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Interleukin-19 contributes as a protective factor in experimental Th2-mediated colitis
Yasuyuki Fujimoto1, Yasu-Taka Azuma2, Yukiko Matsuo1
1Laboratory of Veterinary Pharmacology, Division of Veterinary Science, Osaka Prefecture University Graduate School of Life and Environmental Science, Izumisano, 598-8531, Japan.
Naunyn-Schmiedeberg'S Archives of Pharmacology
|December 13, 2016
Summary
Interleukin-19 (IL-19) plays an anti-inflammatory role in Th2-mediated colitis. Its absence exacerbates inflammation, suggesting IL-19 as a therapeutic target for inflammatory bowel disease.
Area of Science:
- Immunology
- Gastroenterology
Background:
- Inflammatory bowel disease (IBD) involves immune system dysregulation.
- Interleukin-10 (IL-10) family member IL-19's role in IBD requires further investigation.
- Previous studies indicated IL-19 deficiency exacerbates innate-mediated colitis.
Purpose of the Study:
- To investigate the role of IL-19 in T cell-mediated colitis, specifically Th2 cell-driven inflammation.
- To assess the impact of IL-19 deficiency on experimental colitis induced by oxazolone.
Main Methods:
- Utilized a mouse model of Th2 cell-mediated colitis induced by oxazolone.
- Evaluated colitis severity through body weight loss and colonic histology.
- Assessed cytokine production from lymph node cells in vitro.
Main Results:
- IL-19 knockout mice exhibited exacerbated oxazolone-induced colitis.
- Increased inflammatory cell transport into the colon was observed in IL-19 deficient mice.
- Elevated IgE production and circulating eosinophils were noted, alongside increased IL-4 and IL-9 production.
Conclusions:
- IL-19 demonstrates an anti-inflammatory function in the Th2-mediated colitis model.
- IL-19 deficiency worsens colonic inflammation by promoting inflammatory cell infiltration and specific cytokine production.
- IL-19 emerges as a potential therapeutic target for managing colonic inflammation in IBD.

