IL-22 regulates lymphoid chemokine production and assembly of tertiary lymphoid organs.

Détails

ID Serval
serval:BIB_60D5CE40FF5D
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
IL-22 regulates lymphoid chemokine production and assembly of tertiary lymphoid organs.
Périodique
Proceedings of the National Academy of Sciences of the United States of America
Auteur⸱e⸱s
Barone F., Nayar S., Campos J., Cloake T., Withers D.R., Toellner K.M., Zhang Y., Fouser L., Fisher B., Bowman S., Rangel-Moreno J., Garcia-Hernandez Mde L, Randall T.D., Lucchesi D., Bombardieri M., Pitzalis C., Luther S.A., Buckley C.D.
ISSN
1091-6490 (Electronic)
ISSN-L
0027-8424
Statut éditorial
Publié
Date de publication
2015
Peer-reviewed
Oui
Volume
112
Numéro
35
Pages
11024-11029
Langue
anglais
Notes
Publication types: Journal Article
Publication Status: ppublish
Résumé
The series of events leading to tertiary lymphoid organ (TLO) formation in mucosal organs following tissue damage remain unclear. Using a virus-induced model of autoantibody formation in the salivary glands of adult mice, we demonstrate that IL-22 provides a mechanistic link between mucosal infection, B-cell recruitment, and humoral autoimmunity. IL-22 receptor engagement is necessary and sufficient to promote differential expression of chemokine (C-X-C motif) ligand 12 and chemokine (C-X-C motif) ligand 13 in epithelial and fibroblastic stromal cells that, in turn, is pivotal for B-cell recruitment and organization of the TLOs. Accordingly, genetic and therapeutic blockade of IL-22 impairs and reverses TLO formation and autoantibody production. Our work highlights a critical role for IL-22 in TLO-induced pathology and provides a rationale for the use of IL-22-blocking agents in B-cell-mediated autoimmune conditions.
Mots-clé
IL-22, tertiary lymphoid organs, chemokines, Sjogren's syndrome, autoimmunity
Pubmed
Web of science
Création de la notice
24/09/2015 13:14
Dernière modification de la notice
20/08/2019 14:18
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