Th17 Cytokines and the Gut Mucosal Barrier

Abstract

Local immune responses serve to contain infections by pathogens to the gut while preventing pathogen dissemination to systemic sites. Several subsets of T cells in the gut (T-helper 17 cells, γδ T cells, natural killer (NK), and NK-T cells) contribute to the mucosal response to pathogens by secreting a subset of cytokines including interleukin (IL)-17A, IL-17F, IL-22, and IL-26. These cytokines induce the secretion of chemokines and antimicrobial proteins, thereby orchestrating the mucosal barrier against gastrointestinal pathogens. While the mucosal barrier prevents bacterial dissemination from the gut, it also promotes colonization by pathogens that are resistant to some of the inducible antimicrobial responses. In this review, we describe the contribution of Th17 cytokines to the gut mucosal barrier during bacterial infections.

Up-regulation of small intestinal interleukin-17 immunity in untreated coeliac disease but not in potential coeliac disease or in type 1 diabetes

“…Conversely, a recent study showed that a commensal bacteria strain which mediated protection from autoimmune diabetes in a rodent model caused induction of mucosal IL-17 immunity [30]. Our results suggest that the up-regulation of intestinal IL-17 immunity is related to the mechanisms of protection from tissue damage in the inflamed mucosa, as also suggested by others [31], and could thus explain the beneficial effects of mucosal IL-17 up-regulation in autoimmune diabetes. In this study, we did not see evidence for the up-regulation of small intestinal IL-17 immunity in children with T1D who did not have CD, although we have reported enhanced activation of IL-17 immunity in peripheral blood T cells in children with T1D [21].…”

Delivery strategies to enhance oral vaccination against enteric infections

“…The desired outcome of oral vaccination against diarrhoeal infections is the reinforcement of gut barriers through SIgA antibodies [25,86] and effector/memory T and B cells which enhance frontline defences against pathogen reencounter [83,87]. Other local responses against gut infections include the augmented secretion of host factors such as defensins, cytokines and chemokines [88,89].…”

Expression pattern of T-helper 17 cell signaling pathway and mucosal inflammation in celiac disease

“…In a previous study we showed that IL-17 induced anti-apoptotic rather than apoptotic responses in an epithelial cell line [9]. IL-17 in mucosal anti-microbial defence has been shown to contribute to the gut barrier function and up-regulation of IL-17 diminishes the dissemination of pathogens from the intestinal lumen [15]. Furthermore, the small intestinum seems to be responsible for the control of the response by eliminating Th17 cells and by induction of a phenotype change in Th17 cells, which acquire suppressive phenotype characteristics and participate in the regulation of immune responses in small intestine [16].…”