Smad7 in TGF-β-mediated negative regulation of gut inflammation

Mice with targeted disruptions of the transforming growth factor-β1 ( TGF-β1) gene or TGF-β1 intracellular signalling pathways develop intestinal inflammation. Conversely, TGF-β1-producing regulatory T cells protect against experimental colitis. Paradoxically, however, TGF-β1 production is high in t...

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Bibliographic Details
Published in:Trends in immunology 2004-10, Vol.25 (10), p.513-517
Main Authors: Monteleone, Giovanni, Pallone, Francesco, MacDonald, Thomas T.
Format: Article
Language:English
Subjects:
Animals
DNA-Binding Proteins - immunology
Humans
Inflammation - immunology
Intestinal Mucosa
Intestines - immunology
Signal Transduction - immunology
Smad7 Protein
Trans-Activators - immunology
Transforming Growth Factor beta - immunology
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Summary:Mice with targeted disruptions of the transforming growth factor-β1 ( TGF-β1) gene or TGF-β1 intracellular signalling pathways develop intestinal inflammation. Conversely, TGF-β1-producing regulatory T cells protect against experimental colitis. Paradoxically, however, TGF-β1 production is high in the gut of patients with chronic inflammatory intestinal disease, and yet inflammation proceeds unchecked. Here we discuss the functional role of Smad7, an intracellular inhibitor of TGF-β1 signalling, in the control of gut inflammation by TGF-β1. In particular, we delineate a scenario in which the high expression of Smad7 in inflammatory cells renders them unresponsive to TGF-β1 and propose that control of Smad7, not TGF-β1 production, is a key determinant in understanding how TGF-β1 negatively regulates gut inflammation.
ISSN:1471-4906
1471-4981
DOI:10.1016/j.it.2004.07.008