During nasal polyp (NP) development, activated T cells differentiate into T helper (Th) 1, Th2, and Th17 cells. Additionally, regulatory T cells (Tregs) that have an immune suppressive function are involved in the pathophysiology of chronic rhinosinusitis (CRS) with NP (CRSwNP). Tregs can act as effector cells that produce inflammatory cytokines, such as interleukin (IL)-17A. We sought to identify the cellular expression of IL-17A and Treg markers in sinonasal tissue from CRSwNP patients and to investigate whether Tregs are involved in IL-17A secretion. The uncinate process (UP) and NP tissues were harvested from patients with CRSwNP, CRS without NP (CRSsNP), and normal controls. Expression of IL-17A and Foxp3 in each group was observed with immunohistochemistry and immunofluorescence. Expression of IL-17A in Treg was evaluated by flow cytometry of single cells isolated from sinonasal tissues. UP tissue from controls (n = 17), UP from CRSsNP (n = 24), and UP (n = 19) and NP (n = 29) from CRSwNP were obtained. The percentage of Foxp3 cells was higher in CRS tissues compared with normal controls. IL-17A cells were most increased in NP tissues from CRSwNP patients. Expression of IL-17A in some Foxp3 cells was observed in double immunofluorescence. Foxp3 cells, IL-17A cells, and Foxp3IL-17A cells were increased in the UP and NP tissues from CRSwNP patients. CD45RAFoxp3 cells were increased in CRSwNP, and IL-17A cells were observed most frequently in CD4CD45RAFoxp3 cells from NP tissues. These findings show that CD4CD45RAFoxp3 Tregs are involved in NP pathogenesis by producing IL-17A.