IRAK3 and gastritis: Since TH17 cells have been shown to contribute to the gastritis seen in H. pylori infection as well as to protection against H. pylori in experimental murine vaccine models [21], [44]–[46], we sought to determine whether the proinflammatory phenotype of IRAK-M−/− BMDCs might increase TH17 activation using a DC-T cell coculture system.