Th17-cell responses in Helicobacter-induced intestinal inflammation
The Kullberg lab is interested in the immunology of inflammatory bowel disease (IBD) and the mechanisms by which immune responses are initiated and regulated in the intestinal tract. We use a model of bacterial-induced intestinal inflammation involving infection with Helicobacter hepaticus (Hh). We have previously shown that Hh-induced intestinal inflammation is dependent on IL-23 and associated with CD4+ Th1 and Th17 responses. Moreover, we demonstrated that Th17 cells arising in disease-susceptible hosts are plastic and switch phenotype, transitioning via an IFN-g+IL-17A+ stage to become IFN-g+ ex-Th17 cells. More recently, we have examined the role of Th17-type cytokines to pathology in different regions of the gastrointestinal tract during Hh-induced colitis. Our findings demonstrate that individual Th17-type cytokines can have pro- or anti-inflammatory effects in different regions of the intestine, an observation that may have implications for interventions against human IBD.