13 Dendritic cells (DCs) are classified as professional antigen presenting cells (APCs) and play a central role in both the innate and acquired immune responses. DCs are heterogeneous populations of cells. Migratory Protein Tyrosine Kinase inhibitor and resident DCs are involved in the maintenance of self-tolerance

and the induction of specific immune responses against invading pathogens. DCs act as APCs by phagocytosing pathogens and self-antigens and then presenting the antigens to T and B cells on their cell surface. DCs also produce several cytokines in response to stimulation signals from pathogen-associated molecular patterns (PAMPs) or whole bacteria. Thus, DCs contribute to immunological homeostasis by promoting inflammatory responses to pathogens, inducing tolerance to self-antigens,

and suppressing this website excessive immune responses.14 Dysregulation of DCs can therefore lead to autoimmune diseases and chronic inflammatory disorders. Abnormally strong immune responses to commensal bacteria, food antigens, and self-antigens have been reported in the pathogenesis of these diseases. The article by Long and colleagues in this issue of the Journal compares the phenotype and function of mouse lamina propria DCs (LPDCs) in the acute infectious and post-infectious phases of a PI-IBS mouse model (Fig. 1).15 The model used mice infected with Trichinella spiralis, which showed a prolonged disturbance in intestinal motility, with visceral hyperalgesia observed 8 weeks

after infection.16 In the acute infectious phase (2 weeks after infection), LPDCs displayed low CD86 and MHC class II molecule expression patterns and lesser ability to induce T cell proliferation, although endocytosis function was well maintained. On the other hand, in the PI-IBS phase (8 weeks after infection), LPDCs displayed increased CD86 and MHC class II expression patterns resulting in enhanced induction of T cell proliferation, while endocytosis function was decreased. These results demonstrate that post-infectious LPDCs in the mouse model display the phenotype with higher APC function. Interestingly, co-culture of naïve T cells with LPDCs in the acute infectious phase induced a Th2 response. In contrast, Fenbendazole co-culture of naïve T cells with LPDCs in the post-infectious phase induced Th1 and Th17 responses. Based on these findings, Long and colleagues concluded that phenotypical and functional alterations of LPDCs contribute to the development of PI-IBS. Studies of DC function in human IBS are few, but it has been reported that the plasma concentration of kynurenic acid, which is produced through the tryptophan degradation pathway regulated by indoleamine 2,3-dioxygenase (IDO), is increased in male patients with IBS.17 Since IDO is a key enzyme regulating the metabolism of tryptophan, which plays an important role in DC function, this finding may support the hypothesis that DC function is changed in patients with IBS.