Evidence map›Paper›PMID 39606224›Full record

ArticleFrontiers in immunology2024

Human CFTR deficient iPSC-macrophages reveal impaired functional and transcriptomic response upon

Claudio Rodriguez Gonzalez, Débora Basílio-Queirós, Anna-Lena Neehus, Sylvia Merkert, David Tschritter, Sinem Ünal, Jan Hegermann, Matthias Mörgelin, Jacinta Bustamante, Manuel Manfred Nietert and 4 more

Abstract read
In one paragraph

Article in Frontiers in immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

  1. Review
  2. Article
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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

14 authors.

Claudio Rodriguez GonzalezDepartment of Pediatric Pneumology, Allergology and Neonatology, Hannover Medical School, Hannover, Germany.
Débora Basílio-QueirósDepartment of Pediatric Pneumology, Allergology and Neonatology, Hannover Medical School, Hannover, Germany.
Anna-Lena NeehusLaboratory of Human Genetics of Infectious Diseases, Necker Branch, INSERM U1163, Necker Hospital for Sick Children, Paris, France.
Sylvia MerkertLeibniz Research Laboratories for Biotechnology and Artificial Organs (LEBAO), Department of Cardiothoracic, Transplantation and Vascular Surgery (HTTG), Hannover Medical School, Hannover, Germany.
David TschritterDepartment of Medical Bioinformatics, University Medical Center Göttingen, Göttingen, Germany.
Sinem ÜnalLaboratory of Human Genetics of Infectious Diseases, Necker Branch, INSERM U1163, Necker Hospital for Sick Children, Paris, France.
Jan HegermannBiomedical Research in Endstage and Obstructive Lung Disease Hannover (BREATH), Member of the German Center for Lung Research (DZL), Hannover Medical School, Hannover, Germany.
Matthias MörgelinColzyx AB, Lund, Sweden.
Jacinta BustamanteLaboratory of Human Genetics of Infectious Diseases, Necker Branch, INSERM U1163, Necker Hospital for Sick Children, Paris, France.
Manuel Manfred NietertDepartment of Medical Bioinformatics, University Medical Center Göttingen, Göttingen, Germany.
Ulrich MartinLeibniz Research Laboratories for Biotechnology and Artificial Organs (LEBAO), Department of Cardiothoracic, Transplantation and Vascular Surgery (HTTG), Hannover Medical School, Hannover, Germany.
Burkhard TümmlerDepartment of Pediatric Pneumology, Allergology and Neonatology, Hannover Medical School, Hannover, Germany.
Antje MunderDepartment of Pediatric Pneumology, Allergology and Neonatology, Hannover Medical School, Hannover, Germany.
Nico LachmannDepartment of Pediatric Pneumology, Allergology and Neonatology, Hannover Medical School, Hannover, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: Cystic fibrosis (CF) is a hereditary autosomal recessive disease driven by deleterious variants of the CFTR gene, leading, among other symptoms, to increased lung infection susceptibility. Mucus accumulation in the CF lung is, as of yet, considered as one important factor contributing to its colonization by opportunistic pathogens such as Methods: To address this problem and to evaluate the role of CFTR in human macrophages, we successfully differentiated human induced pluripotent stem cells (iPSC) from a CF p.Phe508del homozygous individual and a healthy donor into primitive macrophages (iMac Results: iMac Conclusion: In summary, we present a defective phenotype in iMac

Indexed as

Cystic FibrosisCystic Fibrosis Transmembrane Conductance RegulatorInduced Pluripotent Stem CellsPseudomonas aeruginosaPseudomonas InfectionsTranscriptomeCell DifferentiationCells, CulturedHumansMacrophagesCFTR protein, humanCystic Fibrosis Transmembrane Conductance Regulatorcystic fibrosisinfectioniPSClung immunitymacrophagesPseudomonas aeruginosa

Identifiers

PMID39606224
PMCPMC11601075

What OpenQuestion holds

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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.