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Cambridge Immunology Network



At the epithelial barrier site of the intestine our body comes into intense contact with a large variety of environmental cues, which influence the immune system. Research on the mechanisms of the interaction of host, commensal microbiota and environmental stimuli, like invading pathogens and dietary components, is receiving growing attention. To dissect these processes, our models of choice are parasites of the genus Eimeria. These protozoa belong to the phylum Apicomplexa, which also contains important human pathogens like Toxoplasma gondii, Plasmodium spp. and Cryptosporidium parvum. In contrast to the latter, Eimeria spp. are host specific and, uniquely, even specific for different parts of the murine intestine. While Eimeria falciformis infects epithelial cells of the crypts of caecum and upper colon, Eimeria vermiformis is restricted to the distal parts of the small intestine - jejunum and ileum. We are utilizing these two parasite species to dissect the mucosal immune response in the large and small intestine, respectively. Replication of the small intestinal parasite E. vermiformis is tightly controlled by αβT cells and dependent on IFN-γ. In contrast, the life cycle of the large intestinal species E. falciformis seems to be largely self-limiting and independent of the adaptive immune system. However, the lack of certain components of the immune system leads to exacerbation of the clinical signs of infection in the case of E. falciformis, whereas this is less apparent in infections with E. vermiformis. We are interested in the mechanisms that lead to limitation of parasite replication and / or tight regulation of the local immune response to prevent overt immunopathology.


Key publications: 

Stange, J., and M. Veldhoen. 2013. The aryl hydrocarbon receptor in innate T cell immunity. Semin. Immunopathol. 35: 645-655.

Stange, J., M. R. Hepworth, S. Rausch, L. Zajic, A. A. Kuhl, C. Uyttenhove, J. C. Renauld, S. Hartmann, and R. Lucius. 2012. IL-22 mediates host defense against an intestinal intracellular parasite in the absence of IFN-gamma at the cost of Th17-driven immunopathology. J. Immunol. 188: 2410-2418.

Wiedmer, S., J. Stange, T. Kurth, W. Bleiss, R. Entzeroth, and M. Kurth. 2011. New insights into the excystation process and oocyst morphology of rodent Eimeria species. Protist 162: 668-678.

Rausch, S., J. Held, J. Stange, M. Lendner, M. R. Hepworth, C. Klotz, R. Lucius, T. Pogonka, and S. Hartmann. 2010. A matter of timing: early, not chronic phase intestinal nematode infection restrains control of a concurrent enteric protozoan infection. Eur. J. Immunol. 40: 2804-2815.

Pogonka, T., K. Schelzke, J. Stange, K. Papadakis, S. Steinfelder, O. Liesenfeld, and R. Lucius. 2010. CD8+ cells protect mice against reinfection with the intestinal parasite Eimeria falciformis. Microbes Infect. 12: 218-226.

Frevert, U., S. Engelmann, S. Zougbede, J. Stange, B. Ng, K. Matuschewski, L. Liebes, and H. Yee. 2005. Intravital observation of Plasmodium berghei sporozoite infection of the liver. PLoS Biol 3: e192.

Dr Jörg  Stange
Not available for consultancy


Collaborator profiles: 
Departments and institutes: 
Person keywords: 
intestinal immune system
host-pathogen interaction
innate immunity
Apicomplexan parasites
Eimeria spp.