Innate and adaptive immune responses related to IBD pathogenesis

Although the adaptive immune system traditionally has been the primary focus of investigations into the pathogenesis of inflammatory bowel disease (IBD), it is now clear that innate immune responses play an equally important, or perhaps even primary, role in disease initiation. Intestinal barrier function defects and genetic associations with the nucleotide-binding oligomerization domain and Toll-like receptor pathways suggest that the innate immune system has failed to protect the host against the vast array of commensal bacteria in the gut. This hypothesis is supported further by the observation that probiotic agents exert anti-inflammatory effects in the intestine through stimulation, rather than suppression, of the mucosal innate immune system. Moreover, it is now clear that adaptive immune responses involved in IBD pathogenesis are more complex than the traditionally dichotomous Th1/Th2 paradigm. Finally, mounting evidence suggests that the Th17 effector pathway may contribute to Crohn's disease pathogenesis.