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

Author

Listed:
  • 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)

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.

Suggested Citation

  • Nicolas Rochereau & Xavier Roblin & Eva Michaud & Rémi Gayet & Blandine Chanut & Fabienne Jospin & Blaise Corthésy & Stéphane Paul, 2021. "NOD2 deficiency increases retrograde transport of secretory IgA complexes in Crohn’s disease," Nature Communications, Nature, vol. 12(1), pages 1-13, December.
    • Handle: RePEc:nat:natcom:v:12:y:2021:i:1:d:10.1038_s41467-020-20348-0
    DOI: 10.1038/s41467-020-20348-0
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