Evidence map›Paper›PMID 28824627›Full record

ArticleFrontiers in immunology2017

IL-1β As Mediator of Resolution That Reprograms Human Peripheral Monocytes toward a Suppressive Phenotype.

Katharina Giesbrecht, Mariel-Esther Eberle, Sabine J Wölfle, Delal Sahin, Aline Sähr, Valerie Oberhardt, Zach Menne, Konrad A Bode, Klaus Heeg, Dagmar Hildebrand

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

16 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
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  5. NURR1 expression regulates retinal pigment epithelial-mesenchymal transition and age-related macular degeneration phenotypes.Proceedings of the National Academy of Sciences of the United States of America · 2022
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  11. Observational
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  15. The Interplay of Notch Signaling and STAT3 in TLR-Activated Human Primary Monocytes.Frontiers in cellular and infection microbiology · 2018
    Article
  16. 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

10 authors at 3 institutions in 1 country.

Katharina GiesbrechtMedical Microbiology and Hygiene, Centre for Infectious Diseases, University Hospital Heidelberg, Heidelberg, Germany.
Mariel-Esther EberleMedical Microbiology and Hygiene, Centre for Infectious Diseases, University Hospital Heidelberg, Heidelberg, Germany.
Sabine J WölfleMedical Microbiology and Hygiene, Centre for Infectious Diseases, University Hospital Heidelberg, Heidelberg, Germany.
Delal SahinMedical Microbiology and Hygiene, Centre for Infectious Diseases, University Hospital Heidelberg, Heidelberg, Germany.
Aline SährMedical Microbiology and Hygiene, Centre for Infectious Diseases, University Hospital Heidelberg, Heidelberg, Germany.
Valerie OberhardtMedical Microbiology and Hygiene, Centre for Infectious Diseases, University Hospital Heidelberg, Heidelberg, Germany.
Zach MenneMedical Microbiology and Hygiene, Centre for Infectious Diseases, University Hospital Heidelberg, Heidelberg, Germany.
Konrad A BodeMedical Microbiology and Hygiene, Centre for Infectious Diseases, University Hospital Heidelberg, Heidelberg, Germany.
Klaus HeegMedical Microbiology and Hygiene, Centre for Infectious Diseases, University Hospital Heidelberg, Heidelberg, Germany.
Dagmar HildebrandMedical Microbiology and Hygiene, Centre for Infectious Diseases, University Hospital Heidelberg, Heidelberg, Germany.
Heidelberg University · DEUniversity Hospital Heidelberg · DEGerman Center for Infection Research · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

During infection pathogen-associated molecular patterns activate immune cells to initiate a cascade of reactions leading to inflammation and the activation of the adaptive immune response culminating in the elimination of foreign pathogens. However, shortly after activation of the host defense machinery, a return to homeostasis is preferred to prevent inflammation-induced tissue damage. This switch from the initial immunogenic to the subsequent tolerogenic phase after clearance of the infection can be mediated through highly plastic peripheral monocytes. Our studies reveal that an early encounter with toll-like receptor 7/8-ligand R848 mediates a strong pro-inflammatory monocytic phenotype that primes its own reprogramming toward an immunosuppressive one. Previously, we showed that these R848-treated antigen-presenting cells (APCs) fail to activate allogeneic T cells and induce regulatory T cells (Tregs) through signal transducer and activator of transcription 3 (STAT3)-dependent PD-L1. Here, we further demonstrate that R848-treated APCs suppress CD3/CD28-mediated and dendritic cell-mediated T cell activation and that adenosine and indoleamine 2,3-dioxygenase/kynurenin pathways are involved in tolerance induction. Reprogramming of monocytes after R848 stimulation requires the pro-inflammatory cytokine IL-1β and a boosted IL-6 release. The subsequent autocrine prolonged activation of STAT3 induces direct upregulation of tolerogenic factors which finally downregulate proliferation of activated T cells and mediate Tregs. Thereby our study suggests that inflammatory cytokines, such as IL-1β and IL-6, should be considered as mediators of resolution of inflammation.

Indexed as

adenosineIL-1βindoleamine 2,3-dioxygenasePD-L1resolution of inflammationsignal transducer and activator of transcription 3tolerogenic factorstoll-like receptor-ligand

Identifiers

PMID28824627
PMCPMC5540955
OpenAlexW2741310108

What OpenQuestion holds

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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.