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Cutting Edge: TGF-β Induces a Regulatory Phenotype in CD4+CD25− T Cells through Foxp3 Induction and Down-Regulation of Smad7
- M. Fantini, C. Becker, G. Monteleone, F. Pallone, P. Galle, M. Neurath
- BiologyJournal of Immunology
- 1 May 2004
It is demonstrated that TGF-β induces a regulatory phenotype in CD4+CD25− T cells through the induction of Foxp3 and a positive autoregulatory loop of T GF-β signaling due to the absence of Smad7.
Aryl hydrocarbon receptor-induced signals up-regulate IL-22 production and inhibit inflammation in the gastrointestinal tract.
AhR is down-regulated in intestinal tissue of patients with IBD; AhR signaling, via IL-22, inhibits inflammation and colitis in the gastrointestinal tract of mice.
IL‐23/IL‐17 axis in IBD
- M. Sarra, F. Pallone, T. Macdonald, G. Monteleone
- Medicine, BiologyInflammatory Bowel Diseases
- 1 October 2010
The available data regarding the role of Th17 cells and IL‐23 in chronic intestinal inflammation are reviewed and it is shown that Th17‐related cytokines, such as IL‐17A andIL‐22, can exert protective rather than detrimental effects in the gut.
Bioactive IL-18 expression is up-regulated in Crohn's disease.
The data indicate that IL-18 up-regulation is a feature of CD and suggest thatIL-18 may contribute to the local immunoinflammatory response in CD.
Interleukin-21 enhances T-helper cell type I signaling and interferon-gamma production in Crohn's disease.
The data suggest that IL-21 contributes to the ongoing Th1 mucosal response in Crohn's disease, as well as in tissues and cells isolated from patients with inflammatory bowel disease.
Interleukin 12 is expressed and actively released by Crohn's disease intestinal lamina propria mononuclear cells.
IL-21 Counteracts the Regulatory T Cell-Mediated Suppression of Human CD4+ T Lymphocytes1
Data indicate that IL-21 renders human CD4+CD25− T cells resistant to Treg-mediated suppression and suggest a novel mechanism by which IL- 21 could augment T cell-activated responses in human immune-inflammatory diseases.
A Failure of Transforming Growth Factor-β1 Negative Regulation Maintains Sustained NF-κB Activation in Gut Inflammation*
TGF-β1 is a negative regulator of NF-κB activation in the gut and that Smad7 maintains high NF-kkB activity in gut inflammation by blocking TGF- β1 signaling, as well as stimulating IκBα promoter transcriptional activity in Gut fibroblasts in vitro.
Hepatitis B and C Virus Infection in Crohn's Disease
HBV prevalence is higher in CD than in C at all ages, whereas HCV prevalence Is increased in young patients with CD, because of a greater need for surgery, which suggests that the host immune response may influence the risk of HCV infection.
Mongersen, an oral SMAD7 antisense oligonucleotide, and Crohn's disease.
It was found that study participants with Crohn's disease who received mongersen had significantly higher rates of remission and clinical response than those who received placebo.