In the present study, to test whether, and if so, how the increased IL-17A expression was responsible for inhibition of Th1 cell function in IBD, we used the human colonic epithelial cell line HT-29 cells, as we have found that the expression of IL-17A in and IL-17R on CEC cells is significantly increased in mice with TNBS-induced colitis, which is an animal model of Crohn’s disease (CD). The gene discussed is IL17A; the disease is Cowden disease.