Evidence map›Paper›PMID 21426948›Full record

ReviewInternational immunopharmacology2011

Hematopoietic cytokine-induced transcriptional regulation and Notch signaling as modulators of MDSC expansion.

Sheinei J Saleem, Daniel H Conrad

Open access · greenAbstract readReview
In one paragraph

Review in International immunopharmacology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
0.9field-weighted citation impact, top 28% 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

18 citing papers in PubMed, 35 citations in OpenAlex.

  1. Review
  2. Article
  3. Notch signaling pathway: architecture, disease, and therapeutics.Signal transduction and targeted therapy · 2022
    Review
  4. Review
  5. Review
  6. Review
  7. Article
  8. Review
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Review
  15. Myeloid-derived suppressor cells in B cell malignancies.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015
    Review
  16. Article
  17. Review
  18. Article
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

2 authors at 1 institution in 1 country.

Sheinei J SaleemDepartment of Microbiology and Immunology, Virginia Commonwealth University, School of Medicine, Richmond, VA 23298, USA.
Daniel H Conrad
Virginia Commonwealth University · US

Funding

STRUCTURE/FUNCTION OF THE LYMPHOCYTE FCE RECEPTORR01AI018697 · NIAID · VIRGINIA COMMONWEALTH UNIVERSITY · PI MARTIN, REBECCA KELLEY · 1985 to 2018
$6.5M
IGE CONTROL BY OVEREXPRESSION OF CD23R01AI044163 · NIAID · VIRGINIA COMMONWEALTH UNIVERSITY · PI CONRAD, DANIEL H · 1999 to 2003
$1.0M
NIAID NIH HHS R01 AI018697NIAID NIH HHS R01 AI044163
6 · The paper itself

Abstract

Hematopoietic stem cells (HSCs) differentiate into mature lineage restricted blood cells under the influence of a complex network of hematopoietic cytokines, cytokine-mediated transcriptional regulators, and manifold intercellular signaling pathways. The classical model of hematopoiesis proposes that progenitor cells undergo a dichotomous branching into myelo-erythroid and lymphoid lineages. Nonetheless, erythroid and lymphoid restricted progenitors retain their myeloid potential, supporting the existence of an alternative 'myeloid-based' mechanism of hematopoiesis. In this case, abnormal pathology is capable of dysregulating hematopoiesis in favor of myelopoiesis. The accumulation of immature CD11b+Gr-1+ myeloid-derived suppressor cells (MDSCs) has been shown to correlate with the presence of several hematopoietic cytokines, transcription factors and signaling pathways, lending support to this hypothesis. Although the negative role of MDSCs in cancer development is firmly established, it is now understood that MDSCs can exert a paradoxical, positive effect on transplantation, autoimmunity, and sepsis. Our conflicted understanding of MDSC function and the complexity of hematopoietic cytokine signaling underscores the need to elucidate molecular pathways of MDSC expansion for the development of novel MDSC-based therapeutics.

Indexed as

AnimalsAutoimmune DiseasesCell DedifferentiationCell LineageCell ProliferationCytokinesHematopoietic Stem CellsHumansImmunosuppression TherapyMyeloid CellsMyelopoiesisNeoplasmsReceptors, NotchSignal TransductionTranscriptional ActivationCytokinesReceptors, Notch

Identifiers

PMID21426948
PMCPMC3119497
OpenAlexW2042741856

What OpenQuestion holds

Textmetadata
LicenceTDM
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.