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

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

Research output: Contribution to journalArticlepeer-review

105 Citations (Scopus)

Abstract

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 receptor 4 ligand (TLR4, lipopolysaccharide) stimulation. Intestinal TLR signalling has a dual role-maintaining intestinal homeostasis and protection from injury as well as initiating inflammatory responses. TLR9 is functional in the intestinal epithelium where it is most strongly expressed in Paneth cells.
Original languageEnglish
Pages (from-to)1553-7
Number of pages5
JournalGut
Volume54
Issue number11
DOIs
Publication statusPublished - Nov 2005

Keywords

  • Acetylmuramyl-Alanyl-Isoglutamine
  • Adult
  • Blotting, Western
  • Cells, Cultured
  • CpG Islands
  • Crohn Disease
  • Drug Synergism
  • Enzyme-Linked Immunosorbent Assay
  • Female
  • Humans
  • Immunity, Mucosal
  • Interleukin-8
  • Intestinal Mucosa
  • Intracellular Signaling Peptides and Proteins
  • Ligands
  • Male
  • Membrane Glycoproteins
  • Middle Aged
  • Mutation
  • Nod2 Signaling Adaptor Protein
  • Receptors, Cell Surface
  • Reverse Transcriptase Polymerase Chain Reaction
  • Toll-Like Receptor 4
  • Toll-Like Receptor 9
  • Toll-Like Receptors
  • Tumor Necrosis Factor-alpha

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