IL-21 is required for maintaining mucosal Th1 and Th17 responses during Helicobacter pylori infection (P3184)
| Autor: | Adria Carbo, Raquel Hontecillas, M. Kay Washington, Rupesh Chaturvedi, Danyvid Olivares-Villagómez, Keith T. Wilson, Josep Bassaganya-Riera, Holly M. Algood |
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| Rok vydání: | 2013 |
| Předmět: | |
| Zdroj: | The Journal of Immunology. 190:124.3-124.3 |
| ISSN: | 1550-6606 0022-1767 |
| DOI: | 10.4049/jimmunol.190.supp.124.3 |
| Popis: | CD4+ T cells play a major role in the modulation of immune responses at the gastric mucosa during Helicobacter pylori infection. The relative contributions of CD4+ T cell subsets to gastritis and control of H. pylori colonization and clearance are not completely understood. Expression of IL-21, which is produced by a number of T cell subsets, increases during H. pylori infection. To elucidate the mechanisms of action of IL-21 in effector and regulatory CD4+ T cells during H. pylori infection, we combined computational modeling of CD4+ T cell differentiation and in vivo challenge studies in mice. Our computational modeling predicted activated production of IFNγ and IL-17 by IL-21, and the expression of T-bet, RORγt and phosphorylation of STAT3. To investigate the role of IL-21 in vivo, we infected IL-21-/- and wild-type mice with H. pylori SS1, and assessed colonization, gastric inflammation, cellular infiltration and cytokine profiles in the gastric mucosa. During chronic infection, IL-21-/- mice had higher H. pylori colonization, less gastritis and reduced expression of inflammatory cytokines and chemokines. Moreover, H. pylori infected IL-21-/- mice had reduced levels of CD4+ T cell specific RORγt and T-bet when compared to infected wild-type mice. Our results indicate that IL-21 contributes to the control of infection and severity of gastritis, suggesting a role for induction of gastritis in response to H. pylori through activation of both Th17 and Th1 effector responses. |
| Databáze: | OpenAIRE |
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