Journal
JOURNAL OF CLINICAL IMMUNOLOGY
Volume 30, Issue 1, Pages 80-89Publisher
SPRINGER/PLENUM PUBLISHERS
DOI: 10.1007/s10875-009-9345-1
Keywords
Inflammatory bowel disease; Crohn's disease; ulcerative colitis; regulatory T cells; Th17 effector cells
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Funding
- Department of Gastroenterology and Hepatology
- Queen Elizabeth Hospital
- Queen Elizabeth Hospital Research Foundation
- University of Adelaide
- Australian Crohn's and Colitis Association
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Inflammatory bowel disease (IBD) is thought to result from an aberrant immune response. Inflammation in IBD may be caused by the loss of homeostasis between CD4(+) CD25(high) Foxp3(+) regulatory cells (T (reg)) and proinflammatory Th17 cells. The aim of this study was to investigate T (reg) and Th17 cells in the peripheral blood and intestinal mucosa of IBD patients and to assess the mucosal cytokine environment. T (reg) and Th17 cells were measured in peripheral blood of 63 IBD patients and 28 controls by flow cytometry. Forkhead box p3 (Foxp3), interleukin (IL)-17a, IL-1 beta, IL-6, IL-21, IL-23, and transforming growth factor (TGF)-beta mRNA were analyzed using real-time reverse transcription polymerase chain reaction in intestinal biopsies of 24 IBD and 18 control subjects. A decrease in T (reg) and increase in Th17 cells was observed in the peripheral blood of IBD patients. When measured in the same patient and expressed as a ratio, a significant decrease in T (reg)/Th17 ratio was observed in IBD. Elevated expression of Foxp3, IL-17a, IL-1 beta, and IL-6 was observed in the mucosa of IBD patients, while TGF-beta was only elevated in ulcerative colitis. IBD is associated with a reduced ratio of T (reg) to Th17 cells in peripheral blood and is characterized by a proinflammatory cytokine microenvironment, which supports the continued generation of Th17 cells.
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