role, but instead appear to play a protective role, which has most clearly been illustrated in the case of IL-22. On the other hand, mice deficient in RORgT a critical master regulator of the Th17 lineage, or in IL-23 a cytokine with complicated but important role in Th17 responses, are protected from several types of autoimmune diseases, including EAE ad colitis. This raises a question as to the specific mechanism and effector T cells types involved in these pathogenic responses. We will discuss our recent findings suggesting a potentially dichotomous role of Th17 responses in the development of colitis, as well as the possible innate immune signaling pathways involved in their generation in the gut. Finally, it is increasingly appreciated that commensal flora plays an important role in the activation of various T cell effector responses in the gut [4]. Commensal bacteria can contribute to the initiation of immune responses for two reasons: First, they provide a source of ligands for various pattern recognition receptors, such as TLRs, which is necessary for the activation of T cell responses when other regulatory mechanisms are intact. Second, commensal bacteria provide a source of nonself antigens, which can be recognized by naïve T cells in the intestine, and these T cells can potentially differentiate into pathogenic effector T cells. It is becoming clear from recent studies, that the commensal composition may play a critical role in affecting the type of T cell responses that can develop in the intestine. Therefore, a possible contribution of commensal flora on the differential induction of pathogenic and protective T cell responses in the intestine will also be discussed.