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Induction of Intestinal Inflammation by Adoptive Transfer of CBir1 TCR Transgenic CD4+ T Cells to Immunodeficient Mice
Published on: December 16, 2021
Interleukin-21 triggers effector cell responses in the gut
Daniela De Nitto1, Massimiliano Sarra, Francesco Pallone
1Department of Internal Medicine, University Tor Vergata of Rome, Rome, Italy.
World Journal of Gastroenterology
|August 3, 2010
Summary
Interleukin-21 (IL-21) drives inflammation in inflammatory bowel diseases (IBD). Excessive IL-21 production by immune cells exacerbates gut mucosal inflammation, highlighting its pathogenic role in Crohn's disease and ulcerative colitis.
Area of Science:
- Immunology
- Gastroenterology
Background:
- Inflammatory bowel diseases (IBD), including Crohn's disease and ulcerative colitis, involve complex immune responses in the gut.
- Cytokines are key mediators in initiating and perpetuating the pathological processes observed in IBD.
Purpose of the Study:
- To review existing data on the role of interleukin-21 (IL-21) in the pathogenesis of IBD.
- To highlight IL-21 as a significant cytokine in the inflammatory cascade of IBD.
Main Methods:
- Review of accumulated evidence from in vitro and in vivo studies.
- Analysis of data concerning cytokine production and signaling pathways in IBD patients.
Main Results:
- Interleukin-21 (IL-21) is found in excess in the inflamed intestines of IBD patients.
- IL-21 is primarily produced by activated CD4+ T helper cells, including those co-expressing interferon-gamma and follicular T helper cells.
- Excessive IL-21 production activates signaling pathways that sustain mucosal inflammation.
Conclusions:
- Interleukin-21 (IL-21) plays a significant pathogenic role in inflammatory bowel diseases (IBD).
- Targeting IL-21 may offer a therapeutic strategy for managing IBD.
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