Evidence map›Paper›PMID 40097330›Full record

ReviewHelicobacter

Innate Immunity in Helicobacter pylori Infection and Gastric Oncogenesis.

Yuheng Zhang, Zhiyu Yan, Yuhao Jiao, Yunlu Feng, Shengyu Zhang, Aiming Yang

Abstract readReview
In one paragraph

Review in Helicobacter. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

10 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Clinical and experimental gastroenterology · 2026
    Review
  6. Article
  7. Review
  8. Towards EffectiveInternational journal of molecular sciences · 2025
    Review
  9. Mapping immune trajectories fromFrontiers in immunology · 2025
    Review
  10. MicroRNA-Mediated Regulatory Networks inBiochemistry research international · 2025
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors.

Yuheng ZhangDepartment of Gastroenterology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China.ORCID https://orcid.org/0009-0008-8949-2297
Zhiyu YanDepartment of Gastroenterology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China.
Yuhao JiaoDepartment of Gastroenterology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China.
Yunlu FengDepartment of Gastroenterology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China.
Shengyu ZhangDepartment of Gastroenterology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China.
Aiming YangDepartment of Gastroenterology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China.

Funding

National High Level Hospital Clinical Research Funding 2022-PUMCH-B-024National High Level Hospital Clinical Research Funding 2022-PUMCH-C-063National Key Clinical Specialist Construction Project ZK108000National Key Research and Development Program of China 2022YFC3602103
6 · The paper itself

Abstract

Helicobacter pylori is an extremely common cause of gastritis that can lead to gastric adenocarcinoma over time. Approximately half of the world's population is infected with H. pylori, making gastric cancer the fourth leading cause of cancer-related deaths worldwide. Innate immunity significantly contributes to systemic and local immune responses, maintains homeostasis, and serves as the vital link to adaptive immunity, and in doing so, mediates H. pylori infection outcomes and consequent cancer risk and development. The gastric innate immune system, composed of gastric epithelial and myeloid cells, is uniquely challenged by its need to interact simultaneously and precisely with commensal microbiota, exogenous pathogens, ingested substances, and endogenous exfoliated cells. Additionally, innate immunity can be detrimental by promoting chronic infection and fibrosis, creating an environment conducive to tumor development. This review summarizes and discusses the complex role of innate immunity in H. pylori infection and subsequent gastric oncogenesis, and in doing so, provides insights into how these pathways can be exploited to improve prevention and treatment.

Indexed as

CarcinogenesisHelicobacter InfectionsHelicobacter pyloriImmunity, InnateStomach NeoplasmsAnimalsHumansgastric cancergastric epithelial cellsHelicobacter pyloriinfectioninnate immunitymucosal immunology

Identifiers

PMID40097330
PMCPMC11913635

What OpenQuestion holds

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LicenceCC BY-NC-ND
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Registered trials

None linked

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.