Evidence map›Paper›PMID 27315114›Full record

ArticleBlood cancer journal2016

Systemic TLR2 agonist exposure regulates hematopoietic stem cells via cell-autonomous and cell-non-autonomous mechanisms.

A C Herman, D A Monlish, M P Romine, S T Bhatt, S Zippel, L G Schuettpelz

Open access · goldAbstract read
In one paragraph

Article in Blood cancer journal, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

41 citing papers in PubMed, 52 citations in OpenAlex.

  1. Review
  2. Article
  3. Ruxolitinib reduces macrophage pyroptosis in aplastic anaemia.Clinical and experimental medicine · 2026
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  9. The TLR2/TLR6 ligand FSL-1 mitigates radiation-induced hematopoietic injury in mice and nonhuman primates.Proceedings of the National Academy of Sciences of the United States of America · 2023
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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

6 authors at 1 institution in 1 country.

A C HermanDepartment of Pediatrics, Washington University School of Medicine, St Louis, MO, USA.
D A MonlishDepartment of Pediatrics, Washington University School of Medicine, St Louis, MO, USA.
M P RomineDepartment of Pediatrics, Washington University School of Medicine, St Louis, MO, USA.
S T BhattDepartment of Pediatrics, Washington University School of Medicine, St Louis, MO, USA.
S ZippelDepartment of Pediatrics, Washington University School of Medicine, St Louis, MO, USA.
L G SchuettpelzDepartment of Pediatrics, Washington University School of Medicine, St Louis, MO, USA.
Washington University in St. Louis · US

Funding

Washington University Center for Cellular ImagingP30CA091842 · NCI · WASHINGTON UNIVERSITY · PI TIMOTHY J. EBERLEIN · 2001 to 2026
$128.0M
Child Health Research CenterK12HD076224 · NICHD · WASHINGTON UNIVERSITY · PI MARK E. LOWE · 2013 to 2026
$6.2M
Training Program in Development HematologyT32HD007499 · NICHD · WASHINGTON UNIVERSITY · PI RUBIN, JOSHUA B · 1999 to 2019
$2.3M
ELUCIDATING THE ROLE OF KRUPPEL LIKE FACTOR 7 IN T CELL DEVELOPMENTK08HL118367 · NHLBI · WASHINGTON UNIVERSITY · PI SCHUETTPELZ, LAURA G. · 2014 to 2016
$283k
NCI NIH HHS P30 CA091842NHLBI NIH HHS K08 HL118367NICHD NIH HHS K12 HD076224NICHD NIH HHS T32 HD007499
6 · The paper itself

Abstract

Toll-like receptor 2 (TLR2) is a member of the TLR family of receptors that play a central role in innate immunity. In addition to regulating effector immune cells, where it recognizes a wide variety of pathogen-associated and nonpathogen-associated endogenous ligands, TLR2 is expressed in hematopoietic stem cells (HSCs). Its role in HSCs, however, is not well understood. Furthermore, augmented TLR2 signaling is associated with myelodysplastic syndrome, an HSC disorder characterized by ineffective hematopoiesis and a high risk of transformation to leukemia, suggesting that aberrant signaling through this receptor may have clinically significant effects on HSCs. Herein, we show that systemic exposure of mice to a TLR2 agonist leads to an expansion of bone marrow and spleen phenotypic HSCs and progenitors, but a loss of HSC self-renewal capacity. Treatment of chimeric animals shows that these effects are largely cell non-autonomous, with a minor contribution from cell-autonomous TLR2 signaling, and are in part mediated by granulocyte colony-stimulating factor and tumor necrosis factor-α. Together, these data suggest that TLR2 ligand exposure influences HSC cycling and function via unique mechanisms from TLR4, and support an important role for TLR2 in the regulation of HSCs.

Indexed as

AnimalsBiomarkersBone Marrow CellsBone Marrow TransplantationColony-Forming Units AssayCytokinesGranulocyte Colony-Stimulating FactorHematopoietic Stem CellsMiceMice, KnockoutPhenotypeRadiation ToleranceSignal TransductionSpleenToll-Like Receptor 2Tumor Necrosis Factor-alphaBiomarkersCytokinesGranulocyte Colony-Stimulating FactorToll-Like Receptor 2Tumor Necrosis Factor-alpha

Identifiers

PMID27315114
PMCPMC5141360
OpenAlexW2442550790

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.