Evidence map›Paper›PMID 26491068›Full record

ArticleBlood2015

IFN-γ-mediated hematopoietic cell destruction in murine models of immune-mediated bone marrow failure.

Jichun Chen, Xingmin Feng, Marie J Desierto, Keyvan Keyvanfar, Neal S Young

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

62 citing papers in PubMed, 93 citations in OpenAlex.

  1. Trial
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  4. Macrophages in Hematopoiesis and Related Blood Diseases.Genomics, proteomics & bioinformatics · 2025
    Review
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  6. Article
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  16. Influence of Housing Temperature and Genetic Diversity on Allogeneic T Cell-Induced Tissue Damage in Mice.Pathophysiology : the official journal of the International Society for Pathophysiology · 2023
    Article
  17. Review
  18. Article
  19. Article
  20. Article

2 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

5 authors at 2 institutions in 1 country.

Jichun ChenHematology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD.
Xingmin FengHematology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD.
Marie J DesiertoHematology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD.
Keyvan KeyvanfarHematology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD.
Neal S YoungHematology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD.
National Heart Lung and Blood Institute · USNational Institutes of Health · US

Funding

Pathogenesis And Treatment Of Aplastic AnemiaZIAHL002315 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI YOUNG, NEAL S · 2009 to 2025
$60.1M
NHLBI Animal Program DivisionZIGHL006020 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI CLARK, TANNIA · 2009 to 2025
$47.3M
Intramural NIH HHS
6 · The paper itself

Abstract

Interferon gamma (IFN-γ) has been reported to have both negative and positive activity on hematopoietic cells, adding complexity to the interpretation of its pleiotropic functions. We examined the effects of IFN-γ on murine hematopoietic stem cells (HSCs) and progenitors in vitro and in vivo by using mouse models. IFN-γ treatment expanded bone marrow (BM) c-Kit(+)Sca1(+)Lin(-) (KSL) cell number but reduced BM KLCD150(+) and KLCD150(+)CD48(-) cells. IFN-γ-expanded KSL cells engrafted poorly when tested by competitive repopulation in vivo. KSL, KLCD150(+), and KLCD150(+)CD48(-) cells from IFN-γ-treated animals all showed significant upregulation in Fas expression. When cocultured with activated T cells in vitro, KSL and KLCD150(+) cells from IFN-γ-treated donors showed increased apoptosis relative to those from untreated animals, and infusion of activated CD8 T cells into IFN-γ-injected animals in vivo led to partial elimination of KSL cells. Exposure of BM cells or KSL cells to IFN-γ increased expression of Fas, caspases, and related proapoptotic genes and decreased expression of Ets-1 and other hematopoietic genes. In mouse models of BM failure, mice genetically deficient in IFN-γ receptor expression showed attenuation of immune-mediated marrow destruction, whereas effector lymphocytes from IFN-γ-deficient donors were much less potent in initiating BM damage. We conclude that the activity of IFN-γ on murine hematopoiesis is context dependent. IFN-γ-augmented apoptotic gene expression facilitates destruction of HSCs and progenitors in the presence of activated cytotoxic T cells, as occurs in human BM failure.

Indexed as

Anemia, AplasticAnimalsApoptosisBone Marrow DiseasesBone Marrow Failure DisordersBone Marrow TransplantationCells, CulturedCoculture TechniquesColony-Forming Units AssayDisease Models, AnimalFas Ligand Proteinfas ReceptorGene Expression RegulationHematopoiesisHematopoietic Stem CellsHemoglobinuria, ParoxysmalFas Ligand ProteinFasl protein, mouseFas protein, mousefas ReceptorInterferon-gammaInterferon gamma ReceptorReceptors, Interferon

Identifiers

PMID26491068
PMCPMC4671109
OpenAlexW2333387353

What OpenQuestion holds

Textmetadata
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.