Evidence map›Paper›PMID 40894252›Full record

ReviewJournal of translational autoimmunity2025

When the victim becomes the villain: Platelets as drivers of immune dysregulation in ITP.

Fatemeh Farhid, Hadi Rezaeeyan, Reza Habibi, Ehsan Kamali Yazdi, Michael R Hamblin, Jalal Naghinezhad

Abstract readReview
In one paragraph

Review in Journal of translational autoimmunity, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing 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

9 citing papers in PubMed.

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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.

Fatemeh FarhidBlood Transfusion Research Center, High Institute for Research and Education in Transfusion Medicine, Iranian Blood Transfusion Organization Building, Next to the Milad Tower, Hemmat Exp. Way, P.O.Box:14665-1157, Tehran, Iran.
Hadi RezaeeyanAsadabad School of Medical Sciences, Asadabad, Iran.
Reza HabibiTehran University of Medical Science, Tehran, Iran.
Ehsan Kamali YazdiAlborz University of Medical Sciences, Alborz, Iran.
Michael R HamblinLaser Research Centre, University of Johannesburg, Doornfontein, 2028, South Africa.
Jalal NaghinezhadBlood Transfusion Research Center, High Institute for Research and Education in Transfusion Medicine, Iranian Blood Transfusion Organization Building, Next to the Milad Tower, Hemmat Exp. Way, P.O.Box:14665-1157, Tehran, Iran.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Immune thrombocytopenia (ITP) is a heterogeneous autoimmune disorder characterized by immune-mediated destruction of platelets and impaired platelet production. Although autoantibodies have historically been central to the understanding of ITP, current evidence demonstrates that its pathogenesis extends well beyond humoral mechanisms to involve complex dysregulation of both innate and adaptive immune responses. Multiple immune pathways-including autoreactive B and T cells, dendritic cell activation, and regulatory T cell deficiency-contribute to disease onset, progression, and chronicity. Moreover, ITP encompasses a broad spectrum of clinical and immunological subtypes, including primary idiopathic forms and secondary ITP associated with autoimmune diseases, infections, and inborn errors of immunity. This review offers a novel perspective on ITP pathogenesis, emphasizing the active immunoregulatory role of platelets as contributors to immune dysregulation. Far from being passive targets, platelets in ITP actively shape immune responses through crosstalk with immune cells, particularly CD4

Indexed as

Hairy plateletsImmune dysregulationImmune thrombocytopeniaPlatelet activationP-SelectinP-Selectin glycoprotein ligand 1Transforming growth factor β

Identifiers

PMID40894252
PMCPMC12398799

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.