ArticleFrontiers in immunology2012
IL-23 Contributes to Control of Chronic Helicobacter Pylori Infection and the Development of T Helper Responses in a Mouse Model.
Article in Frontiers in immunology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
26 citing papers in PubMed, 47 citations in OpenAlex.
- Inflammatory factors collaboratively linkFrontiers in immunology · 2025Review
- Strategies ofFrontiers in cellular and infection microbiology · 2024Review
- Immune Biology and Persistence of Helicobacter pylori in Gastric Diseases.Current topics in microbiology and immunology · 2023Article
- Article
- The Roles of IL-17, IL-21, and IL-23 in theToxins · 2021Review
- Acceptive Immunity: The Role of Fucosylated Glycans in Human Host-Microbiome Interactions.International journal of molecular sciences · 2021Review
- Helicobacter-stimulated IL-10-producing B cells suppress differentiation of lipopolysaccharide/Helicobacter felis-activated stimulatory dendritic cells.Turkish journal of biology = Turk biyoloji dergisi · 2021Article
- From genes polymorphisms to mucosal expression of cytokines: evaluating IL-23/IL-17 axis in adult patients with gastritis.African health sciences · 2020Article
- Th17 Cells in Helicobacter pylori Infection: a Dichotomy of Help and Harm.Infection and immunity · 2019Review
- Altered cytokine expression in Helicobacter pylori infected patients with bleeding duodenal ulcer.BMC research notes · 2019Article
- Proinflammatory Cytokine IL-17 Shows a Significant Association withGastroenterology research and practice · 2017Article
- Current views of the relationship between Helicobacter pylori and Henoch-Schonlein purpura in children.World journal of clinical pediatrics · 2016Review
- Article
- Article
- The host protein calprotectin modulates the Helicobacter pylori cag type IV secretion system via zinc sequestration.PLoS pathogens · 2014Article
- Article
- The emerging role of dendritic cells in the host immune response against Helicobacter pylori.Frontiers in microbiology · 2014Article
- CagA-dependent downregulation of B7-H2 expression on gastric mucosa and inhibition of Th17 responses during Helicobacter pylori infection.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- Article
- Inflammatory cytokine and microRNA responses of primary human dendritic cells cultured with Helicobacter pylori strains.Frontiers in microbiology · 2013Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
The immune response to Helicobacter pylori involves a mixed T helper-1, T helper-2, and T helper-17 response. It has been suggested that T helper cells contribute to the gastric inflammatory response during infection, and that T helper 1 (Th1) and T helper 17 (Th17) subsets may be required for control of H. pylori colonization in the stomach. The relative contributions of these subsets to gastritis and control of infection are still under investigation. IL-23 plays a role in stabilizing and expanding Th17 cell cytokine expression. Expression of IL-23, which is induced in dendritic cells and macrophages following co-culture with H. pylori, has also been reported to increase during H. pylori infection in humans and animal models. To investigate the role of IL-23 in H. pylori, we infected IL-23p19 deficient mice (IL-23-/-) and wild-type littermates with H. pylori strain SS1. At various time points post-infection, we assessed colonization, gastric inflammation, and cytokine profiles in the gastric tissue. Specifically, H. pylori-infected IL-23-/- mice have higher levels of H. pylori in their stomachs, significantly less chronic gastritis, and reduced expression of IL-17 and IFNγ compared to H. pylori-infected wild-type mice. While many of these differences were significant, the H. pylori infected IL-23-/- had mild increases in our measurements of disease severity. Our results indicate that IL-23 plays a role in the activation of the immune response and induction of gastritis in response to H. pylori by contributing to the control of infection and severity of gastritis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.