Cutting edge: IL-23 cross-regulates IL-12 production in T cell-dependent experimental colitis.

Details

Serval ID
serval:BIB_A2DF52A63C21
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
Cutting edge: IL-23 cross-regulates IL-12 production in T cell-dependent experimental colitis.
Journal
Journal of Immunology
Author(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
Publication state
Published
Issued date
2006
Peer-reviewed
Oui
Volume
177
Number
5
Pages
2760-2764
Language
english
Abstract
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.
Keywords
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
Create date
29/01/2008 18:33
Last modification date
20/08/2019 15:08
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