Regulatory T (Treg) cells take part in immune homeostasis and play a pivotal role in maintaining peripheral tolerance. The aim of this study was to evaluate the frequency and function of Treg cells in active and untreated ulcerative colitis (UC) patients. Thirty-two subjects with newly diagnosed UC and 31 age-matched healthy controls were included in this survey. The frequency of Tregs was analyzed with flow cytometry using CD4, CD25, CD127 and FoxP3 markers. We used surface expression of CD4(+), CD25(+) and CD127(low) markers for isolation of a relatively pure Treg population. Suppressive activity of Tregs was determined by measuring their ability to inhibit the proliferation of T responder cells. UC patients had a lower frequency of CD4(+) CD25(+) CD127(low) FoxP3(+) Treg cells. Additionally, Treg cell-mediated suppression was lower in UC patients compared to controls. The frequency and suppressive capacity of Tregs and MFI of FoxP3 were inversely correlated with disease activity. These results suggest that CD4(+) CD25(+) CD127(low) FoxP3(+) Treg cells may contribute to immunopathogenesis of UC, and assessment of Treg cell frequency and function may have clinical value.

Regulatory T (Treg) cells are essential for maintenance of peripheral tolerance and prevention of autoimmune diseases in part by producing immunosuppressive cytokines. Recently, microRNAs (miRNAs) have also been involved in autoimmune disorders, not least for their crucial role in the regulation of Treg biology and function. We simultaneously investigated the concentration of IL-35, IL-10, TGF-β, and sCD25 in supernatant of cell culture and the expression patterns of several miRNAs in CD4(+)CD25(+) CD127(-/low) FoxP3(+) Tregs of ulcerative colitis (UC) patients. Significantly lower levels of IL-10 and IL-35 were observed in Treg cultures of UC patients. miR-21, miR-146a, and miR-155 levels were downregulated and miR-31 level was upregulated in Tregs of patients. Our results suggest that microRNAs may serve as a novel regulator in function and homoeostasis of UC Treg cells, providing a key role for them in pathophysiology of UC.

The frequency of CD4+ CD25+ CD127low FoxP3+ Tregs decreased in active stage of CD but there was no impaired suppressive function of CD4+ CD25+ CD127low FoxP3+ Treg cells. We suggest that an alteration in the balance of Tregs and T effectors may contribute to pathogenesis of CD.

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