Source:http://linkedlifedata.com/resource/pubmed/id/16949315
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
3
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| pubmed:dateCreated |
2006-9-18
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| pubmed:abstractText |
In this study, we determined conditions leading to the development of colitis in mice with nucleotide binding oligomerization domain 2 (NOD2) deficiency, a susceptibility factor in Crohn's disease. We found that NOD2-deficient antigen-presenting cells (APCs) produced increased amounts of interleukin (IL)-12 in the presence of ovalbumin (OVA) peptide and peptidoglycan or recombinant E. coli that express OVA peptide (ECOVA). Furthermore, these APCs elicited heightened interferon-gamma (IFN-gamma) responses from cocultured OVA-specific CD4+ T cells. We then demonstrated that NOD2-deficient mice adoptively transferred OVA-specific CD4+ T cells and that administered intrarectal ECOVA developed colitis associated with the expansion of OVA-specific CD4+ T cells producing IFN-gamma. Importantly, this colitis was highly dependent on Toll-like receptor 2 (TLR2) function since it was suppressed in NOD2 and TLR2 double-deficient mice. Thus, NOD2-deficient mice become susceptible to colitis as a result of increased TLR2 responses when they have the capacity to respond to an antigen expressed by mucosal bacteria.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, Bacterial,
http://linkedlifedata.com/resource/pubmed/chemical/Epitopes,
http://linkedlifedata.com/resource/pubmed/chemical/Intracellular Signaling Peptides...,
http://linkedlifedata.com/resource/pubmed/chemical/NOD2 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Nod2 Signaling Adaptor Protein,
http://linkedlifedata.com/resource/pubmed/chemical/TLR2 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Toll-Like Receptor 2
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| pubmed:status |
MEDLINE
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| pubmed:month |
Sep
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| pubmed:issn |
1074-7613
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:volume |
25
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
473-85
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| pubmed:dateRevised |
2008-5-13
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| pubmed:meshHeading |
pubmed-meshheading:16949315-Animals,
pubmed-meshheading:16949315-Antigen-Presenting Cells,
pubmed-meshheading:16949315-Antigens, Bacterial,
pubmed-meshheading:16949315-Cells, Cultured,
pubmed-meshheading:16949315-Colitis,
pubmed-meshheading:16949315-Epitopes,
pubmed-meshheading:16949315-Humans,
pubmed-meshheading:16949315-Inflammatory Bowel Diseases,
pubmed-meshheading:16949315-Intestinal Mucosa,
pubmed-meshheading:16949315-Intracellular Signaling Peptides and Proteins,
pubmed-meshheading:16949315-Male,
pubmed-meshheading:16949315-Mice,
pubmed-meshheading:16949315-Mice, Knockout,
pubmed-meshheading:16949315-Mice, Transgenic,
pubmed-meshheading:16949315-Nod2 Signaling Adaptor Protein,
pubmed-meshheading:16949315-Protein Structure, Tertiary,
pubmed-meshheading:16949315-Signal Transduction,
pubmed-meshheading:16949315-Toll-Like Receptor 2
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| pubmed:year |
2006
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| pubmed:articleTitle |
Nucleotide binding oligomerization domain 2 deficiency leads to dysregulated TLR2 signaling and induction of antigen-specific colitis.
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| pubmed:affiliation |
Mucosal Immunity Section, Laboratory of Host Defenses, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Building 10-CRC, Room 5W3940, 10 Center Drive, Bethesda, Maryland 20892, USA.
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| pubmed:publicationType |
Journal Article
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