ArticlePloS one2016
IL-17a and IL-22 Induce Expression of Antimicrobials in Gastrointestinal Epithelial Cells and May Contribute to Epithelial Cell Defense against Helicobacter pylori.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
47 citing papers in PubMed, 91 citations in OpenAlex.
- The Dual Role of Zinc Homeostasis in Gram-Negative Bacterial Pathogenicity and Host Immune Defense.Microorganisms · 2026Review
- Context-specific roles for IL-17 in tuberculosis.PLoS pathogens · 2026Review
- Biphasic Regulation of Epithelial Antimicrobial Peptides DuringJournal of fungi (Basel, Switzerland) · 2026Article
- Managing dangerous liaisons: lessons fromJournal of bacteriology · 2026Review
- Mucosal vaccination with enzymatically activeFrontiers in microbiology · 2026Article
- IL-17-mediated antifungal immunity restricts Candida albicans pathogenicity in the oral cavity.Nature microbiology · 2026Article
- DOCK8 in T cells promotes Th17 and Treg cell functionality to restrain mucosal mast cells and limit susceptibility to oral anaphylaxis.Immunity · 2025Article
- The role of IL-22 in cancer.Medical oncology (Northwood, London, England) · 2024Review
- IL-8 (CXCL8) Correlations with Psychoneuroimmunological Processes and Neuropsychiatric Conditions.Journal of personalized medicine · 2024Review
- IL-17RA-Mediated Epithelial Cell Activity Prevents Severe Inflammatory Response to Helicobacter pylori Infection.ImmunoHorizons · 2024Article
- IL-17 receptor A functions to help maintain barrier integrity and limit activation of immunopathogenic response toInfection and immunity · 2024Article
- Strategies ofFrontiers in cellular and infection microbiology · 2024Review
- Viral Persistence in the Gut-Associated Lymphoid Tissue and Barriers to HIV Cure.AIDS research and human retroviruses · 2023Article
- Microbial Reprogramming in Obsessive-Compulsive Disorders: A Review of Gut-Brain Communication and Emerging Evidence.International journal of molecular sciences · 2023Review
- A Th17 cell-intrinsic glutathione/mitochondrial-IL-22 axis protects against intestinal inflammation.bioRxiv : the preprint server for biology · 2023Article
- Current Knowledge of Th22 Cell and IL-22 Functions in Infectious Diseases.Pathogens (Basel, Switzerland) · 2023Review
- Dermatophyte infection: from fungal pathogenicity to host immune responses.Frontiers in immunology · 2023Review
- IL-17: Balancing Protective Immunity and Pathogenesis.Journal of immunology research · 2023Review
- The correlation of Th22 and regulatory T cells with Helicobacter pylori infection in patients with chronic gastritis.Immunity, inflammation and disease · 2023Article
- Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Helicobacter pylori colonization of the human stomach can lead to adverse clinical outcomes including gastritis, peptic ulcers, or gastric cancer. Current data suggest that in addition to bacterial virulence factors, the magnitude and types of immune responses influence the outcome of colonization. Specifically, CD4+ T cell responses impact the pathology elicited in response to H. pylori. Because gastritis is believed to be the initiating host response to more detrimental pathological outcomes, there has been a significant interest in pro-inflammatory T cell cytokines, including the cytokines produced by T helper 17 cells. Th17 cells produce IL-17A, IL-17F, IL-21 and IL-22. While these cytokines have been linked to inflammation, IL-17A and IL-22 are also associated with anti-microbial responses and control of bacterial colonization. The goal of this research was to determine the role of IL-22 in activation of antimicrobial responses in models of H. pylori infection using human gastric epithelial cell lines and the mouse model of H. pylori infection. Our data indicate that IL-17A and IL-22 work synergistically to induce antimicrobials and chemokines such as IL-8, components of calprotectin (CP), lipocalin (LCN) and some β-defensins in both human and primary mouse gastric epithelial cells (GEC) and gastroids. Moreover, IL-22 and IL-17A-activated GECs were capable of inhibiting growth of H. pylori in vitro. While antimicrobials were activated by IL-17A and IL-22 in vitro, using a mouse model of H. pylori infection, the data herein indicate that IL-22 deficiency alone does not render mice more susceptible to infection, change their antimicrobial gene transcription, or significantly change their inflammatory response.
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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.