Publication Date:
2005-02-05
Description:
The gene encoding the Nod2 protein is frequently mutated in Crohn's disease (CD) patients, although the physiological function of Nod2 in the intestine remains elusive. Here we show that protective immunity mediated by Nod2 recognition of bacterial muramyl dipeptide is abolished in Nod2-deficient mice. These animals are susceptible to bacterial infection via the oral route but not through intravenous or peritoneal delivery. Nod2 is required for the expression of a subgroup of intestinal anti-microbial peptides, known as cryptdins. The Nod2 protein is thus a critical regulator of bacterial immunity within the intestine, providing a possible mechanism for Nod2 mutations in CD.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kobayashi, Koichi S -- Chamaillard, Mathias -- Ogura, Yasunori -- Henegariu, Octavian -- Inohara, Naohiro -- Nunez, Gabriel -- Flavell, Richard A -- New York, N.Y. -- Science. 2005 Feb 4;307(5710):731-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Immunobiology, Yale University School of Medicine, New Haven, CT 06510, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15692051" target="_blank"〉PubMed〈/a〉
Keywords:
Acetylmuramyl-Alanyl-Isoglutamine/*immunology
;
Animals
;
*Antibody Formation
;
Female
;
Gene Expression
;
Gene Targeting
;
Ileum/*immunology/microbiology
;
*Immunity, Innate
;
Immunity, Mucosal
;
Immunoglobulins/biosynthesis
;
Interleukins/biosynthesis
;
Intestinal Diseases/immunology/microbiology
;
Intestinal Mucosa/immunology/microbiology
;
Intracellular Signaling Peptides and Proteins/*physiology
;
Ligands
;
Lipopolysaccharides/toxicity
;
Listeria monocytogenes/growth & development/immunology/isolation & purification
;
Listeriosis/*immunology/microbiology
;
Liver/microbiology
;
Macrophages/immunology
;
Male
;
Membrane Glycoproteins/physiology
;
Mice
;
Nod2 Signaling Adaptor Protein
;
Oligonucleotide Array Sequence Analysis
;
Protein Precursors/biosynthesis/genetics
;
Receptors, Cell Surface/physiology
;
Serum Albumin/immunology
;
Signal Transduction
;
Spleen/microbiology
;
Toll-Like Receptors
;
Tumor Necrosis Factor-alpha/biosynthesis
;
alpha-Defensins/*biosynthesis/genetics
Print ISSN:
0036-8075
Electronic ISSN:
1095-9203
Topics:
Biology
,
Chemistry and Pharmacology
,
Computer Science
,
Medicine
,
Natural Sciences in General
,
Physics
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