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Blockade of interleukin 6 trans signaling suppresses T-cell resistance against apoptosis in chronic intestinal inflammation: Evidence in Crohn disease and experimental colitis in vivo
Assessment of the contribution of the pro-inflammatory cytokine interleukin (IL)-6 to the increased resistance of mucosal T cells against apoptosis in Crohn disease indicates that a pathway of T-cell activation driven by IL-6–sIL-6R contributes to the perpetuation of chronic intestinal inflammation.
CD28-dependent Rac1 activation is the molecular target of azathioprine in primary human CD4+ T lymphocytes.
It is suggested that 6-Thio-GTP derivates may be useful as potent immunosuppressive agents in autoimmune diseases and organ transplantation and in the control of T cell apoptosis by modulation of Rac1 activation upon CD28 costimulation.
NF‐κB in inflammatory bowel disease
The nuclear transcription factor kappaB (NF‐κB) is identified as one of the key regulators in this immunological setting and its activation is markedly induced in IBD patients and through its ability to promote the expression of various pro‐inflammatory genes, NF‐κBs strongly influences the course of mucosal inflammation.
Involvement of IL-6 in the pathogenesis of inflammatory bowel disease and colon cancer
Understanding concerning the predominant pathogenic role of an IL-6-dependent inflammatory cascade may lead to the development of new therapeutic strategies in the treatment of IBD, which consists of Crohn's disease and ulcerative colitis.
TH9 cells that express the transcription factor PU.1 drive T cell–mediated colitis via IL-9 receptor signaling in intestinal epithelial cells
The findings suggest that the TH9 subset of helper T cells serves an important role in driving ulcerative colitis by regulating intestinal epithelial cells and that TH9 cells represent a likely target for the treatment of chronic intestinal inflammation.
Antibodies against tumor necrosis factor (TNF) induce T-cell apoptosis in patients with inflammatory bowel diseases via TNF receptor 2 and intestinal CD14⁺ macrophages.
Clinically effective anti-TNF antibodies are able to induce T-cell apoptosis in IBD only when mucosal TNFR2(+) T cells are cocultured with mTNF-expressing CD14(+) macrophages.
Vedolizumab provides clinical benefit over 1 year in patients with active inflammatory bowel disease – a prospective multicenter observational study
- A. Stallmach, C. Langbein, C. Schmidt
- Medicine, BiologyAlimentary Pharmacology and Therapeutics
- 1 December 2016
Vedolizumab, a monoclonal antibody targeting the α4β7‐integrin, is effective in inducing and maintaining clinical remission in Crohn's disease and ulcerative colitis according to randomised clinical…
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.
Molecular mechanism of action of anti-tumor necrosis factor antibodies in inflammatory bowel diseases
- U. Billmeier, W. Dieterich, M. Neurath, R. Atreya
- Medicine, BiologyWorld Journal of Gastroenterology
- 14 November 2016
The anti-TNF agent etanercept is effective in the treatment of rheumatoid arthritis but failed to induce clinical response in Crohn’s disease patients, suggesting different contributions of TNF in the pathogenesis of these inflammatory diseases.
IL-9 and its receptor are predominantly involved in the pathogenesis of UC
Evidence is provided that IL- 9 is predominantly involved in the pathogenesis of UC suggesting that targeting IL-9 might become a therapeutic option for patients with UC.