Impaired dendritic cell function in Crohn's disease patients with NOD2 3020insC mutation.
Publication year
2006Source
Journal of Leukocyte Biology, 79, 4, (2006), pp. 860-866ISSN
Publication type
Article / Letter to editor

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Organization
Tumorimmunology
Internal Medicine
Gastroenterology
Journal title
Journal of Leukocyte Biology
Volume
vol. 79
Issue
iss. 4
Page start
p. 860
Page end
p. 866
Subject
EBP 3: Effective Primary Care and Public Health; N4i 1: Pathogenesis and modulation of inflammation; N4i 2: Invasive mycoses and compromised host; NCMLS 1: Immunity, infection and tissue repair; NCMLS 1: Infection and autoimmunity; NCMLS 2: Immune Regulation; ONCOL 3: Translational research; UMCN 4.1: Microbial pathogenesis and host defense; UMCN 5.1: Genetic defects of metabolismAbstract
The nucleotide oligomerization domain 2 (NOD2) 3020insC (NOD2fs) mutation increases susceptibility to Crohn's disease (CD), but the mechanism remains controversial. Loss-of-function and gain-of-function phenotypes have been described as a result of NOD2fs. Here, we show that dendritic cells (DC) derived from CD patients homozygous for this mutation respond normally to purified Toll-like receptor (TLR) ligands but fail to up-regulate the costimulatory molecules CD80 and CD86 in response to the NOD2 ligand muramyl dipeptide (MDP). Moreover, they lack MDP-induced enhancement of TLR-mediated tumor necrosis factor alpha, interleukin (IL)-12, and IL-10 production, which is observed in control DC with intact NOD2. These data indicate that the NOD2fs mutation results in a loss-of-function phenotype in human myeloid DC and imply decreased immune regulation by IL-10 as a possible mechanism for this mutation in CD.
This item appears in the following Collection(s)
- Academic publications [204994]
- Electronic publications [103242]
- Faculty of Medical Sciences [81051]
- Open Access publications [71780]
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