Secretory IgA Induces Tolerogenic Dendritic Cells through SIGNR1 Dampening Autoimmunity in Mice.

Détails

ID Serval
serval:BIB_356149D09B53
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
Secretory IgA Induces Tolerogenic Dendritic Cells through SIGNR1 Dampening Autoimmunity in Mice.
Périodique
Journal of Immunology
Auteur(s)
Diana J., Moura I.C., Vaugier C., Gestin A., Tissandie E., Beaudoin L., Corthésy B., Hocini H., Lehuen A., Monteiro R.C.
ISSN
1550-6606 (Electronic)
ISSN-L
0022-1767
Statut éditorial
Publié
Date de publication
2013
Volume
191
Numéro
5
Pages
2335-2343
Langue
anglais
Notes
Publication types: Journal ArticlePublication Status: ppublish
Résumé
IgA plays ambivalent roles in the immune system. The balance between inhibitory and activating responses relies on the multimerization status of IgA and interaction with their cognate receptors. In mucosal sites, secretory IgA (SIgA) protects the host through immune-exclusion mechanisms, but its function in the bloodstream remains unknown. Using bone marrow-derived dendritic cells, we found that both human and mouse SIgA induce tolerogenic dendritic cells (DCs) following binding to specific ICAM-3 grabbing nonintegrin receptor 1. This interaction was dependent on Ca(2+) and mannose residues. SIgA-primed DCs (SIgA-DCs) are resistant to TLR-dependent maturation. Although SIgA-DCs fail to induce efficient proliferation and Th1 differentiation of naive responder T cells, they generate the expansion of regulatory T cells through IL-10 production. SIgA-DCs are highly potent in inhibiting autoimmune responses in mouse models of type 1 diabetes and multiple sclerosis. This discovery may offer new insights about mucosal-derived DC immunoregulation through SIgA opening new therapeutic approaches to autoimmune diseases.
Pubmed
Web of science
Open Access
Oui
Création de la notice
03/10/2013 18:03
Dernière modification de la notice
20/08/2019 14:22
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