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
Auteur⸱e⸱s
Becker C., Dornhoff H., Neufert C., Fantini M.C., Wirtz S., Huebner S., Nikolaev A., Lehr H.A., Murphy A.J., Valenzuela D.M., Yancopoulos G.D., Galle P.R., Karow M., Neurath M.F.
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
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