Journal of Leukocyte Biology
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Originally published online as doi:10.1189/jlb.0805484 on February 3, 2006

Published online before print February 3, 2006
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(Journal of Leukocyte Biology. 2006;79:860-866.)
© 2006 by Society for Leukocyte Biology

Impaired dendritic cell function in Crohn’s disease patients with NOD2 3020insC mutation

Matthijs Kramer*, Mihai G. Netea{dagger},{ddagger}, Dirk J. de Jong§, Bart Jan Kullberg{dagger},{ddagger} and Gosse J. Adema*,1

* Departments of Tumor Immunology, Nijmegen Centre for Molecular Life Sciences,
§ Gastroenterology and Hepatology, and
{dagger} Medicine,
{ddagger} Nijmegen University Centre for Infectious Diseases, Radboud University Nijmegen Medical Centre, The Netherlands

1Correspondence: Department of Tumor Immunology, Nijmegen Centre for Molecular Life Sciences, Radboud University Nijmegen Medical Centre, Geert Grooteplein 28, 6525 GA, Nijmegen, The Netherlands. E-mail: g.adema{at}ncmls.ru.nl

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.

Key Words: human • cytokines • Toll-like receptor




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