Journal of Clinical Immunology

, Volume 30, Issue 1, pp 80-89

Foxp3+ Regulatory T Cells, Th17 Effector Cells, and Cytokine Environment in Inflammatory Bowel Disease

  • Nicola Eastaff-LeungAffiliated withDepartment of Gastroenterology and Hepatology, The Queen Elizabeth HospitalDiscipline of Pathology, University of Adelaide
  • , Nicholas MabarrackAffiliated withDiscipline of Microbiology and Immunology, University of Adelaide
  • , Angela BarbourAffiliated withDiscipline of Pathology, University of Adelaide
  • , Adrian CumminsAffiliated withDepartment of Gastroenterology and Hepatology, The Queen Elizabeth HospitalDiscipline of Medicine, University of Adelaide Email author 
  • , Simon BarryAffiliated withDiscipline of Pediatrics, University of Adelaide

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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+ CD25high 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-1β, IL-6, IL-21, IL-23, and transforming growth factor (TGF)-β 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-1β, and IL-6 was observed in the mucosa of IBD patients, while TGF-β 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.


Inflammatory bowel disease Crohn’s disease ulcerative colitis regulatory T cells Th17 effector cells