The pathogenesis of nasal polyposis remains unclear; it severely affects patients' quality of life and complicates inflammation in adjacent organs such as sinusitis and asthma. Aberrant immune regulatory function in these patients is proposed. The present study aims to examine the regulatory T cells (T(reg) ) in nasal mucosa of patients with allergic rhinitis (AR) and nasal polyposis (NP). Patients with AR or AR/NP were treated with inferior turbinectomy for their inferior turbinate hyperplasia. Surgically removed nasal mucosa was collected to examine the T(reg) by immunohistochemistry and flow cytometry. The results showed that more forkhead box P3 (FoxP3)(+) cells were found in AR with polyps than in those with AR alone. Further studies revealed that these FoxP3(+) T cells from AR/NP group also expressed interleukin (IL)-17. In vitro study showed that staphylococcal enterotoxin B (SEB) induced CD4(+) FoxP3(+) T cells to become FoxP3(+) IL-17(+) cells via facilitating the expression of IL-6, that in synergy with transforming growth factor-beta, induce the expression of IL-17 in FoxP3(+) cells. We conclude that FoxP3(+) IL-17(+) T cells were localized in the nasal mucosa of patients with AR and NP. SEB may play a role in converting FoxP3(+) T(reg) to FoxP3(+) IL-17(+) T cells. The presence of IL-17(+) FoxP3(+) T cells may play a role in the remodelling of the nasal airways in certain people who develop polyps, irrespective of whether or not they are atopic.