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Secretory IgA induces tolerogenic dendritic cells through SIGNR1 dampening autoimmunity in mice.

Authors
  • Diana, Julien
  • Moura, Ivan C
  • Vaugier, Céline
  • Gestin, Aurélie
  • Tissandie, Emilie
  • Beaudoin, Lucie
  • Corthésy, Blaise
  • Hocini, Hakim
  • Agnès Lehuen
  • Monteiro, Renato C
Type
Published Article
Journal
The Journal of Immunology
Publisher
The American Association of Immunologists
Publication Date
Sep 04, 2013
Volume
191
Issue
5
Pages
2335–2343
Identifiers
DOI: 10.4049/jimmunol.1300864
PMID: 23926325
Source
USPC - SET - SVS
License
Green

Abstract

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.

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