Evidence map›Paper›PMID 24992931›Full record

ReviewCell death and differentiation2015

Regulation of hematopoietic and leukemic stem cells by the immune system.

C Riether, C M Schürch, A F Ochsenbein

Open access · hybridAbstract readReview
In one paragraph

Review in Cell death and differentiation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 118 papers.

0numbers the graph read from it
0cells of the map it votes in
118citing papers in PubMed
11.6field-weighted citation impact, top 1% 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

118 citing papers in PubMed, 238 citations in OpenAlex.

  1. Trial
  2. Review
  3. Review
  4. Reconceptualizing Aplastic Anemia-Seed, Worm, Soil.Journal of clinical laboratory analysis · 2026
    Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
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  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
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  17. Article
  18. Leukemic Stem Cells and Hematological Malignancies.International journal of molecular sciences · 2024
    Review
  19. Review
  20. Article

58 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

3 authors at 1 institution in 1 country.

C RietherTumor Immunology, Department of Clinical Research, University of Bern, Bern, Switzerland.
C M Schürch1] Tumor Immunology, Department of Clinical Research, University of Bern, Bern, Switzerland [2] Institute of Pathology, University of Bern, Bern, Switzerland.
A F Ochsenbein1] Tumor Immunology, Department of Clinical Research, University of Bern, Bern, Switzerland [2] Department of Medical Oncology, Inselspital, Bern University Hospital and University of Bern, Bern, Switzerland.
University of Bern · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hematopoietic stem cells (HSCs) are rare, multipotent cells that generate via progenitor and precursor cells of all blood lineages. Similar to normal hematopoiesis, leukemia is also hierarchically organized and a subpopulation of leukemic cells, the leukemic stem cells (LSCs), is responsible for disease initiation and maintenance and gives rise to more differentiated malignant cells. Although genetically abnormal, LSCs share many characteristics with normal HSCs, including quiescence, multipotency and self-renewal. Normal HSCs reside in a specialized microenvironment in the bone marrow (BM), the so-called HSC niche that crucially regulates HSC survival and function. Many cell types including osteoblastic, perivascular, endothelial and mesenchymal cells contribute to the HSC niche. In addition, the BM functions as primary and secondary lymphoid organ and hosts various mature immune cell types, including T and B cells, dendritic cells and macrophages that contribute to the HSC niche. Signals derived from the HSC niche are necessary to regulate demand-adapted responses of HSCs and progenitor cells after BM stress or during infection. LSCs occupy similar niches and depend on signals from the BM microenvironment. However, in addition to the cell types that constitute the HSC niche during homeostasis, in leukemia the BM is infiltrated by activated leukemia-specific immune cells. Leukemic cells express different antigens that are able to activate CD4(+) and CD8(+) T cells. It is well documented that activated T cells can contribute to the control of leukemic cells and it was hoped that these cells may be able to target and eliminate the therapy-resistant LSCs. However, the actual interaction of leukemia-specific T cells with LSCs remains ill-defined. Paradoxically, many immune mechanisms that evolved to activate emergency hematopoiesis during infection may actually contribute to the expansion and differentiation of LSCs, promoting leukemia progression. In this review, we summarize mechanisms by which the immune system regulates HSCs and LSCs.

Indexed as

Cell DifferentiationHematopoiesisImmune SystemHematopoietic Stem CellsHumansLeukemiaNeoplastic Stem CellsStem Cell Niche

Identifiers

PMID24992931
PMCPMC4291501
OpenAlexW2076966192

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.