Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Synergy between TLR9 and NOD2 innate immune responses is lost in genetic Crohn's disease.

Gut - 1 Nov 2005

van Heel D A, Ghosh S, Hunt K A, Mathew C G, Forbes A, Jewell D P, Playford R J

Abstract excerpt

BACKGROUND: Nucleotide binding oligomerisation domain 2 (NOD2; also known as CARD15) mutations are associated with Crohn's disease but how mutations cause disease is poorly understood. Innate immune responses are reportedly enhanced by combined NOD2 ligand (muramyl dipeptide, MDP) and Toll-like r...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Drug Synergism
Share to Immunity, Mucosal
Share to Interleukin-8

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Intestinal Mucosa

Share to Nod2 Signaling Adaptor Protein

Share to Toll-Like Receptor 4

Share to Toll-Like Receptor 9

Share to Toll-Like Receptors

Source

Open in PubMed Open full text

Identifiers

PMID: 15928043
DOI: 10.1136/gut.2005.065888
PMCID: PMC1774767

Genes

NOD2
TLR9
TNF
TLR4

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 2 Sept 2026. Prepared record publication-15928043-2026-09-02.2. Manifest publication-graph-cohort-2026-09-02.2.

Source receipt: PubMed via Helena Literature Corpus, retrieved 2 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Synergy between TLR9 and NOD2 innate immune responses is lost in genetic Crohn's disease.PMID 15928043Read ↗

Toll-like receptor-induced granulocyte-macrophage colony-stimulating factor secretion is impaired in Crohn's disease by nucleotide oligomerization domain 2-dependent and -independent pathways.Semantic proximity Read ↗

Muramyl dipeptide and toll-like receptor sensitivity in NOD2-associated Crohn's disease.Semantic proximity Read ↗

NOD2, an intracellular innate immune sensor involved in host defense and Crohn's disease.Semantic proximity Read ↗

NOD2 mutations affect muramyl dipeptide stimulation of human B lymphocytes and interact with other IBD-associated genes.Semantic proximity Read ↗

Functional consequences of NOD2 (CARD15) mutations.Semantic proximity Read ↗

The molecular basis of NOD2 susceptibility mutations in Crohn's disease.Semantic proximity Read ↗

Normal responses to specific NOD1-activating peptidoglycan agonists in the presence of the NOD2 frameshift and other mutations in Crohn's disease.Semantic proximity Read ↗

Towards an understanding of the role of NOD2/CARD15 in the pathogenesis of Crohn's disease.Semantic proximity Read ↗

Muramyl dipeptide activation of nucleotide-binding oligomerization domain 2 protects mice from experimental colitisSemantic proximity Read ↗

Engagement of NOD2 has a dual effect on proIL-1beta mRNA transcription and secretion of bioactive IL-1beta.Semantic proximity Read ↗

Crohn's disease: a role of gut microbiota and Nod2 gene polymorphisms in disease pathogenesis.Semantic proximity Read ↗

Insights into the molecular basis of the NOD2 signalling pathwaySemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.