ArticleInternational journal of hematology2009
Cross-reaction of antibody against Helicobacter pylori urease B with platelet glycoprotein IIIa and its significance in the pathogenesis of immune thrombocytopenic purpura.
Article in International journal of hematology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 41 citations in OpenAlex.
- Complex regulatory effects of gut microbial short-chain fatty acids on immune tolerance and autoimmunity.Cellular & molecular immunology · 2023Review
- Eradication therapy may decrease the risk of immune thrombocytopenia after Helicobacter pylori infection: a retrospective cohort study in Taiwan.BMC gastroenterology · 2023Article
- Role ofJournal of clinical medicine · 2020Review
- H. pylori infection and extra-gastroduodenal diseases.Journal of biomedical science · 2018Review
- The Impact ofFrontiers in microbiology · 2017Article
- Clinical significance of Helicobacter pylori infection in patients with acute coronary syndromes: an overview of current evidence.Clinical research in cardiology : official journal of the German Cardiac Society · 2014Review
- Helicobacter pylori-associated immune thrombocytopenia: clinical features and pathogenic mechanisms.World journal of gastroenterology · 2014Review
- VacA, the vacuolating cytotoxin of Helicobacter pylori, binds to multimerin 1 on human platelets.Thrombosis journal · 2013Article
- Development of corpus atrophic gastritis may be associated with Helicobacter pylori-related idiopathic thrombocytopenic purpura.Journal of gastroenterology · 2011Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Many clinical investigations have suggested that Helicobacter pylori (H. pylori) infection might be associated with immune thrombocytopenic purpura (ITP), but its role in the pathogenesis of ITP is unsettled. In this study, we cultured H. pylori, produced recombinant H. pylori urease (ure) B, and then prepared monoclonal antibody (MoAb) against ureB, 1F11, both 1F11 and MoAb against human platelet glycoprotein (GP) IIIa, SZ21, could bind to the band of GP IIIa of normal platelet lysate, but not to that from a patient with Glanzmann thrombasthenia (GT) whose GP IIb-IIIa complex was absent. Flow cytometry showed that normal platelets were reacted with 1F11 and SZ21, while GT platelets were not. In immuno-radiometric assay, the binding of (125)I-labeled 1F11 to GP IIIa was higher than that to GP Ib, GP IIb, GP VI, and P-selectin. 1F11 could partly compete with SZ21 in a binding to platelet surface. In addition, 1F11 inhibited platelet aggregation induced by adenosine diphosphate, but had no effect on platelet P-selectin expression or Thromboxane B(2) production of platelets. These results indicate that H. pylori ureB antibody could cross-react with human platelet GP IIIa and partly inhibit platelet aggregation. UreB may be a crucial component of H. pylori involved in the pathogenesis of a subset of ITP.
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