Evidence map›Paper›PMID 31520477›Full record

ArticleImmunology2019

Siglec-F is induced by granulocyte-macrophage colony-stimulating factor and enhances interleukin-4-induced expression of arginase-1 in mouse macrophages.

Hiroyuki Tateyama, Yusuke Murase, Hiroshi Higuchi, Yui Inasaka, Hidenori Kaneoka, Shinji Iijima, Ken-Ichi Nishijima

Open access · bronzeAbstract read
In one paragraph

Article in Immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.9field-weighted citation impact, top 25% 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

13 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Review
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  4. Article
  5. Macrophage variants in laboratory research: most are well done, but some are RAW.Frontiers in cellular and infection microbiology · 2024
    Review
  6. Article
  7. Article
  8. Article
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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

7 authors at 1 institution in 1 country.

Hiroyuki TateyamaDepartment of Biomolecular Engineering, Graduate School of Engineering, Nagoya University, Nagoya, Japan.
Yusuke MuraseDepartment of Biomolecular Engineering, Graduate School of Engineering, Nagoya University, Nagoya, Japan.
Hiroshi HiguchiDepartment of Biomolecular Engineering, Graduate School of Engineering, Nagoya University, Nagoya, Japan.
Yui InasakaDepartment of Biomolecular Engineering, Graduate School of Engineering, Nagoya University, Nagoya, Japan.
Hidenori KaneokaDepartment of Biomolecular Engineering, Graduate School of Engineering, Nagoya University, Nagoya, Japan.
Shinji IijimaDepartment of Biomolecular Engineering, Graduate School of Engineering, Nagoya University, Nagoya, Japan.
Ken-Ichi NishijimaDepartment of Biomolecular Engineering, Graduate School of Engineering, Nagoya University, Nagoya, Japan.ORCID 0000-0002-7189-465X
Nagoya University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Siglecs are cell surface lectins that recognize sialic acids and are primarily expressed in hematopoietic cells. Previous studies showed that some Siglecs regulate macrophage function. In the present study, we examined the induction and putative roles of mouse Siglec-F in bone-marrow-derived macrophages in mice. A quantitative RT-PCR analysis showed that the basal expression of Siglec-F was weak in bone-marrow-derived macrophages differentiated by macrophage colony-stimulating factor. However, a 24-hr stimulation with granulocyte-macrophage colony-stimulating factor (GM-CSF) enhanced Siglec-F expression. GM-CSF also enhanced Siglec-F expression in thioglycollate-induced peritoneal macrophages. The inhibition of signal transducer and activator of transcription 5 (STAT5), but not that of phosphoinositide 3-kinase or mitogen-activated protein kinase kinase, significantly reduced the induction of Siglec-F. Interleukin-3, which uses a common β-chain shared with the GM-CSF receptor to stimulate the STAT5 pathway, also enhanced Siglec-F expression. The knockdown of Siglec-F by a specific small interfering RNA enhanced GM-CSF-induced STAT5 phosphorylation, suggesting that Siglec-F down-regulates its own expression upon prolonged GM-CSF stimulation. Furthermore, the knockdown of Siglec-F reduced the STAT6 phosphorylation and expression of arginase-1 in interleukin-4-stimulated macrophages. These results suggest that Siglec-F fine-tunes the immune responses of macrophages.

Indexed as

AnimalsAntigens, Differentiation, MyelomonocyticArginaseCells, CulturedGranulocyte-Macrophage Colony-Stimulating FactorInterleukin-4MacrophagesMaleMiceMice, Inbred C57BLPhosphorylationRNA, Small InterferingSialic Acid Binding Immunoglobulin-like LectinsSTAT5 Transcription FactorSTAT6 Transcription FactorUp-RegulationAntigens, Differentiation, MyelomonocyticArg1 protein, mouseArginaseGranulocyte-Macrophage Colony-Stimulating FactorInterleukin-4RNA, Small InterferingSialic Acid Binding Immunoglobulin-like LectinsSiglecf protein, mouseSTAT5 Transcription FactorSTAT6 Transcription Factorarginasegranulocyte-macrophage colony-stimulating factorinterleukin-4macrophageSiglec-Fsignal transducer and activator of transcription 5

Identifiers

PMID31520477
PMCPMC6856935
OpenAlexW2972612467

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.