NOD2 deficiency increases retrograde transport of secretory IgA complexes in Crohn's disease.
basic_science · Level V
Where this comes from
- Record sourced from PubMed, PMID 33431850.
- Also identified by DOI 10.1038/s41467-020-20348-0 and PMC identifier 7801705.
- Licence recorded as CC BY.
- The licence permits redistribution, so the abstract is shown in full and the full text is available from the publisher.
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.
Medical subject headings
- Crohn Disease
- Immunoglobulin A, Secretory
- Nod2 Signaling Adaptor Protein