ArticleStem cells (Dayton, Ohio)2014
Type II interferon promotes differentiation of myeloid-biased hematopoietic stem cells.
Article in Stem cells (Dayton, Ohio), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers.
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.
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.
Who cites it
85 citing papers in PubMed, 129 citations in OpenAlex.
- Aldehyde Detoxification in Cancer: Metabolic Guardians of the Genome.Biomolecules · 2026Review
- IFN-γ induces hematopoietic stem cell myelopoiesis through Meis1 in tumor.Stem cell research & therapy · 2026Article
- Rare epigenetic alterations are conserved across hematopoietic differentiation stages after mycobacterial infection.JCI insight · 2026Article
- IL-27 limits HSPC differentiation during infection and protects from stem cell exhaustion.eLife · 2025Article
- Interferons in Autoimmunity: From Loss of Tolerance to Chronic Inflammation.Biomedicines · 2025Review
- Review
- Niche-derived Semaphorin 4A safeguards functional identity of myeloid-biased hematopoietic stem cells.Nature aging · 2025Article
- Article
- A distinct metabolic and epigenetic state drives trained immunity in HSC-derived macrophages from autoimmune mice.Cell stem cell · 2024Article
- Forged in the fire: Lasting impacts of inflammation on hematopoietic progenitors.Experimental hematology · 2024Review
- STAT3 protects hematopoietic stem cells by preventing activation of a deleterious autocrine type-I interferon response.Leukemia · 2024Article
- Clonal hematopoiesis in people with advanced HIV and associated inflammatory syndromes.JCI insight · 2024Article
- Single-cell time series analysis reveals the dynamics of HSPC response to inflammation.Life science alliance · 2024Article
- The impact of gut microbial signals on hematopoietic stem cells and the bone marrow microenvironment.Frontiers in immunology · 2024Review
- Hematopoietic stem cell a reservoir of innate immune memory.Frontiers in immunology · 2024Review
- Article
- Article
- Antiretrovirals to CCR5 CRISPR/Cas9 gene editing - A paradigm shift chasing an HIV cure.Clinical immunology (Orlando, Fla.) · 2023Review
- Hematopoietic stem and progenitor cells confer cross-protective trained immunity in mouse models.iScience · 2023Article
- Genotoxic aldehyde stress prematurely ages hematopoietic stem cells in a p53-driven manner.Molecular cell · 2023Article
25 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Interferon gamma (IFNγ) promotes cell division of hematopoietic stem cells (HSCs) without affecting the total HSC number. We postulated that IFNγ stimulates differentiation of HSCs as part of the innate immune response. Here, we report that type II interferon signaling is required, both at baseline and during an animal model of LCMV infection, to maintain normal myeloid development. By separately evaluating myeloid-biased and lymphoid-biased HSC subtypes, we found that myeloid-biased HSCs express higher levels of IFNγ receptor and are specifically activated to divide after recombinant IFNγ exposure in vivo. While both HSC subtypes show increased expression of the transcription factor C/EBPβ after infection, only the myeloid-biased HSCs are transiently depleted from the marrow during the type II interferon-mediated immune response to Mycobacterium avium infection, as measured both functionally and phenotypically. These findings indicate that IFNγ selectively permits differentiation of myeloid-biased HSCs during an innate immune response to infection. This represents the first report of a context and a mechanism for discriminate utilization of the alternate HSC subtypes. Terminal differentiation, at the expense of self-renewal, may compromise HSC populations during states of chronic inflammation.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.