NOD2 deficiency increases retrograde transport of secretory IgA complexes in Crohn’s disease

Nicolas Rochereau (), Xavier Roblin, Eva Michaud, Rémi Gayet, Blandine Chanut, Fabienne Jospin, Blaise Corthésy and Stéphane Paul
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Nicolas Rochereau: GIMAP/EA3064, Université de Lyon, CIC 1408 Vaccinology
Xavier Roblin: GIMAP/EA3064, Université de Lyon, CIC 1408 Vaccinology
Eva Michaud: GIMAP/EA3064, Université de Lyon, CIC 1408 Vaccinology
Rémi Gayet: GIMAP/EA3064, Université de Lyon, CIC 1408 Vaccinology
Blandine Chanut: GIMAP/EA3064, Université de Lyon, CIC 1408 Vaccinology
Fabienne Jospin: GIMAP/EA3064, Université de Lyon, CIC 1408 Vaccinology
Blaise Corthésy: R&D Laboratory of the Division of Immunology and Allergy, CHUV, Centre des Laboratoires d’Epalinges
Stéphane Paul: GIMAP/EA3064, Université de Lyon, CIC 1408 Vaccinology

Nature Communications, 2021, vol. 12, issue 1, 1-13

Abstract: 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.

Date: 2021
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DOI: 10.1038/s41467-020-20348-0

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