Evidence map›Paper›PMID 35199503›Full record

ArticleHaematologica2022

Antiplatelet antibody predicts platelet desialylation and apoptosis in immune thrombocytopenia.

Shiying Silvia Zheng, Zohra Ahmadi, Halina Hoi Laam Leung, Rose Wong, Feng Yan, Jose Sail Perdomo, Beng Hock Chong

Open access · goldAbstract read
In one paragraph

Article in Haematologica, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
6.6field-weighted citation impact, top 2% of its field
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

34 citing papers in PubMed, 49 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. The glycan fingerprint in immune thrombocytopenia.Research and practice in thrombosis and haemostasis · 2026
    Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Review
  15. Review
  16. Review
  17. Review
  18. Haemostasis alterations in immune thrombocytopenia and their clinical significance.Research and practice in thrombosis and haemostasis · 2025
    Article
  19. Natural killer cell granule protein 7 contributes to CD8Research and practice in thrombosis and haemostasis · 2025
    Article
  20. 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

7 authors at 3 institutions in 2 countries.

Shiying Silvia ZhengHaematology Research Unit, St. George and Sutherland Clinical School, University of New South Wales, Sydney, Australia; Department of Haematology, St. George Hospital, Kogarah, New South Wales. silvia.zheng@health.nsw.gov.au.
Zohra AhmadiHaematology Research Unit, St. George and Sutherland Clinical School, University of New South Wales, Sydney.
Halina Hoi Laam LeungHaematology Research Unit, St. George and Sutherland Clinical School, University of New South Wales, Sydney.
Rose WongHaematology Research Unit, St. George and Sutherland Clinical School, University of New South Wales, Sydney, Australia; Department of Haematology, St. George Hospital, Kogarah, New South Wales.
Feng YanHaematology Research Unit, St. George and Sutherland Clinical School, University of New South Wales, Sydney, Australia; Department of Haematology, St. George Hospital, Kogarah, New South Wales.
Jose Sail PerdomoHaematology Research Unit, St. George and Sutherland Clinical School, University of New South Wales, Sydney.
Beng Hock ChongHaematology Research Unit, St. George and Sutherland Clinical School, University of New South Wales, Sydney, Australia; Department of Haematology, St. George Hospital, Kogarah, New South Wales.
Sutherland Hospital · AUUNSW Sydney · AUSt. George Hospital · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Immune thrombocytopenia (ITP) is a bleeding disorder caused by dysregulated B- and T- cell functions, which lead to platelet destruction. A well-recognized mechanism of ITP pathogenesis involves anti-platelet and anti-megakaryocyte antibodies recognizing membrane glycoprotein (GP) complexes, mainly GPIb/IX and GPIIb/IIIa. In addition to the current view of phagocytosis of the opsonised platelets by splenic and hepatic macrophages via their Fc γ receptors, antibodyinduced platelet desialylation and apoptosis have also been reported to contribute to ITP pathogenesis. Nevertheless, the relationship between the specific thrombocytopenic mechanisms and various types of anti-platelet antibodies has not been established. In order to ascertain such association, we used sera from 61 ITP patients and assessed the capacity of anti-platelet antibodies to induce neuraminidase 1 (NEU1) surface expression, RCA-1 lectin binding and loss of mitochondrial inner membrane potential on donors' platelets. Sera from ITP patients with detectable antibodies caused significant platelet desialylation and apoptosis. Anti-GPIIb/IIIa antibodies appeared more capable of causing NEU1 surface translocation while anti-GPIb/IX complex antibodies resulted in a higher degree of platelet apoptosis. In ITP patients with anti-GPIIb/IIIa antibodies, both desialylation and apoptosis were dependent on FcγRIIa signaling rather than platelet activation. Finally, we confirmed in a murine model of ITP that destruction of human platelets induced by anti-GPIIb/IIIa antibodies can be prevented with the NEU1 inhibitor oseltamivir. A collaborative clinical trial is warranted to investigate the utility of oseltamivir in the treatment of ITP.

Indexed as

Purpura, Thrombocytopenic, IdiopathicThrombocytopeniaAnimalsAntibodiesApoptosisAutoantibodiesBlood PlateletsHumansMiceOseltamivirPlatelet Glycoprotein GPIb-IX ComplexPlatelet Glycoprotein GPIIb-IIIa ComplexAntibodiesAutoantibodiesOseltamivirPlatelet Glycoprotein GPIb-IX ComplexPlatelet Glycoprotein GPIIb-IIIa Complex

Identifiers

PMID35199503
PMCPMC9425302
OpenAlexW4213423463

What OpenQuestion holds

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LicenceCC BY-NC
Read underepoch 390

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.