Evidence map›Paper›PMID 34095758›Full record

ReviewHemaSphere2021

Immune Thrombocytopenia: Recent Advances in Pathogenesis and Treatments.

Sylvain Audia, Matthieu Mahévas, Martin Nivet, Sethi Ouandji, Marion Ciudad, Bernard Bonnotte

Open access · goldAbstract readReview
In one paragraph

Review in HemaSphere, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed
12.1field-weighted citation impact, top 1% 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

71 citing papers in PubMed, 131 citations in OpenAlex.

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  11. The glycan fingerprint in immune thrombocytopenia.Research and practice in thrombosis and haemostasis · 2026
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11 more citing papers are in PubMed but not listed here.

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 at 2 institutions in 1 country.

Sylvain AudiaService de Médecine Interne et Immunologie Clinique, Centre de Référence Constitutif des Cytopénies Auto-immunes de l'adulte, Centre Hospitalo-Universitaire Dijon Bourgogne, Université de Bourgogne Franche-Comté, Dijon, France.
Matthieu MahévasService de Médecine Interne, Centre de Référence des Cytopénies Auto-immunes de l'adulte, Centre Hospitalier Universitaire Henri-Mondor, Assistance Publique-Hôpitaux de Paris (AP-HP), Université Paris-Est Créteil (UPEC), Créteil, France.
Martin NivetService de Médecine Interne et Immunologie Clinique, Centre de Référence Constitutif des Cytopénies Auto-immunes de l'adulte, Centre Hospitalo-Universitaire Dijon Bourgogne, Université de Bourgogne Franche-Comté, Dijon, France.
Sethi OuandjiService de Médecine Interne et Immunologie Clinique, Centre de Référence Constitutif des Cytopénies Auto-immunes de l'adulte, Centre Hospitalo-Universitaire Dijon Bourgogne, Université de Bourgogne Franche-Comté, Dijon, France.
Marion CiudadService de Médecine Interne et Immunologie Clinique, Centre de Référence Constitutif des Cytopénies Auto-immunes de l'adulte, Centre Hospitalo-Universitaire Dijon Bourgogne, Université de Bourgogne Franche-Comté, Dijon, France.
Bernard BonnotteService de Médecine Interne et Immunologie Clinique, Centre de Référence Constitutif des Cytopénies Auto-immunes de l'adulte, Centre Hospitalo-Universitaire Dijon Bourgogne, Université de Bourgogne Franche-Comté, Dijon, France.
Université de Bourgogne · FRUniversité Paris Cité · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Immune thrombocytopenia (ITP) is a rare autoimmune disease due to both a peripheral destruction of platelets and an inappropriate bone marrow production. Although the primary triggering factors of ITP remain unknown, a loss of immune tolerance-mostly represented by a regulatory T-cell defect-allows T follicular helper cells to stimulate autoreactive splenic B cells that differentiate into antiplatelet antibody-producing plasma cells. Glycoprotein IIb/IIIa is the main target of antiplatelet antibodies leading to platelet phagocytosis by splenic macrophages, through interactions with Fc gamma receptors (FcγRs) and complement receptors. This allows macrophages to activate autoreactive T cells by their antigen-presenting functions. Moreover, the activation of the classical complement pathway participates to platelet opsonization and also to their destruction by complement-dependent cytotoxicity. Platelet destruction is also mediated by a FcγR-independent pathway, involving platelet desialylation that favors their binding to the Ashwell-Morell receptor and their clearance in the liver. Cytotoxic T cells also contribute to ITP pathogenesis by mediating cytotoxicity against megakaryocytes and peripheral platelets. The deficient megakaryopoiesis resulting from both the humoral and the cytotoxic immune responses is sustained by inappropriate levels of thrombopoietin, the major growth factor of megakaryocytes. The better understanding of ITP pathogenesis has provided important therapeutic advances. B cell-targeting therapies and thrombopoietin-receptor agonists (TPO-RAs) have been used for years. New emerging therapeutic strategies that inhibit FcγR signaling, the neonatal Fc receptor or the classical complement pathway, will deeply modify the management of ITP in the near future.

Identifiers

PMID34095758
PMCPMC8171374
OpenAlexW3170272567

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.