Evidence map›Paper›PMID 31213716›Full record

ReviewNature immunology2019

Hematopoietic progenitor cells as integrative hubs for adaptation to and fine-tuning of inflammation.

Triantafyllos Chavakis, Ioannis Mitroulis, George Hajishengallis

Open access · greenAbstract readReview
In one paragraph

Review in Nature immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 196 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
196citing papers in PubMed, 2 pooled it
11.7field-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

196 citing papers in PubMed, 2 syntheses or guidelines pooled it, 305 citations in OpenAlex.

  1. Pooled it
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  11. Antioxidants (Basel, Switzerland) · 2026
    Review
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  14. Galectin-9Aging cell · 2026
    Article
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136 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 3 institutions in 3 countries.

Triantafyllos ChavakisInstitute for Clinical Chemistry and Laboratory Medicine, University Hospital and Faculty of Medicine Carl Gustav Carus of TU Dresden, Dresden, Germany. triantafyllos.chavakis@uniklinikum-dresden.de.ORCID http://orcid.org/0000-0002-1869-5141
Ioannis MitroulisInstitute for Clinical Chemistry and Laboratory Medicine, University Hospital and Faculty of Medicine Carl Gustav Carus of TU Dresden, Dresden, Germany.
George HajishengallisUniversity of Pennsylvania, Penn Dental Medicine, Department of Microbiology, Philadelphia, PA, USA.ORCID http://orcid.org/0000-0001-7392-8852
Democritus University of Thrace · GRUniversity Hospital Carl Gustav Carus · DEUniversity of Pennsylvania · US

Funding

P. gingivalis as a keystone pathogenR01DE015254 · NIDCR · UNIVERSITY OF PENNSYLVANIA · PI HAJISHENGALLIS, GEORGIOS · 2004 to 2018
$4.6M
Local endogenous regulators of functional immune plasticity in the periodontiumR37DE026152 · NIDCR · UNIVERSITY OF PENNSYLVANIA · PI HAJISHENGALLIS, GEORGIOS · 2016 to 2025
$3.5M
Neutrophil homeostasis and periodontitis: Novel concepts and treatmentsR01DE024153 · NIDCR · UNIVERSITY OF PENNSYLVANIA · PI HAJISHENGALLIS, GEORGIOS · 2016 to 2020
$2.0M
Del-1: Molecular and Cellular Targets in PeriodontitisR01DE024716 · NIDCR · UNIVERSITY OF PENNSYLVANIA · PI HAJISHENGALLIS, GEORGIOS · 2015 to 2019
$2.0M
European Research Council 683145NIDCR NIH HHS R01 DE015254NIDCR NIH HHS R01 DE024153NIDCR NIH HHS R01 DE024716NIDCR NIH HHS R37 DE026152
6 · The paper itself

Abstract

Recent advances have highlighted the ability of hematopoietic stem and progenitor cells in the bone marrow to sense peripheral inflammation or infection and adapt through increased proliferation and skewing toward the myeloid lineage. Such adaptations can meet the increased demand for innate immune cells and can be beneficial in response to infection or myeloablation. However, the inflammation-induced adaptation of hematopoietic and myeloid progenitor cells toward enhanced myelopoiesis might also perpetuate inflammation in chronic inflammatory or cardio-metabolic diseases by generating a feed-forward loop between inflammation-adapted hematopoietic progenitor cells and the inflammatory disorder. Sustained adaptive responses of progenitor cells in the bone marrow can also contribute to trained immunity, a non-specific memory of earlier encounters that in turn facilitates the heightened response of these cells, as well as that of their progeny, to future challenges. Here we discuss the mechanisms that govern the adaptation of hematopoietic progenitor cells to inflammation and its sequelae in the pathogenesis of human disease.

Indexed as

Adaptation, BiologicalAnimalsCytokinesHematopoietic Stem CellsHumansImmunityImmunomodulationInflammationIntercellular Signaling Peptides and ProteinsInterferonsMyelopoiesisSignal TransductionToll-Like ReceptorsCytokinesIntercellular Signaling Peptides and ProteinsInterferonsToll-Like Receptors

Identifiers

PMID31213716
PMCPMC6709414
OpenAlexW2952520385

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.