FOXP3+ Treg cells and interleukin-23 expression in the intestinal mucosa of children with ulcerative colitis

Background/Aims Ulcerative colitis (UC) is thought to result from an aberrant immune response. Forkhead box P3 (FOXP3) regulatory T (Treg) cells and Interleukin (IL)-23/T-helper 17 pathway play an important role in the pathogenesis of inflammatory bowel disease, but little is known about their role in children with UC. The aim of this study was to investigate the role of FOXP3 and IL-23 in the pathogenesis of UC by determining them in intestinal tissues of children with the disease. Materials and Methods We studied 29 patients with UC (18 pancolitis, nine left-sided colitis, and two proctocolitis) and 11 control subjects. Immunohistochemistry was used to examine FOXP3+ Treg cells and IL-23 in intestinal biopsy specimens from UC patients and from non-inflamed tissues in the control group. Results UC patients’ FOXP3+ Treg cells were significantly higher than those of the control group (45.67% ± 10.83 vs. 22.06% ± 8.09, p=0.007). IL-23 expression in patients with UC were significantly higher than those of the control subjects (24.33% ± 13.81 vs. 12.91% ± 5.06, p=0.009). FOXP3+ Treg cells (43.21% ± 16.97) and IL-23 (25.12% ± 14.98) expression in patients with pancolitis were higher than in the control group (p=0.012 vs p=0.022). However, no differences were determined in FOXP3+ Treg cells and IL-23 in patients with left colon involvement and proctocolitis compared to the control group. Conclusions FOXP3+ Treg cell and IL-23 expression were higher in the intestinal mucosa of children with UC. These data indicate that new therapeutic options directed toward inhibiting the IL23 pathway and raising Treg cell numbers may permit more efficacious treatment of UC