Evidence map›Paper›PMID 36203578›Full record

ArticleFrontiers in immunology2022

P2Y6 receptor-mediated signaling amplifies TLR-induced pro-inflammatory responses in microglia.

Raissa Timmerman, Ella A Zuiderwijk-Sick, Jeffrey J Bajramovic

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

10 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. The microglial P2YTranslational neurodegeneration · 2024
    Review
  7. Article
  8. Article
  9. Article
  10. 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 1 institution in 1 country.

Raissa TimmermanAlternatives Unit, Biomedical Primate Research Centre, Rijswijk, Netherlands.
Ella A Zuiderwijk-SickAlternatives Unit, Biomedical Primate Research Centre, Rijswijk, Netherlands.
Jeffrey J BajramovicAlternatives Unit, Biomedical Primate Research Centre, Rijswijk, Netherlands.
Biomedical Primate Research Centre · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

TLR-induced signaling initiates inflammatory responses in cells of the innate immune system. These responses are amongst others characterized by the secretion of high levels of pro-inflammatory cytokines, which are tightly regulated and adapted to the microenvironment. Purinergic receptors are powerful modulators of TLR-induced responses, and we here characterized the effects of P2Y6 receptor (P2RY6)-mediated signaling on TLR responses of rhesus macaque primary bone marrow-derived macrophages (BMDM) and microglia, using the selective P2RY6 antagonist MRS2578. We demonstrate that P2RY6-mediated signaling enhances the levels of TLR-induced pro-inflammatory cytokines in microglia in particular. TLR1, 2, 4, 5 and 8-induced responses were all enhanced in microglia, whereas such effects were much less pronounced in BMDM from the same donors. Transcriptome analysis revealed that the overall contribution of P2RY6-mediated signaling to TLR-induced responses in microglia leads to an amplification of pro-inflammatory responses. Detailed target gene analysis predicts that P2RY6-mediated signaling regulates the expression of these genes

Indexed as

MicrogliaNF-kappa BAnimalsCytokinesHeat-Shock ProteinsMacaca mulattaReceptors, Purinergic P2Toll-Like Receptor 1CytokinesHeat-Shock ProteinsNF-kappa Bpurinoceptor P2Y6Receptors, Purinergic P2Toll-Like Receptor 1bone marrow-derived macrophagesheat shock proteinsmicroglianeuroinflammationP2RY6TLR

Identifiers

PMID36203578
PMCPMC9531012
OpenAlexW4296483449

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.