Dectin-1 (gene symbol: Clec7a), one of C-type lectin family members, is the receptor for 1, 3-b-glucans and plays an important role for the host defense against fungal infection by inducing ROS and Th17-inducing cytokines. Because various foods, such as mushrooms and yeasts, contain b-glucans and Dectin-1 is expressed in intestinal myeloid cells, we examined the effects of Dectin-1 deficiency on the intestinal immune system. We found that Clec7a–/– mice are resistant against Dextran Sodium Sulfate (DSS)-induced colitis due to over expansion of Treg cells. Treg cell expansion was caused by Lactobacillus murinus, whose population was expanded in Clec7a–/– mouse colon due to a decrease of a group of antimicrobial proteins that specifically suppress L. murinus growth. IL-17F, but not IL-17A, was induced in the downstream of Dectin-1, and induced these antimicrobial proteins. Actually, Il17f–/– mice also showed resistance against DSS-induced colitis associated with expansion of Treg cells. Oral administration of short chain b-glucans, a Dectin-1 antagonist, or i. p. injection of anti-IL-17F suppressed development of DSS-colitis. Thus, these observations suggest that treatment with anti-IL-17F or short chain b-glucans should be beneficial for the treatment of inflammatory bowel diseases by inducing Treg cells through modification of intestinal microflora.