Evidence map›Paper›PMID 29445154›Full record

ArticleCell death & disease2018

Interleukin 4 modulates microglia homeostasis and attenuates the early slowly progressive phase of amyotrophic lateral sclerosis.

Chiara Rossi, Melania Cusimano, Martina Zambito, Annamaria Finardi, Alessia Capotondo, Jose Manuel Garcia-Manteiga, Giancarlo Comi, Roberto Furlan, Gianvito Martino, Luca Muzio

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed, 1 pooled it
6.8field-weighted citation impact, top 3% 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

49 citing papers in PubMed, 1 synthesis or guideline pooled it, 76 citations in OpenAlex.

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  15. Causal ALS genes impact the MHC class II antigen presentation pathway.Proceedings of the National Academy of Sciences of the United States of America · 2023
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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

10 authors at 2 institutions in 1 country.

Chiara RossiNeuroimmunology Unit, Division of Neuroscience, Institute of Experimental Neurology (INSPE), San Raffaele Scientific Institute, 20132, Milan, Italy.
Melania CusimanoNeuroimmunology Unit, Division of Neuroscience, Institute of Experimental Neurology (INSPE), San Raffaele Scientific Institute, 20132, Milan, Italy.
Martina ZambitoNeuroimmunology Unit, Division of Neuroscience, Institute of Experimental Neurology (INSPE), San Raffaele Scientific Institute, 20132, Milan, Italy.
Annamaria FinardiNeuroimmunology Unit, Division of Neuroscience, Institute of Experimental Neurology (INSPE), San Raffaele Scientific Institute, 20132, Milan, Italy.
Alessia CapotondoNeuroimmunology Unit, Division of Neuroscience, Institute of Experimental Neurology (INSPE), San Raffaele Scientific Institute, 20132, Milan, Italy.
Jose Manuel Garcia-ManteigaCentre for Translational Genomics and Bioinformatics, San Raffaele Scientific Institute, 20132, Milan, Italy.ORCID 0000-0002-5481-040X
Giancarlo ComiDepartment of Neurology, Institute of Experimental Neurology (INSPE), Vita Salute San Raffaele University, 20132, Milan, Italy.
Roberto FurlanNeuroimmunology Unit, Division of Neuroscience, Institute of Experimental Neurology (INSPE), San Raffaele Scientific Institute, 20132, Milan, Italy.
Gianvito MartinoNeuroimmunology Unit, Division of Neuroscience, Institute of Experimental Neurology (INSPE), San Raffaele Scientific Institute, 20132, Milan, Italy.
Luca MuzioNeuroimmunology Unit, Division of Neuroscience, Institute of Experimental Neurology (INSPE), San Raffaele Scientific Institute, 20132, Milan, Italy. muzio.luca@hsr.it.
Neuroscience Institute · ITVita-Salute San Raffaele University · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Microglia activation is a commonly pathological hallmark of neurodegenerative diseases, such as amyotrophic lateral sclerosis (ALS), a devastating disorder characterized by a selective motor neurons degeneration. Whether such activation might represent a causal event rather than a secondary epiphenomenon remains elusive. Here, we show that CNS-delivery of IL-4-via a lentiviral-mediated gene therapy strategy-skews microglia to proliferate, inducing these cells to adopt the phenotype of slowly proliferating cells. Transcriptome analysis revealed that IL-4-treated microglia express a broad number of genes normally encoded by embryonic microglia. Since embryonic microglia sustain CNS development, we then hypothesized that turning adult microglia to acquire such phenotype via IL-4 might be an efficient in vivo strategy to sustain motor neuron survival in ALS. IL-4 gene therapy in SOD1

Indexed as

Bone Marrow TransplantationAmyotrophic Lateral SclerosisAnimalsDisease Models, AnimalDisease ProgressionGene Expression RegulationGenes, ReporterGenetic TherapyGreen Fluorescent ProteinsHomeostasisInterleukin-4MiceMice, Inbred C57BLMice, TransgenicMicrogliaNerve Tissue ProteinsGreen Fluorescent ProteinsIl4 protein, mouseInterleukin-4Nerve Tissue ProteinsSod1 protein, mouseSuperoxide Dismutase-1

Identifiers

PMID29445154
PMCPMC5833860
OpenAlexW2790138775

What Socratic 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 Socratic graph.