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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
1
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pubmed:dateCreated |
2011-7-4
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pubmed:abstractText |
The pathogenesis of inflammatory bowel disease (IBD) is believed to involve an altered balance between effector and regulatory T cells. Aryl hydrocarbon receptor (AhR), a ligand-dependent transcription factor that mediates the toxicity of dioxins, controls T-cell responses. We investigated the role of AhR in inflammation and pathogenesis of IBD in humans and mouse models.
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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/6-formylindolo(3,2-b)carbazole,
http://linkedlifedata.com/resource/pubmed/chemical/AHR protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Ahr protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Basic Helix-Loop-Helix...,
http://linkedlifedata.com/resource/pubmed/chemical/Carbazoles,
http://linkedlifedata.com/resource/pubmed/chemical/Dextran Sulfate,
http://linkedlifedata.com/resource/pubmed/chemical/Inflammation Mediators,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukins,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Aryl Hydrocarbon,
http://linkedlifedata.com/resource/pubmed/chemical/Trinitrobenzenesulfonic Acid,
http://linkedlifedata.com/resource/pubmed/chemical/interleukin-22
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pubmed:status |
MEDLINE
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pubmed:month |
Jul
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pubmed:issn |
1528-0012
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pubmed:author |
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pubmed:copyrightInfo |
Copyright © 2011 AGA Institute. Published by Elsevier Inc. All rights reserved.
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pubmed:issnType |
Electronic
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pubmed:volume |
141
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
237-48, 248.e1
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pubmed:meshHeading |
pubmed-meshheading:21600206-Adult,
pubmed-meshheading:21600206-Animals,
pubmed-meshheading:21600206-Basic Helix-Loop-Helix Transcription Factors,
pubmed-meshheading:21600206-Biopsy,
pubmed-meshheading:21600206-Carbazoles,
pubmed-meshheading:21600206-Case-Control Studies,
pubmed-meshheading:21600206-Cells, Cultured,
pubmed-meshheading:21600206-Dextran Sulfate,
pubmed-meshheading:21600206-Disease Models, Animal,
pubmed-meshheading:21600206-Dose-Response Relationship, Drug,
pubmed-meshheading:21600206-Female,
pubmed-meshheading:21600206-Flow Cytometry,
pubmed-meshheading:21600206-Humans,
pubmed-meshheading:21600206-Inflammation Mediators,
pubmed-meshheading:21600206-Inflammatory Bowel Diseases,
pubmed-meshheading:21600206-Interleukins,
pubmed-meshheading:21600206-Intestines,
pubmed-meshheading:21600206-Mice,
pubmed-meshheading:21600206-Mice, Inbred BALB C,
pubmed-meshheading:21600206-Middle Aged,
pubmed-meshheading:21600206-Polymerase Chain Reaction,
pubmed-meshheading:21600206-Receptors, Aryl Hydrocarbon,
pubmed-meshheading:21600206-Severity of Illness Index,
pubmed-meshheading:21600206-Signal Transduction,
pubmed-meshheading:21600206-T-Lymphocytes,
pubmed-meshheading:21600206-Time Factors,
pubmed-meshheading:21600206-Trinitrobenzenesulfonic Acid,
pubmed-meshheading:21600206-Up-Regulation
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pubmed:year |
2011
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pubmed:articleTitle |
Aryl hydrocarbon receptor-induced signals up-regulate IL-22 production and inhibit inflammation in the gastrointestinal tract.
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pubmed:affiliation |
Dipartimento di Medicina Interna, Università Tor Vergata, Rome, Italy. ivan.monteleone@uniroma2.it
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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