Evidence map›Paper›PMID 29777026›Full record

ArticleThe Journal of cell biology2018

Endosomal TLR3, TLR7, and TLR8 control neuronal morphology through different transcriptional programs.

Yun-Fen Hung, Chiung-Ya Chen, Yi-Chun Shih, Hsin-Yu Liu, Chiao-Ming Huang, Yi-Ping Hsueh

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in The Journal of cell biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
3.6field-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

50 citing papers in PubMed, 71 citations in OpenAlex.

  1. Review
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  7. Microglia and immune signaling as architects of the brain.Frontiers in cellular neuroscience · 2026
    Review
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  9. Article
  10. Innate and adaptive immunity in neurodegenerative disease.Cellular and molecular life sciences : CMLS · 2025
    Review
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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

6 authors at 2 institutions in 1 country.

Yun-Fen HungDepartment of Life Sciences and Institute of Genome Sciences, National Yang-Ming University, Taipei, Taiwan.ORCID 0000-0002-6944-9370
Chiung-Ya ChenInstitute of Molecular Biology, Academia Sinica, Taipei, Taiwan.
Yi-Chun ShihInstitute of Molecular Biology, Academia Sinica, Taipei, Taiwan.
Hsin-Yu LiuInstitute of Molecular Biology, Academia Sinica, Taipei, Taiwan.ORCID 0000-0002-1637-5814
Chiao-Ming HuangInstitute of Molecular Biology, Academia Sinica, Taipei, Taiwan.ORCID 0000-0002-0116-1098
Yi-Ping HsuehInstitute of Molecular Biology, Academia Sinica, Taipei, Taiwan yph@gate.sinica.edu.tw.ORCID 0000-0002-0866-6275
Institute of Molecular Biology, Academia Sinica · TWNational Yang Ming Chiao Tung University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neuroinflammation is associated with diverse neurological disorders. Endosomal Toll-like receptors (TLRs) including TLR3, TLR7, and TLR8 cell-autonomously regulate neuronal differentiation. However, the mechanisms by which these three TLRs affect neuronal morphology are unclear. In this study, we compare these TLRs in mouse neurons. By combining in vitro neuronal cultures, in utero electroporation, and transcriptomic profiling, we show that TLR8, TLR7, and TLR3 promote dendritic pruning via MYD88 signaling. However, they induce different transcriptomic profiles related to innate immunity, signaling, and neuronal development. The temporal expression patterns and the effects on neuronal morphology are not identical upon activation of these endosomal TLRs. Pathway analyses and in vitro studies specifically implicate mitogen-activated protein kinase signaling in TLR8-mediated dendritic pruning. We further show that TLR8 is more critical for dendritic arborization at a late development stage in vivo. The activation of TLR8, TLR7, or TLR3 results in dendritic shortening, and TLR7 and TLR3 but not TLR8 also control axonal growth. In-depth transcriptomic analyses show that TLRs use different downstream pathways to control neuronal morphology, which may contribute to neuronal development and pathological responses.

Indexed as

AnimalsCell EnlargementElectroporationEndosomesFemaleGene Expression ProfilingGene Expression RegulationMaleMembrane GlycoproteinsMiceMice, Inbred C57BLMyeloid Differentiation Factor 88Neuronal PlasticityNeuronsSignal TransductionToll-Like Receptor 3Membrane GlycoproteinsMyd88 protein, mouseMyeloid Differentiation Factor 88TLR3 protein, mouseTlr7 protein, mouseTLR8 protein, mouseToll-Like Receptor 3Toll-Like Receptor 7Toll-Like Receptor 8

Identifiers

PMID29777026
PMCPMC6080926
OpenAlexW2804100187

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.