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

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.

journal_name

Nat Commun

journal_title

Nature communications

authors

Rochereau N,Roblin X,Michaud E,Gayet R,Chanut B,Jospin F,Corthésy B,Paul S

doi

10.1038/s41467-020-20348-0

subject

Has Abstract

pub_date

2021-01-11 00:00:00

pages

261

issue

1

issn

2041-1723

pii

10.1038/s41467-020-20348-0

journal_volume

12

pub_type

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