The etiology of cancer is unclear. Recent studies indicate that some cytokines, such as interleukin (IL)-17, and regulatory T cells are involved in the development of cancer. This study aims to detect a subset of T cell, IL17+Foxp3+ T cell, in the pathogenesis of esophageal cancer (Eca). Twelve patients with squamous Eca were recruited in this study. The surgically removed Eca tissue was collected. Cells isolated from Eca tissue were analyzed by flow cytometry. The results showed that 2-10% Eca tissue-derived CD4(+) T cells expressed Foxp3; only 0.2-0.8% non-ca tissue-derived CD4(+) T cells expressed Foxp3. Further analysis showed that 3-15% Eca-isolated CD4(+) T cells were also IL-17 positive whereas only 0.4-1.5% non-ca tissue-isolated CD4(+) T cells were IL-17 positive. We also found that about 4.8-11.2% Foxp3(+) IL-17(+) T cells in isolated CD4(+) T cells from Eca tissue that were significantly less than in non-ca tissue derived CD4(+) T cells. Less than 1% Foxp3(+) IL-17(+) T cells in isolated CD4(+) T cells in both Eca patients and healthy controls. Treatment with hypoxia markedly increased the expression of IL-6 in peripheral CD68+ cells. Coculturing CD68+ cells and Foxp3+ T cells under hypoxic environment resulted in abundant expression of IL-17 in Foxp3+ T cells that could be blocked by pretreatment with either anti-IL-17 or anti-transforming growth factor beta antibodies. We conclude that IL-17+Foxp3+ T cells may contribute to the development of Eca.