Cutting edge: IL-23 cross-regulates IL-12 production in T cell-dependent experimental colitis.
Détails
ID Serval
serval:BIB_A2DF52A63C21
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
Cutting edge: IL-23 cross-regulates IL-12 production in T cell-dependent experimental colitis.
Périodique
Journal of Immunology
ISSN
0022-1767
Statut éditorial
Publié
Date de publication
2006
Peer-reviewed
Oui
Volume
177
Numéro
5
Pages
2760-2764
Langue
anglais
Résumé
Although IL-12 and IL-23 share the common p40 subunit, IL-23, rather than IL-12, seems to drive the pathogenesis of experimental autoimmune encephalomyelitis and arthritis, because IL-23/p19 knockout mice are protected from disease. In contrast, we describe in this study that newly created LacZ knockin mice deficient for IL-23 p19 were highly susceptible for the development of experimental T cell-mediated TNBS colitis and showed even more severe colitis than wild-type mice by endoscopic and histologic criteria. Subsequent studies revealed that dendritic cells from p19-deficient mice produce elevated levels of IL-12, and that IL-23 down-regulates IL-12 expression upon TLR ligation. Finally, in vivo blockade of IL-12 p40 in IL-23-deficient mice rescued mice from lethal colitis. Taken together, our data identify cross-regulation of IL-12 expression by IL-23 as novel key regulatory pathway during initiation of T cell dependent colitis.
Mots-clé
Animals, Cells, Cultured, Colitis, Disease Models, Animal, Disease Susceptibility, Down-Regulation, Interleukin-12, Interleukin-23, Interleukin-23 Subunit p19, Interleukins, Mice, Mice, Transgenic, Protein Subunits, Survival Rate, T-Lymphocytes
Pubmed
Web of science
Création de la notice
29/01/2008 18:33
Dernière modification de la notice
20/08/2019 15:08