingly, we also show that this effect is likely due to changes on the levels of AP-1 activation induced by IL-2 receptor signaling in T cells. Our data identifies a mechanism that can explain how IL-2 may prevent or reverse the establishment of anergy in T cells and, therefore, helps to understand how the cytokine environment can be determinant to shape the outcome of T cell responses - tolerance or activation - when antigen is encountered.
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pubmed:grant |
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/18990450-10072524,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18990450-10201984,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18990450-10605005,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18990450-10970869,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18990450-11356007,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18990450-11745394,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18990450-11750878,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18990450-12086671,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18990450-12172553,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18990450-12271141,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18990450-12444122,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18990450-12471050,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18990450-12705856,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18990450-12869586,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18990450-14527511,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18990450-14661020,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18990450-14973438,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18990450-15023415,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18990450-15067056,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18990450-15210761,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18990450-15238074,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18990450-15308098,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18990450-15347678,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18990450-15585857,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18990450-15834410,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18990450-15928679,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18990450-15999806,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18990450-16493028,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18990450-16581297,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18990450-17013388,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18990450-17028587,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18990450-17028589,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18990450-17114425,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18990450-17148585,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18990450-17277121,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18990450-17383196,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18990450-17387022,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18990450-17400472,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18990450-17612584,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18990450-18025173,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18990450-18203138,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18990450-2153162,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18990450-3035012,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18990450-7973657
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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/Interleukin-2,
http://linkedlifedata.com/resource/pubmed/chemical/Jak3 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Janus Kinase 3,
http://linkedlifedata.com/resource/pubmed/chemical/Protein Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Interleukin-2,
http://linkedlifedata.com/resource/pubmed/chemical/TOR Serine-Threonine Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/Transcription Factor AP-1,
http://linkedlifedata.com/resource/pubmed/chemical/mTOR protein, mouse
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pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
0161-5890
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
46
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
999-1006
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pubmed:dateRevised |
2011-9-26
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pubmed:meshHeading |
pubmed-meshheading:18990450-Animals,
pubmed-meshheading:18990450-Cell Cycle,
pubmed-meshheading:18990450-Clonal Anergy,
pubmed-meshheading:18990450-Gene Expression Regulation,
pubmed-meshheading:18990450-Interleukin-2,
pubmed-meshheading:18990450-Janus Kinase 3,
pubmed-meshheading:18990450-Mice,
pubmed-meshheading:18990450-Mice, Inbred BALB C,
pubmed-meshheading:18990450-Protein Kinases,
pubmed-meshheading:18990450-Receptors, Interleukin-2,
pubmed-meshheading:18990450-Signal Transduction,
pubmed-meshheading:18990450-T-Lymphocytes,
pubmed-meshheading:18990450-TOR Serine-Threonine Kinases,
pubmed-meshheading:18990450-Transcription Factor AP-1
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pubmed:year |
2009
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pubmed:articleTitle |
IL-2 signaling prevents T cell anergy by inhibiting the expression of anergy-inducing genes.
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pubmed:affiliation |
Department of Pathology, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY 10461, USA.
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pubmed:publicationType |
Journal Article
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