Basic—Alimentary TractInterleukin-25 Inhibits Interleukin-12 Production and Th1 Cell-Driven Inflammation in the Gut
Section snippets
Mucosal Samples
Colonic mucosal biopsy specimens were taken from 16 patients with CD and 8 patients with ulcerative colitis (UC). Surgical specimens from 13 CD patients and 4 UC patients undergoing resection for a chronically active disease poorly responsive to medical treatment were also analyzed. Twenty-four patients with CD and 9 patients with UC were receiving corticosteroids and mesalazine, whereas the remaining patients were untreated. Additional biopsy samples were taken from 5 patients with IBD (2 CD
Intestinal Mucosal CD14+ Cells Express IL-25R and Respond to IL-25
The proportion of mucosal CD14+ cells was markedly increased in IBD LPMC compared with control LPMC (15% ± 5% vs 1% ± 0.5%, respectively). Nonetheless, the percentage of CD14+ cells that expressed IL-25R did not differ between IBD and controls (Figure 1A). CD3+ T cells expressed IL-25R, with no significant difference between IBD and controls (Figure 1B). Because in CD mucosa the CD14+ monocytes are a major source of IL-12,6 we next examined whether IL-25 inhibited IL-12 transcripts. Initially,
Discussion
In recent years, it has become evident that CD results from a dysregulated immune reaction within the intestinal wall directed against luminal antigens and is characterized by exaggerated production of Th1-associated cytokines.24, 25, 26 These advances led to the development of novel therapeutic agents that are currently being studied for their capacity to specifically target the mucosal Th1-inflammatory pathways occurring in CD patients.27
We identify a new mechanism in this paper by which
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Could IL-25 be a potential therapeutic target for intestinal inflammatory diseases?
2023, Cytokine and Growth Factor ReviewsIL-25 (IL-17E) in epithelial immunology and pathophysiology
2021, Journal of Allergy and Clinical ImmunologyCitation Excerpt :In contrast, McHenga et al132 reported that the IL-25 injections in parallel with dextran sulfate sodium administration resulted in elevated levels of IL-23 and TGF-β1 (but not IL-17A) in colon tissues and decreased inflammation. IL-25 administration was able to protect mice from peptidoglycan-induced TH1-driven colitis.77 Using a model for colitis-induced colon cancer, Thelen et al133 showed that IL-25 suppression by blocking antibody resulted in increased colitis scores but greater tumor burdens compared with isotype control–treated mice; however, IL-25 knockouts showed no difference in colonic tumor development compared with the wild type.
IL-17E (IL-25) and IL-17A Differentially Affect the Functions of Human Keratinocytes
2020, Journal of Investigative Dermatology
Conflicts of interest The authors disclose the following: G.M. has filed a patent entitled “A treatment for inflammatory diseases” (patent No. 08154101.3). The remaining authors disclose no conflicts.