The type of immunity elicited by the pathogenic bacteria Yersinia enterocolitica is now shown to depend on the route of infection (J. Exp. Med. 209, 1437–1444).

R. William DePaolo et al. showed that oral infection of mice with Y. enterocolitica promotes T helper type 17 (TH17) immunity, whereas systemic infection with the same pathogen leads to a TH1 response. They found that the TH17 response induced by oral Y. enterocolitica was dependent on the presence of Toll-like receptor 1 (TLR1). TLR1-deficient mice produced reduced levels of the cytokines interleukin-6 (IL-6) and IL-23, which are involved in TH17 polarization, compared with infected control mice. Consistent with this, the authors found that TLR1 signaling in dendritic cells (DCs) was involved in the production of IL-6 and IL-23 in the presence of Y. enterocolitica. TLR1 may also influence DC migration in response to oral Y. enterocolitica infection, as De Paolo et al. showed that TLR1-deficient mice had a reduced number of DCs in their mesenteric lymph nodes compared with infected controls.

These findings may have implications for vaccine development, indicating the importance of understanding the type of pathogen and its effects on specific tissues for designing a vaccine to elicit an appropriate immune response.