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

doi:10.1136/gut.2005.065888

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 journal › Article › peer-review

115 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 language	English
Pages (from-to)	1553-7
Number of pages	5
Journal	Gut
Volume	54
Issue number	11
DOIs	https://doi.org/10.1136/gut.2005.065888
Publication status	Published - 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

Access to Document

10.1136/gut.2005.065888

Cite this

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

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.",

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author = "{van Heel}, {D A} and S Ghosh and Hunt, {K A} and Mathew, {C G} and A Forbes and Jewell, {D P} and Playford, {R J}",

year = "2005",

month = nov,

doi = "10.1136/gut.2005.065888",

language = "English",

volume = "54",

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T1 - Synergy between TLR9 and NOD2 innate immune responses is lost in genetic Crohn's disease

AU - van Heel, D A

AU - Ghosh, S

AU - Hunt, K A

AU - Mathew, C G

AU - Forbes, A

AU - Jewell, D P

AU - Playford, R J

PY - 2005/11

Y1 - 2005/11

N2 - 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.

AB - 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.

KW - Acetylmuramyl-Alanyl-Isoglutamine

KW - Adult

KW - Blotting, Western

KW - Cells, Cultured

KW - CpG Islands

KW - Crohn Disease

KW - Drug Synergism

KW - Enzyme-Linked Immunosorbent Assay

KW - Female

KW - Humans

KW - Immunity, Mucosal

KW - Interleukin-8

KW - Intestinal Mucosa

KW - Intracellular Signaling Peptides and Proteins

KW - Ligands

KW - Male

KW - Membrane Glycoproteins

KW - Middle Aged

KW - Mutation

KW - Nod2 Signaling Adaptor Protein

KW - Receptors, Cell Surface

KW - Reverse Transcriptase Polymerase Chain Reaction

KW - Toll-Like Receptor 4

KW - Toll-Like Receptor 9

KW - Toll-Like Receptors

KW - Tumor Necrosis Factor-alpha

U2 - 10.1136/gut.2005.065888

DO - 10.1136/gut.2005.065888

M3 - Article

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VL - 54

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EP - 1557

JO - Gut

JF - Gut

SN - 0017-5749

IS - 11

ER -