http://purl.uniprot.org/cit... | rdf:type | uniprot:Journal_Citation | lld:uniprot |
http://purl.uniprot.org/cit... | rdfs:comment | The mechanism by which mutations in CARD15, which encodes nucleotide-binding oligomerization domain 2 (NOD2), cause Crohn disease is poorly understood. Because signaling via mutated NOD2 proteins leads to defective activation of the transcription factor NF-kappa B, one proposal is that mutations cause deficient NF-kappa B-dependent T helper type 1 (T(H)1) responses and increased susceptibility to infection. However, this idea is inconsistent with the increased T(H)1 responses characteristic of Crohn disease. Here we used Card15(-/-) mice to show that intact NOD2 signaling inhibited Toll-like receptor 2-driven activation of NF-kappa B, particularly of the NF-kappa B subunit c-Rel. Moreover, NOD2 deficiency or the presence of a Crohn disease-like Card15 mutation increased Toll-like receptor 2-mediated activation of NF-kappa B-c-Rel, and T(H)1 responses were enhanced. Thus, CARD15 mutations may lead to disease by causing excessive T(H)1 responses. | lld:uniprot |
http://purl.uniprot.org/cit... | skos:exactMatch | http://purl.uniprot.org/pub... | lld:uniprot |
http://purl.uniprot.org/cit... | uniprot:name | Nat. Immunol. | lld:uniprot |
http://purl.uniprot.org/cit... | uniprot:author | Watanabe T. | lld:uniprot |
http://purl.uniprot.org/cit... | uniprot:author | Strober W. | lld:uniprot |
http://purl.uniprot.org/cit... | uniprot:author | Murray P.J. | lld:uniprot |
http://purl.uniprot.org/cit... | uniprot:author | Kitani A. | lld:uniprot |
http://purl.uniprot.org/cit... | uniprot:date | 2004 | lld:uniprot |
http://purl.uniprot.org/cit... | uniprot:pages | 800-808 | lld:uniprot |
http://purl.uniprot.org/cit... | uniprot:title | NOD2 is a negative regulator of Toll-like receptor 2-mediated T helper type 1 responses. | lld:uniprot |
http://purl.uniprot.org/cit... | uniprot:volume | 5 | lld:uniprot |
http://purl.uniprot.org/cit... | dc-term:identifier | doi:10.1038/ni1092 | lld:uniprot |
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