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Updated: Nov 21, 2025
A TNBS-Induced Rodent Model to Study the Pathogenic Role of Mechanical Stress in Crohn's Disease
Published on: March 1, 2022
NOD2 deficiency increases retrograde transport of secretory IgA complexes in Crohn's disease
Nicolas Rochereau1, Xavier Roblin2, Eva Michaud2
1GIMAP/EA3064, Université de Lyon, CIC 1408 Vaccinology, F42023, Saint-Etienne, France. nicolas.rochereau@univ-st-etienne.fr.
Abstract:
Intestinal microfold cells are the primary pathway for translocation of secretory IgA (SIgA)-pathogen complexes to gut-associated lymphoid tissue. Uptake of SIgA/commensals complexes is important for priming adaptive immunity in the mucosa. This study aims to explore the effect of SIgA retrograde transport of immune complexes in Crohn's disease (CD). Here we report a significant increase of SIgA transport in CD patients with NOD2-mutation compared to CD patients without NOD2 mutation and/or healthy individuals. NOD2 has an effect in the IgA transport through human and mouse M cells by downregulating Dectin-1 and Siglec-5 expression, two receptors involved in retrograde transport. These findings define a mechanism of NOD2-mediated regulation of mucosal responses to intestinal microbiota, which is involved in CD intestinal inflammation and dysbiosis.
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