| First Author | Moyat M | Year | 2017 |
| Journal | Mucosal Immunol | Volume | 10 |
| Issue | 1 | Pages | 271-281 |
| PubMed ID | 27143303 | Mgi Jnum | J:315988 |
| Mgi Id | MGI:6832073 | Doi | 10.1038/mi.2016.38 |
| Citation | Moyat M, et al. (2017) IL-22-induced antimicrobial peptides are key determinants of mucosal vaccine-induced protection against H. pylori in mice. Mucosal Immunol 10(1):271-281 |
| abstractText | Despite the recent description of the mucosal vaccine-induced reduction of Helicobacter pylori natural infection in a phase 3 clinical trial, the absence of immune correlates of protection slows the final development of the vaccine. In this study, we evaluated the role of interleukin (IL)-22 in mucosal vaccine-induced protection. Gastric IL-22 levels were increased in mice intranasally immunized with urease+cholera toxin and challenged with H. felis, as compared with controls. Flow cytometry analysis showed that a peak of CD4(+)IL-22(+)IL-17(+) T cells infiltrating the gastric mucosa occurred in immunized mice in contrast to control mice. The inhibition of the IL-22 biological activity prevented the vaccine-induced reduction of H. pylori infection. Remarkably, anti-microbial peptides (AMPs) extracted from the stomachs of vaccinated mice, but not from the stomachs of non-immunized or immunized mice, injected with anti-IL-22 antibodies efficiently killed H. pylori in vitro. Finally, H. pylori infection in vaccinated RegIIIbeta-deficient mice was not reduced as efficiently as in wild-type mice. These results demonstrate that IL-22 has a critical role in vaccine-induced protection, by promoting the expression of AMPs, such as RegIIIbeta, capable of killing Helicobacter. Therefore, it can be concluded that urease-specific memory Th17/Th22 cells could constitute immune correlates of vaccine protection in humans. |
