Evidence map›Paper›PMID 41650961›Full record

ArticleStem cell reports2026

Erythropoietin exposure disrupts B cell development and drives the emergence of myeloid-biased biphenotypic progenitors.

Andrada Chiron-Margerie, Stéphanie Bessoles, Guillaume Sarrabayrouse, Kutaiba Alhaj-Hussen, Corentin Joulain, Thomas Darde, Pierre de la Grange, Amine M Abina, Bruno Canque, Roman Krzysiek and 1 more

Abstract read
In one paragraph

Article in Stem cell reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

11 authors.

Andrada Chiron-MargerieUniversité Paris Cité, CNRS 8258, INSERM U1267, Unité des Technologies Chimiques et Biologiques pour La Santé, Paris, France; Clinical Immunology Laboratory, Groupe Hospitalier Universitaire Paris-Saclay, Hôpital Bicêtre, Assistance Publique-Hôpitaux de Paris, Le-Kremlin-Bicêtre, France.
Stéphanie BessolesUniversité Paris Cité, CNRS 8258, INSERM U1267, Unité des Technologies Chimiques et Biologiques pour La Santé, Paris, France.
Guillaume SarrabayrouseUniversité Paris Cité, CNRS 8258, INSERM U1267, Unité des Technologies Chimiques et Biologiques pour La Santé, Paris, France.
Kutaiba Alhaj-HussenDepartment of Biological Hematology, Groupe Hospitalier Universitaire Paris-Saclay, Hôpital Bicêtre, Assistance Publique-Hôpitaux de Paris, Le-Kremlin-Bicêtre, France; INSERM 1151, Université de Paris, École Pratique des Hautes Études/PSL Research University, Institut Necker Enfants Malades (INEM), Paris, France.
Corentin JoulainUniversité Paris Cité, CNRS 8258, INSERM U1267, Unité des Technologies Chimiques et Biologiques pour La Santé, Paris, France.
Thomas DardeSciLicium, Rennes, France.
Pierre de la GrangeGenoSplice Technology, Paris, France.
Amine M AbinaUniversité Paris Cité, CNRS 8258, INSERM U1267, Unité des Technologies Chimiques et Biologiques pour La Santé, Paris, France.
Bruno CanqueINSERM 1151, Université de Paris, École Pratique des Hautes Études/PSL Research University, Institut Necker Enfants Malades (INEM), Paris, France.
Roman KrzysiekClinical Immunology Laboratory, Groupe Hospitalier Universitaire Paris-Saclay, Hôpital Bicêtre, Assistance Publique-Hôpitaux de Paris, Le-Kremlin-Bicêtre, France; UMR-996 INSERM, Inflammation, Microbiome and Immunosurveillance, Paris-Saclay University, Orsay, France.
Salima Hacein-Bey-AbinaUniversité Paris Cité, CNRS 8258, INSERM U1267, Unité des Technologies Chimiques et Biologiques pour La Santé, Paris, France; Clinical Immunology Laboratory, Groupe Hospitalier Universitaire Paris-Saclay, Hôpital Bicêtre, Assistance Publique-Hôpitaux de Paris, Le-Kremlin-Bicêtre, France. Electronic address: salima.hacein-bey@aphp.fr.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recombinant human erythropoietin (EPO) is widely used to treat anemia. EPO has immunomodulatory effects extending beyond erythropoiesis, but its impact on lympho-hematopoiesis remains insufficiently explored. The objective of this study was to investigate B lymphopoiesis in the context of hyper-EPOemia-induced stress hematopoiesis. Using an EPO supplementation model in C57BL/6 mice, we found that EPO exerts contrasting effects on early B cell development. EPO supplementation promotes the transition from common lymphoid progenitors (CLPs) to pre-pro-B cells but impairs the pre-pro-B to pro-B transition, in part by downregulating interleukin-7 (IL-7) receptor expression. Remarkably, EPO promotes the emergence of atypical B cell precursors, including M-CSFR/CD115-expressing CLPs and CD11b and CD16/32-expressing pre-pro-B cells. Gene expression profiling revealed that EPO reprograms early B cell precursors, upregulating myeloid-type genes, while downregulating B lymphoid identity genes. In conclusion, our results show that hyper-EPOemia interferes with the earliest stages of B cell development, while promoting the emergence of mixed-lineage "myeloid-like" B cells.

Indexed as

B-LymphocytesCell DifferentiationErythropoietinMyeloid CellsAnimalsLymphopoiesisMiceMice, Inbred C57BLPrecursor Cells, B-LymphoidReceptors, Interleukin-7ErythropoietinReceptors, Interleukin-7biphenotypic progenitorsB lymphopoiesiserythropoietinM-CSF receptormyelopoiesisprogenitor fatestress hematopoiesis

Identifiers

PMID41650961
PMCPMC12985362

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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.