Helicobacter species are potent drivers of colonic T cell responses in homeostasis and inflammation

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Science Immunology  21 Jul 2017:
Vol. 2, Issue 13, eaal5068
DOI: 10.1126/sciimmunol.aal5068

Context is critical in IBD

The intestine hosts trillions of commensal microbes; however, exactly how these microbes contribute to a balanced immune response in the intestine is still being explored. Now, Chai et al. report that mucosal-associated Helicobacter species can trigger either regulatory T (Treg) or effector T (Teff) cell activation in mouse intestine, depending on context. T cells specific to the bacteria activated Treg cells in homeostatic conditions. In contrast, in a mouse model of colitis, Helicobacter species induced Teff cells. These data suggest that a pathobiont such as Helicobacter species may induce immune tolerance in homeostatic conditions but switch to contribute to pathogenesis in the presence of inflammation.


Specific gut commensal bacteria improve host health by eliciting mutualistic regulatory T (Treg) cell responses. However, the bacteria that induce effector T (Teff) cells during inflammation are unclear. We addressed this by analyzing bacterial-reactive T cell receptor (TCR) transgenic cells and TCR repertoires in a murine colitis model. Unexpectedly, we found that mucosal-associated Helicobacter species triggered both Treg cell responses during homeostasis and Teff cell responses during colitis, as suggested by an increased overlap between the Teff/Treg TCR repertoires with colitis. Four of six Treg TCRs tested recognized mucosal-associated Helicobacter species in vitro and in vivo. By contrast, the marked expansion of luminal Bacteroides species seen during colitis did not trigger a commensurate Teff cell response. Unlike other Treg cell–inducing bacteria, Helicobacter species are known pathobionts and cause disease in immunodeficient mice. Thus, our study suggests a model in which mucosal bacteria elicit context-dependent Treg or Teff cell responses to facilitate intestinal tolerance or inflammation.

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