Dectin-1 is essential for reverse transcytosis of glycosylated SIgA-antigen complexes by intestinal M cells.

Détails

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Etat: Public
Version: de l'auteur⸱e
ID Serval
serval:BIB_A55F4DE084BF
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
Dectin-1 is essential for reverse transcytosis of glycosylated SIgA-antigen complexes by intestinal M cells.
Périodique
PLoS Biology
Auteur⸱e⸱s
Rochereau N., Drocourt D., Perouzel E., Pavot V., Redelinghuys P., Brown G.D., Tiraby G., Roblin X., Verrier B., Genin C., Corthésy B., Paul S.
ISSN
1545-7885 (Electronic)
ISSN-L
1544-9173
Statut éditorial
Publié
Date de publication
2013
Volume
11
Numéro
e1001658
Pages
1-18
Langue
anglais
Résumé
Intestinal microfold (M) cells possess a high transcytosis capacity and are able to transport a broad range of materials including particulate antigens, soluble macromolecules, and pathogens from the intestinal lumen to inductive sites of the mucosal immune system. M cells are also the primary pathway for delivery of secretory IgA (SIgA) to the gut-associated lymphoid tissue. However, although the consequences of SIgA uptake by M cells are now well known and described, the mechanisms whereby SIgA is selectively bound and taken up remain poorly understood. Here we first demonstrate that both the Cα1 region and glycosylation, more particularly sialic acid residues, are involved in M cell-mediated reverse transcytosis. Second, we found that SIgA is taken up by M cells via the Dectin-1 receptor, with the possible involvement of Siglec-5 acting as a co-receptor. Third, we establish that transcytosed SIgA is taken up by mucosal CX3CR1⁺ dendritic cells (DCs) via the DC-SIGN receptor. Fourth, we show that mucosal and systemic antibody responses against the HIV p24-SIgA complexes administered orally is strictly dependent on the expression of Dectin-1. Having deciphered the mechanisms leading to specific targeting of SIgA-based Ag complexes paves the way to the use of such a vehicle for mucosal vaccination against various infectious diseases.
Pubmed
Web of science
Open Access
Oui
Création de la notice
01/11/2013 20:59
Dernière modification de la notice
20/08/2019 15:10
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