The small intestine harbors a substantial number of commensal bacteria and is sporadically invaded by pathogens. Double-stranded RNA (dsRNA) of one major commensal species, lactic acid bacteria (LAB), triggered IFN-β production from dendritic cells (DCs) and protected mice from experimental colitis. Further, we clarified that IFN-β production not only improves mucosal immune-homeostasis but also systemic Th1 immunity. We demonstrated that IFN-β secreted in response to LAB enhanced IFN regulatory factor 1 (IRF1) and IRF7 mRNA, which contribute to Il12p35 expression. Dendritic cells from type I IFN-receptor deficient mice fail to enhance IFN-g producing T cells upon recognition of LAB. Thus oral administration of LAB enhances systemic Th1 immunity and suppresses Th2 immune responses. These results identify TLR3 as a sensor to small intestinal commensal bacteria and the resultant induction of IFN-β contribute to the two phases of protective immunity, i.e. maintenance of immunological homeostasis and enhancement of Th1 cellular immunity.