T cell subsets and environmental factors in Citrobacter rodentium infection

Infection with Citrobacter rodentium constitutes an attack on the intestinal barrier and results in concerted action by innate and adaptive immune responses to limit bacterial translocation and destroy those bacteria that have breached the intestinal barrier. Among the many immune cell types that are involved in the defence against this infection, Th17 cells as the major producers of the barrier protective cytokine IL-22 during the adaptive phase of the response are most numerous. Their extensive plasticity furthermore results in the production of additional cytokines that previously were ascribed to Th1 cells, such as IFN-y. The timely and coordinated repair of damaged epithelium requires input from environmental factors derived from diet and microbiota metabolism of tryptophan which are transmitted through the aryl hydrocarbon receptor (AHR). Thus, the combination of a robust immune response, coupled with intestinal stem cell differentiation guided by environmental factors, ensures resistance to barrier destruction by intestinal infection.

Automated summary

Infection with Citrobacter rodentium triggers a threat to the intestinal barrier, prompting a coordinated immune response involving Th17 cells to limit bacterial translocation and repair damaged epithelium with the aid of environmental factors.