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Updated: May 11, 2026

Visualization of IL-22-expressing Lymphocytes Using Reporter Mice
Published on: January 25, 2017
IL-22-producing CD4+ cells are depleted in actively inflamed colitis tissue
J M Leung1, M Davenport2, M J Wolff3
1Division of Parasitology, Department of Microbiology, New York University School of Medicine, New York, New York, USA.
In inflammatory bowel diseases (IBD), T helper 17 (Th17) cells play a role. Ulcerative colitis (UC) patients show reduced IL-22+ cells, linked to increased TGF-β and altered gut microbiota.
Area of Science:
- Immunology
- Gastroenterology
- Microbiology
Background:
- T helper type 17 (Th17) cytokines, including IL-17A and IL-22, are crucial for mucosal barrier integrity.
- These cytokines are implicated in the pathogenesis of inflammatory bowel diseases (IBDs), such as Crohn's disease (CD) and ulcerative colitis (UC).
Purpose of the Study:
- To investigate the role and regulation of Th17-related cytokines (IL-17A, IL-22) in the colonic mucosa of IBD patients.
- To explore the relationship between cytokine levels, inflammatory status, transforming growth factor-beta (TGF-β), and mucosal microbiota in IBD.
Main Methods:
- Analysis of colonic cells from IBD patients (CD and UC) and healthy controls.
- Quantification of IL-17+ and IL-22+ CD4+ cells in relation to mucosal inflammation.
- Assessment of TGF-β expression and its effect on Th22 cell populations in vitro.
- Examination of mucosal microbiota composition in relation to Th22 cell levels.
Main Results:
- Crohn's disease patients exhibited elevated IL-17+ CD4+ cells, irrespective of mucosal inflammation.
- Ulcerative colitis patients with active inflammation showed reduced IL-22+ cells and an increase in mono-IL-17-producing cells.
- Increased TGF-β levels in UC correlated with Th22 cell depletion and altered microbiota (reduced Clostridiales, increased Proteobacteria).
Conclusions:
- Elevated TGF-β during active UC inflammation may drive the loss of protective Th22 cells in the intestinal mucosa.
- These changes in Th22 cells and associated microbiota alterations could contribute to UC pathogenesis.
- The distinct cytokine profiles in CD and UC highlight disease-specific immune dysregulation in IBD.
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