Inflammatory
bowel diseases (IBD) are chronic inflammatory pathologies of the gut,
characterized by a relapsing-remitting course.
Although IBD
pathogenesis is not fully understood, epidemiological
and experimental data suggest that multiple environmental factors can, in
genetically predisposed individuals, trigger an excessive immune response
directed against the antigens of the normal intestinal microflora, which eventually
leads to the tissue damage. Defects in the physiological mechanisms/factors of
counter-regulation contribute to amplify and sustain such a detrimental
response.
For instance, in
inflamed tissue of IBD patients there is diminished activity of the
immunesuppressive cytokine transforming growth factor (TGF)-β1, due to elevated
levels of Smad7, an intracellular inhibitor of TGF-β1 signaling.
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