| pubmed-article:16374251 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:16374251 | lifeskim:mentions | umls-concept:C0012634 | lld:lifeskim |
| pubmed-article:16374251 | lifeskim:mentions | umls-concept:C0021390 | lld:lifeskim |
| pubmed-article:16374251 | lifeskim:mentions | umls-concept:C0231448 | lld:lifeskim |
| pubmed-article:16374251 | lifeskim:mentions | umls-concept:C1882417 | lld:lifeskim |
| pubmed-article:16374251 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:16374251 | pubmed:dateCreated | 2005-12-23 | lld:pubmed |
| pubmed-article:16374251 | pubmed:abstractText | Evidence that a deficient innate immune response toward the bacterial flora of the gut plays a role in the pathogenesis of inflammatory bowel disease (IBD) is growing. This is underscored by the finding of the association between CARD15 variants and Crohn's disease (CD) and D299G in Toll-like receptor (TLR) 4 and IBD. Our aims were to study nonsynonymous polymorphisms in other TLR genes in IBD. | lld:pubmed |
| pubmed-article:16374251 | pubmed:language | eng | lld:pubmed |
| pubmed-article:16374251 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16374251 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:16374251 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:16374251 | pubmed:month | Jan | lld:pubmed |
| pubmed-article:16374251 | pubmed:issn | 1078-0998 | lld:pubmed |
| pubmed-article:16374251 | pubmed:author | pubmed-author:RutgeertsPaul... | lld:pubmed |
| pubmed-article:16374251 | pubmed:author | pubmed-author:VlietinckRobe... | lld:pubmed |
| pubmed-article:16374251 | pubmed:author | pubmed-author:JoossensSofie... | lld:pubmed |
| pubmed-article:16374251 | pubmed:author | pubmed-author:VermeireSever... | lld:pubmed |
| pubmed-article:16374251 | pubmed:author | pubmed-author:Van... | lld:pubmed |
| pubmed-article:16374251 | pubmed:author | pubmed-author:PierikMarieM | lld:pubmed |
| pubmed-article:16374251 | pubmed:author | pubmed-author:Van... | lld:pubmed |
| pubmed-article:16374251 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:16374251 | pubmed:volume | 12 | lld:pubmed |
| pubmed-article:16374251 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:16374251 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:16374251 | pubmed:pagination | 1-8 | lld:pubmed |
| pubmed-article:16374251 | pubmed:dateRevised | 2008-5-13 | lld:pubmed |
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| pubmed-article:16374251 | pubmed:year | 2006 | lld:pubmed |
| pubmed-article:16374251 | pubmed:articleTitle | Toll-like receptor-1, -2, and -6 polymorphisms influence disease extension in inflammatory bowel diseases. | lld:pubmed |
| pubmed-article:16374251 | pubmed:affiliation | Department of Gastroenterology, University Hospital Gasthuisberg, Leuven, Belgium. Marieke.Pierik@uz.kuleuven.ac.be | lld:pubmed |
| pubmed-article:16374251 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:16374251 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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