Evidence map›Paper›PMID 19740375›Full record

ArticleImmunology2009

Regulation of triggering receptor expressed on myeloid cells 1 expression on mouse inflammatory monocytes.

Kai Zanzinger, Carola Schellack, Norman Nausch, Adelheid Cerwenka

Open access · greenAbstract read
In one paragraph

Article in Immunology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

20 citing papers in PubMed, 35 citations in OpenAlex.

  1. Immune Biomarkers of Islet Transplant Rejection Revealed by Synthetic Immunological Niche.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  2. Article
  3. Stored RBC transfusions leads to the systemic inflammatory response syndrome in anemic murine neonates.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024
    Article
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  12. TREM-1-accentuated lung injury via miR-155 is inhibited by LP17 nanomedicine.American journal of physiology. Lung cellular and molecular physiology · 2016
    Article
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  19. Review
  20. Cervical remodeling during pregnancy and parturition.Trends in endocrinology and metabolism: TEM · 2010
    Review
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

4 authors at 2 institutions in 2 countries.

Kai ZanzingerGerman Cancer Research Centre (DKFZ), Innate Immunity, 69120 Heidelberg, Germany.
Carola Schellack
Norman Nausch
Adelheid Cerwenka
Heidelberg University · DEGerman Cancer Research Center · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Triggering receptor expressed on myeloid cells 1 (TREM-1) is an activating receptor involved in inflammatory diseases and septic shock. The TREM-1 ligand(s) (TREM-1L) have not yet been identified. In this study, we performed a detailed analysis of the expression of mouse TREM-1 and its ligand(s). Our results demonstrate that TREM-1 is expressed on bone-marrow-derived dendritic cells (BMDC). On bone-marrow-derived macrophages (BMM) its expression is induced in vitro after stimulation by granulocyte-macrophage colony-stimulating factor, interleukin-3 or by myeloid differentiation primary response gene 88 (MyD88)-dependent Toll-like receptor (TLR) ligands. Under steady-state conditions mouse TREM-1 is detectable on a Gr-1(-) F4/80(+) monocyte subpopulation bearing markers of resident monocytes, but not on Gr-1(+) F4/80(+) inflammatory monocytes. During lipopolysaccharide (LPS)-induced endotoxaemia TREM-1 was also up-regulated on inflammatory Gr-1(+) F4/80(+) cells in vivo. In tumour-bearing mice, TREM-1 was up-regulated on Gr-1(+) F4/80(+) monocytes, which phenotypically and functionally resembled mononuclear myeloid-derived suppressor cells. Using a soluble TREM-1 fusion protein, we demonstrate that after intravenous injection of LPS TREM-1L was induced on Gr-1(+) granulocytes and monocytes but not on other cell populations in peripheral blood. This up-regulation on granulocytes was directly mediated by TLR ligands and required the adapter protein MyD88. In contrast to human, mouse platelets expressed TREM-1L neither under steady-state conditions nor after LPS injection in vivo. Our study reveals differential regulation of TREM-1 expression on mouse monocyte subpopulations and improves our understanding of the biological role of TREM-1 during disease.

Indexed as

AnimalsBone Marrow CellsDendritic CellsEndotoxemiaFemaleGranulocyte-Macrophage Colony-Stimulating FactorGranulocytesImmunity, InnateInterleukin-3LigandsLymphoma, T-CellMembrane GlycoproteinsMiceMice, Inbred C57BLMonocytesNeoplasm TransplantationGranulocyte-Macrophage Colony-Stimulating FactorInterleukin-3LigandsMembrane GlycoproteinsReceptors, ImmunologicToll-Like ReceptorsTREM1 protein, mouseTriggering Receptor Expressed on Myeloid Cells-1Tumor Necrosis Factor-alpha

Identifiers

PMID19740375
PMCPMC2767308
OpenAlexW2059075072

What OpenQuestion holds

Textmetadata
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.