Evidence map›Paper›PMID 25010215›Full record

ArticlePloS one2014

Dendritic cell-secreted lipocalin2 induces CD8+ T-cell apoptosis, contributes to T-cell priming and leads to a TH1 phenotype.

Melanie Floderer, Michaela Prchal-Murphy, Caterina Vizzardelli

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

23 citing papers in PubMed, 38 citations in OpenAlex.

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  15. Regulation of theInfection and immunity · 2021
    Article
  16. Article
  17. Lipocalin-2 Exacerbates Lupus Nephritis by Promoting Th1 Cell Differentiation.Journal of the American Society of Nephrology : JASN · 2020
    Article
  18. Neutrophil Gelatinase-Associated Lipocalin Protects from ANCA-Induced GN by Inhibiting TJournal of the American Society of Nephrology : JASN · 2020
    Article
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  20. 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

3 authors at 3 institutions in 1 country.

Melanie FlodererLaboratory of Tumour Immunology, St. Anna Children's Cancer Research Institute, Vienna, Austria.
Michaela Prchal-MurphyInstitute of Pharmacology and Toxicology, Department for Biomedical Science, University of Veterinary Medicine Vienna, Vienna, Austria.
Caterina VizzardelliLaboratory of Tumour Immunology, St. Anna Children's Cancer Research Institute, Vienna, Austria.
St. Anna Children's Cancer Research InstituteSt Anna Children's Hospital · ATUniversity of Veterinary Medicine Vienna · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lipocalin 2 (LCN2), which is highly expressed by dendritic cells (DCs) when treated with dexamethasone (Dex) and lipopolysaccharide (LPS), plays a key role in the defence against bacteria and is also involved in the autocrine apoptosis of T-cells. However, the function of LCN2 when secreted by DCs is unknown: this is a critical gap in our understanding of the regulation of innate and adaptive immune systems. Tolerance, stimulation and suppression are functions of DCs that facilitate the fine-tuning of the immune responses and which are possibly influenced by LCN2 secretion. We therefore examined the role of LCN2 in DC/T-cell interaction. WT or Lcn2-/- bone marrow-derived DCs were stimulated with LPS or LPS+IFN-γ with and without Dex and subsequently co-cultured with T-cells from ovalbumin-specific TCR transgenic (OT-I and OT-II) mice. We found that CD8+ T-cell apoptosis was highly reduced when Lcn2-/- DCs were compared with WT. An in vivo CTL assay, using LPS-treated DCs, showed diminished killing ability in mice that had received Lcn2-/- DCs compared with WT DCs. As a consequence, we analysed T-cell proliferation and found that LCN2 participates in T-cell-priming in a dose-dependent manner and promotes a TH1 microenvironment. DC-secreted LCN2, whose function has previously been unknown, may in fact have an important role in regulating the balance between TH1 and TH2. Our results yield insights into DC-secreted LCN2 activity, which could play a pivotal role in cellular immune therapy and in regulating immune responses.

Indexed as

PhenotypeAcute-Phase ProteinsAnimalsApoptosisCD8-Positive T-LymphocytesCellular MicroenvironmentCytokinesDendritic CellsFemaleGene Expression RegulationImmunizationInterferon-gammaLipocalin-2LipocalinsLipopolysaccharidesMiceAcute-Phase ProteinsCytokinesInterferon-gammaLcn2 protein, mouseLipocalin-2LipocalinsLipopolysaccharidesOncogene Proteins

Identifiers

PMID25010215
PMCPMC4092100
OpenAlexW1994764722

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.