Evidence map›Paper›PMID 41853894›Full record

ArticleAmerican journal of hematology2026

IFN-I-Mediated Transcriptional Reprogramming Drives Myeloid-Skewed Hematopoiesis in Sickle Cell Anemia.

Marion Serra, Steven Akkaya, Marine Aglave, Mohammad Salma, Sara Bencheikh, Patricia Hermand, Carine Lefevre, Romain Duval, Jade Merrer, Fallou Leye and 6 more

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In one paragraph

Article in American journal of hematology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

16 authors.

Marion SerraUniversité Paris Cité, Université des Antilles, INSERM, EFS, BIGR U1134, Laboratory of Blood Group Antigens, Hematopoiesis and Sickle Cell Disease, Paris, France.
Steven AkkayaUniversité Paris Cité, Université des Antilles, INSERM, EFS, BIGR U1134, Laboratory of Blood Group Antigens, Hematopoiesis and Sickle Cell Disease, Paris, France.
Marine AglaveGustave Roussy, Plateforme de Bioinformatique, Villejuif, France.
Mohammad SalmaIGMM, Univ Montpellier, CNRS, Montpellier, France.ORCID 0000-0002-3648-1809
Sara BencheikhUniversité Paris Cité, Université des Antilles, INSERM, EFS, BIGR U1134, Laboratory of Blood Group Antigens, Hematopoiesis and Sickle Cell Disease, Paris, France.
Patricia HermandUniversité Paris Cité, Université des Antilles, INSERM, EFS, BIGR U1134, Laboratory of Blood Group Antigens, Hematopoiesis and Sickle Cell Disease, Paris, France.
Carine LefevreUniversité Paris Cité, Université des Antilles, INSERM, EFS, BIGR U1134, Laboratory of Blood Group Antigens, Hematopoiesis and Sickle Cell Disease, Paris, France.
Romain DuvalUniversité Paris Cité, Université des Antilles, INSERM, EFS, BIGR U1134, Laboratory of Blood Group Antigens, Hematopoiesis and Sickle Cell Disease, Paris, France.
Jade MerrerUnité d'Epidémiologie Clinique, INSERM CIC 1426, AP-HP, Hôpital Robert Debré, Paris, France.
Fallou LeyeUnité d'Epidémiologie Clinique, INSERM CIC 1426, AP-HP, Hôpital Robert Debré, Paris, France.
Joelle MagneUniversité Paris Cité, Université des Antilles, INSERM, EFS, BIGR U1134, Laboratory of Blood Group Antigens, Hematopoiesis and Sickle Cell Disease, Paris, France.
Isabelle PloInserm UMR 1287, Université Paris Saclay, Villejuif, France.
Lionel BlancNorthwell, New Hyde Park, New York, USA.
Eric SolerIGMM, Univ Montpellier, CNRS, Montpellier, France.
Slim AzouziUniversité Paris Cité, Université des Antilles, INSERM, EFS, BIGR U1134, Laboratory of Blood Group Antigens, Hematopoiesis and Sickle Cell Disease, Paris, France.ORCID 0000-0001-5519-4031
Berengere KoehlUniversité Paris Cité, Université des Antilles, INSERM, EFS, BIGR U1134, Laboratory of Blood Group Antigens, Hematopoiesis and Sickle Cell Disease, Paris, France.ORCID 0000-0001-7087-7199

Funding

Agence Nationale de la Recherche ANR-11-LABX-0051Agence Nationale de la Recherche ANR-24-CE14-6816-01Etablissement Français du SangEuropean Hematology AssociationSickle Cell Disease Center at Robert Debré Hospital
6 · The paper itself

Abstract

Neutrophils and monocytes are persistently elevated in sickle cell anemia (SCA), yet the intrinsic mechanisms driving pathological myelopoiesis and inflammation remain poorly defined. Through single-cell RNA sequencing and functional assays, we demonstrate that hematopoietic stem and multipotent progenitor cells (HSPCs) in SCA are transcriptionally reprogrammed toward myeloid differentiation. This process is orchestrated by aberrant activation of Type I interferon (IFN-I) signaling, which promotes premature myeloid commitment of hematopoietic stem cells. SCA progenitors further exhibit unexpected responsiveness to granulocyte colony-stimulating factor (G-CSF) through upregulation of CSF3R, resulting in skewed myelopoiesis toward the monocytic lineage. Importantly, hydroxyurea treatment attenuates IFN-I signaling in neutrophils, consistent with its therapeutic role in reducing excessive inflammation and granulopoiesis. Collectively, these findings uncover IFN-I-driven remodeling of hematopoiesis as a fundamental mechanism of leukocytosis and chronic inflammation in SCA, and establish a tractable therapeutic axis to mitigate innate immunity activation in this disease.

Indexed as

Anemia, Sickle CellCellular ReprogrammingHematopoiesisInterferon Type IMyelopoiesisTranscription, GeneticGranulocyte Colony-Stimulating FactorHematopoietic Stem CellsHumansHydroxyureaInflammationMonocytesMyeloid CellsNeutrophilsSignal TransductionGranulocyte Colony-Stimulating FactorHydroxyureaInterferon Type I

Identifiers

PMID41853894

What OpenQuestion holds

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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.