The gastrointestinal tract is the major site for constant immunological challenge to the host immune system. The host must be able to mount protective immune responses against pathogenic micro-organisms while maintaining tolerance to most microbes under homeostatic conditions. A number of Helicobacter species, including Helicobacter hepaticus, have been isolated as the etiological agents of gastric ulcer disease or colitis in their respective hosts. H. hepaticus infection induces severe colitis in a number of immunocompromised mouse mutants, but interestingly does not usually cause disease in most WT mouse strains. Although Th17/Th1 responses are known to play an important role in H. hepaticus-mediated inflammation, how the immune response is contained such that it is harmless under homeostatic conditions and how perturbations lead to pathogenicity remain elusive questions. To answer these, it will be important to track H. hepaticus-specific T helper cells, which form a small proportion of total gut T helper cells, under homeostatic conditions. We have characterized TCRs specific for H. hepaticus antigens, which has allowed for development of TCR transgenic mice and MHCII tetramers to interrogate the specific T cell response that can contribute to inflammatory bowel disease in mouse models.
Citation Format: Mo Xu, Dan R. Littman. Helicobacter-specific T cell responses in gut homeostasis and disease. [abstract]. In: Proceedings of the CRI-CIMT-EATI-AACR Inaugural International Cancer Immunotherapy Conference: Translating Science into Survival; September 16-19, 2015; New York, NY. Philadelphia (PA): AACR; Cancer Immunol Res 2016;4(1 Suppl):Abstract nr A098.
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