ReviewJournal of immunology research2015
Helicobacter pylori and T Helper Cells: Mechanisms of Immune Escape and Tolerance.
Review in Journal of immunology research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
54 citing papers in PubMed.
- [Molecular mechanisms of chronic gastric mucosal inflammation induced byZhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2026Review
- A Pathogen Penalty? Associations Between Persistent Infections and Biological Aging in the US.The Journal of infectious diseases · 2026Article
- Computational design of a multi-epitope vaccine against Helicobacter pylori targeting CagA, FliD, urease, and OipA with cholera toxin B subunit (CTB) adjuvant.BMC microbiology · 2026Article
- Helicobacter pylori infection is causally associated with extra-gastric tumors: a Mendelian randomization study.Discover oncology · 2026Article
- Effect ofTherapeutic advances in gastroenterology · 2026Review
- Screening and functional validation of key genes inFrontiers in immunology · 2026Article
- Inflammation as a Unifying Axis: Shared Pathogenic Mechanisms in Coronary Atherosclerosis and Chronic Atrophic Gastritis.Journal of inflammation research · 2026Review
- Nanoemulsion as a promising drug delivery strategy for effective eradication of Helicobacter pylori: current insights.Drug delivery and translational research · 2026Review
- T Helper and Cytotoxic T Cells Play an Important Role in Acute Gastric Injury.Diseases (Basel, Switzerland) · 2025Article
- The gut microbiota in cancer immunity and immunotherapy.Cellular & molecular immunology · 2025Review
- Co-Infection Dynamics ofInternational journal of molecular sciences · 2025Review
- The Potential Role ofMicroorganisms · 2025Review
- A Narrative Review on the Multifaceted Roles of Galectins in Host-Pathogen Interactions DuringInternational journal of molecular sciences · 2025Review
- Single-cell RNA sequencing dissects the immunosuppressive signatures in Helicobacter pylori-infected human gastric ecosystem.Nature communications · 2025Article
- TargetingNutrients · 2025Review
- Immune Cell Interactions and Immune Checkpoints in the Tumor Microenvironment of Gastric Cancer.International journal of molecular sciences · 2025Review
- Review
- The immunoregulatory role of helper T cells inFrontiers in immunology · 2025Review
- Shrimp Lipid Bioactives with Anti-Inflammatory, Antithrombotic, and Antioxidant Health-Promoting Properties for Cardio-Protection.Marine drugs · 2024Review
- Altered Cytokine Production in Patients withMiddle East journal of digestive diseases · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Helicobacter pylori colonizes the gastric mucosa of at least half of the human population, causing a worldwide infection that appears in early childhood and if not treated, it can persist for life. The presence of symptoms and their severity depend on bacterial components, host susceptibility, and environmental factors, which allow H. pylori to switch between commensalism and pathogenicity. H. pylori-driven interactions with the host immune system underlie the persistence of the infection in humans, since the bacterium is able to interfere with the activity of innate and adaptive immune cells, reducing the inflammatory response in its favour. Gastritis due to H. pylori results from a complex interaction between several T cell subsets. In particular, H. pylori is known to induce a T helper (Th)1/Th17 cell response-driven gastritis, whose impaired modulation caused by the bacterium is thought to sustain the ongoing inflammatory condition and the unsuccessful clearing of the infection. In this review we discuss the current findings underlying the mechanisms implemented by H. pylori to alter the T helper lymphocyte proliferation, thus facilitating the development of chronic infections and allowing the survival of the bacterium in the human host.
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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.