IL-21 expression during H. pylori infection

The development of gastritis during Helicobacter pylori infection is dependent on an activated adaptive immune response orchestrated by T helper cells. The relative contributions of T helper 1 (Th1) and T helper 17 (Th17) subsets to gastritis and control of infection are still under investigation. Expression of IL-21, which may be produced by a number of T cell subsets, has been reported to increase during H. pylori infection. To investigate the role of IL-21 in the gastric mucosa during H. pylori infection, we combined mathematical modeling of CD4+ T cell differentiation with in vivo studies to elucidate the impact of IL-21 on H. pylori infection. Our computational modeling efforts predict that IL-21 activates the production of IFN gamma and IL17, the expression of Tbet and RORgamma t, the phosphorylation of STAT3, and suggest a potential role of IL-21 in the modulation of IL-10. To elucidate the role IL-21 in vivo, we infected IL-21 deficient mice and wild-type littermates with H. pylori strain SS1, and assessed colonization, gastric inflammation, cellular infiltration, and cytokine profiles in the gastric tissue.