Mucosal-associated Invariant T (MAIT) cells are innate like T cells that are restricted by the non-classical MHC class I-related molecule, MR1. MAIT cells detect antigens that are derived from microbial vitamin B2 (riboflavin) synthesis, and produce inflammatory cytokines, including IL-17, IFNg and TNF, and cytotoxic granzymes.

Helicobacter pylori is a bacterium that infects the human stomach and is aetiologically associated with gastritis, duodenal ulcers and gastric cancer. Although MAIT cells have been shown to be protective against some pulmonary infections, their production of pro-inflammatory cytokines suggest chronic stimulation of MAIT cells could contribute to pathology. Using highly specific MR1 tetramers and mouse models of H. pylori infection, we have shown that MAIT cells accumulate in the stomach, have a Tc1/Tc17 phenotype and accelerate pathology associated with the recruitment of other immune cells. This occurred both in MAIT TCR transgenic mice, and in a prime-boost model of C57BL/6 mice where MAIT cells were first primed intranasally either with bacteria or with TLR agonists plus synthetic antigen. Thus, we show a pathogenic role for MAIT cells for the first time in H. pylori associated inflammation, revealing a broader potential role for MAIT cell-driven immunopathology in chronic bacterial infection.