rdf:type |
|
lifeskim:mentions |
umls-concept:C0017337,
umls-concept:C0021467,
umls-concept:C0021469,
umls-concept:C0026809,
umls-concept:C0038952,
umls-concept:C0039194,
umls-concept:C0040300,
umls-concept:C0242184,
umls-concept:C0332161,
umls-concept:C0333348,
umls-concept:C0599894,
umls-concept:C0965644,
umls-concept:C1292733,
umls-concept:C1333897,
umls-concept:C1442161,
umls-concept:C1521840,
umls-concept:C1704838
|
pubmed:issue |
9
|
pubmed:dateCreated |
2007-9-5
|
pubmed:abstractText |
Sepsis patients may die either from an overwhelming systemic immune response and/or from an immunoparalysis-associated lack of anti-bacterial immune defence. We hypothesized that bacterial superantigen-activated T cells may be prevented from contribution into anti-bacterial response due to the inhibition of their effector functions by the hypoxia inducible transcription factor (HIF-1alpha) in inflamed and hypoxic areas.
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pubmed:grant |
|
pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/17786224-10395324,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17786224-10569781,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17786224-10611972,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17786224-11714773,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17786224-11780065,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17786224-11854513,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17786224-12482987,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17786224-12628185,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17786224-12668645,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17786224-12787889,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17786224-15032592,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17786224-15630139,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17786224-15857155,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17786224-16110315,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17786224-16155188,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17786224-16172258,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17786224-16330813,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17786224-16950761,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17786224-16971487,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17786224-17015677,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17786224-1740105,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17786224-8016642,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17786224-8627516,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17786224-9143706,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17786224-9697772
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pubmed:language |
eng
|
pubmed:journal |
|
pubmed:citationSubset |
IM
|
pubmed:chemical |
|
pubmed:status |
MEDLINE
|
pubmed:issn |
1932-6203
|
pubmed:author |
|
pubmed:issnType |
Electronic
|
pubmed:volume |
2
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
e853
|
pubmed:dateRevised |
2011-9-26
|
pubmed:meshHeading |
pubmed-meshheading:17786224-Animals,
pubmed-meshheading:17786224-Anoxia,
pubmed-meshheading:17786224-Flow Cytometry,
pubmed-meshheading:17786224-Hypoxia-Inducible Factor 1, alpha Subunit,
pubmed-meshheading:17786224-Lymphocyte Activation,
pubmed-meshheading:17786224-Mice,
pubmed-meshheading:17786224-NF-kappa B,
pubmed-meshheading:17786224-Peritonitis,
pubmed-meshheading:17786224-Reverse Transcriptase Polymerase Chain Reaction,
pubmed-meshheading:17786224-Sepsis,
pubmed-meshheading:17786224-Survival Rate,
pubmed-meshheading:17786224-T-Lymphocytes
|
pubmed:year |
2007
|
pubmed:articleTitle |
Targeted deletion of HIF-1alpha gene in T cells prevents their inhibition in hypoxic inflamed tissues and improves septic mice survival.
|
pubmed:affiliation |
Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, United States of America.
|
pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
|