Evidence map›Paper›PMID 23661549›Full record

ArticleEuropean journal of immunology2013

Detection of a TLR2 agonist by hematopoietic stem and progenitor cells impacts the function of the macrophages they produce.

Alberto Yáñez, Nargess Hassanzadeh-Kiabi, Madelena Y Ng, Javier Megías, Aparna Subramanian, George Y Liu, David M Underhill, M Luisa Gil, Helen S Goodridge

Open access · bronzeAbstract read
In one paragraph

Article in European journal of immunology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed, 1 pooled it
4.0field-weighted citation impact, top 6% 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

43 citing papers in PubMed, 1 synthesis or guideline pooled it, 71 citations in OpenAlex.

  1. Trained innate immunity.Immunologic research · 2021
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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

9 authors at 3 institutions in 2 countries.

Alberto YáñezRegenerative Medicine Institute, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA.
Nargess Hassanzadeh-Kiabi
Madelena Y Ng
Javier Megías
Aparna Subramanian
George Y Liu
David M Underhill
M Luisa Gil
Helen S Goodridge
Cedars-Sinai Medical Center · USUniversitat de València · ESUniversity of California, Los Angeles · US

Funding

UCLA Clinical and Translational Science InstituteUL1TR000124 · NCATS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI DUBINETT, STEVEN M. · 2012 to 2015
$57.0M
Non-Toll-like receptor innate immune signalingR01AI071116 · NIAID · CEDARS-SINAI MEDICAL CENTER · PI UNDERHILL, DAVID M. · 2008 to 2023
$6.3M
Effects of Microbial Exposure on MyelopoiesisR21AI082379 · NIAID · CEDARS-SINAI MEDICAL CENTER · PI GOODRIDGE, HELEN S · 2010 to 2011
$451k
NCATS NIH HHS UL1 TR000124NCATS NIH HHS UL1TR000124NIAID NIH HHS R01 AI071116NIAID NIH HHS R21 AI082379
6 · The paper itself

Abstract

Several groups have shown that detection of microbial components by TLRs on hematopoietic stem and progenitor cells (HSPCs) instructs myeloid cell generation, raising interest in the possibility of targeting TLRs on HSPCs to boost myelopoiesis. However, although "TLR-derived" cells exhibit myeloid cell characteristics (phagocytosis, cytokine production, antigen presentation), it is not clear whether they are functionally equivalent to macrophages derived in the absence of TLR activation. Our in vitro and in vivo studies show that macrophages derived from mouse and human HSPC subsets (including stem cells) exposed to a TLR2 agonist prior to or during macrophage differentiation produce lower levels of inflammatory cytokines (TNF-α, IL-6, and IL-1β) and reactive oxygen species. This is in contrast to prior exposure of differentiated macrophages to the TLR2 agonist ("tolerance"), which suppresses inflammatory cytokine production, but elevates reactive oxygen species. Soluble factors produced following exposure of HSPCs to a TLR2 agonist can also act in a paracrine manner to influence the function of macrophages derived from unexposed HSPCs. Our data demonstrate that macrophage function can be influenced by TLR signaling in the HSPCs from which they are derived, and that this may impact the clinical utility of targeting TLRs on HSPCs to boost myelopoiesis.

Indexed as

AnimalsCell DifferentiationCells, CulturedHematopoietic Stem CellsInterleukin-1betaInterleukin-6LipopeptidesMacrophagesMiceMice, Inbred C57BLMice, KnockoutMyeloid CellsMyelopoiesisPhagocytosisReactive Oxygen SpeciesSignal TransductionInterleukin-1betaInterleukin-6LipopeptidesPam(3)CSK(4) peptideReactive Oxygen SpeciesTlr2 protein, mouseToll-Like Receptor 2Tumor Necrosis Factor-alphaHematopoietic progenitor cellsHematopoietic stem cellsMonocytes/ macrophagesMyelopoiesisTLRs

Identifiers

PMID23661549
PMCPMC3783206
OpenAlexW1758327849

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.