Evidence map›Paper›PMID 41322409›Full record

ArticleFrontiers in immunology2025

Extracellular microRNAs modulate human microglial function through TLR8.

Hannah Weidling, Edyta Motta, Leonard D Kuhrt, Christina Krüger, Caio Andreeta Figueiredo, Thomas Wallach, Silke Frahm, Sebastian Diecke, Susanne A Wolf, Helmut Kettenmann and 1 more

Abstract read
In one paragraph

Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

3 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
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

11 authors.

Hannah WeidlingInstitute of Cell Biology and Neurobiology, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Berlin, Germany.
Edyta MottaInstitute of Cell Biology and Neurobiology, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Berlin, Germany.
Leonard D KuhrtMax-Delbrueck-Center for Molecular Medicine in the Helmholtz Association, Berlin, Germany.
Christina KrügerInstitute of Cell Biology and Neurobiology, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Berlin, Germany.
Caio Andreeta FigueiredoMax-Delbrueck-Center for Molecular Medicine in the Helmholtz Association, Berlin, Germany.
Thomas WallachInstitute of Cell Biology and Neurobiology, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Berlin, Germany.
Silke FrahmTechnology Platform for Pluripotent Stem Cells, Max Delbrück Center for Molecular Medicine in the Helmholtz Association, Berlin, Germany.
Sebastian DieckeTechnology Platform for Pluripotent Stem Cells, Max Delbrück Center for Molecular Medicine in the Helmholtz Association, Berlin, Germany.
Susanne A WolfMax-Delbrueck-Center for Molecular Medicine in the Helmholtz Association, Berlin, Germany.
Helmut Kettenmann *Max-Delbrueck-Center for Molecular Medicine in the Helmholtz Association, Berlin, Germany.
Seija Lehnardt *Institute of Cell Biology and Neurobiology, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Berlin, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Objective: MicroRNAs (miRNAs) are abundantly expressed in the brain and are specifically dysregulated in central nervous system (CNS) diseases. They act as post-transcriptional gene regulators but can also serve as ligands for Toll-like receptors (TLRs). This study aims to investigate CNS disease-associated miRNAs as signaling molecules for human microglia. Methods: Using a machine learning algorithm and the disease-linked database PhenoMiR, we identified Alzheimer's disease (AD)- and glioma-associated miRNAs as ligands for TLR7 and TLR8. Expression of human TLR7 and TLR8 in iPSC-derived human microglia-like cells (iMGLs) was validated by RT-qPCR. Using ELISA, scratch assay, and FACS, we investigated the miRNAs' potential to modulate iMGL function, including cytokine release, motility, and phagocytosis, respectively. The selective human TLR8 antagonist CU-CPT9a was used to determine the role of this receptor in miRNA-induced modulation of human microglial activity. Co-cultures of iMGLs and iPSC-derived human cortical neurons (iNeurons) were analyzed by Neurotrack imaging to assess the effects of miRNAs on human neurites. Results: We identified AD- and glioma-associated miR-9-5p, miR-132-5p, miR-340-3p, miR-30e-3p, miR-501-3p, and Discussion: Our data establish that distinct CNS disease-associated miRNAs serve as signaling molecules for human microglia via TLR8, thereby controlling the diverse microglial functions and modulating the neuroinflammatory response.

Indexed as

MicrogliaMicroRNAsToll-Like Receptor 8Alzheimer DiseaseCells, CulturedCoculture TechniquesCytokinesGliomaHumansInduced Pluripotent Stem CellsNeuronsPhagocytosisSignal TransductionToll-Like Receptor 7CytokinesMicroRNAsTLR7 protein, humanTLR8 protein, humanToll-Like Receptor 7Toll-Like Receptor 8Alzheimer's diseaseextracellular microRNAgliomahuman microgliaiPSCmicroglial functionstem cellstoll-like receptor 8

Identifiers

PMID41322409
PMCPMC12660282

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Registered trials

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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.