Evidence map›Paper›PMID 32718316›Full record

ArticleJournal of neuroinflammation2020

CD36-mediated uptake of myelin debris by macrophages and microglia reduces neuroinflammation.

Elien Grajchen, Elien Wouters, Britt van de Haterd, Mansour Haidar, Kévin Hardonnière, Tess Dierckx, Jana Van Broeckhoven, Celine Erens, Sven Hendrix, Saadia Kerdine-Römer and 2 more

Open access · goldAbstract read
In one paragraph

Article in Journal of neuroinflammation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 102 papers.

0numbers the graph read from it
0cells of the map it votes in
102citing papers in PubMed
7.8field-weighted citation impact, top 2% 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

102 citing papers in PubMed, 159 citations in OpenAlex.

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  8. Metabolic Reprogramming of Microglia in Neuroinflammation and Depression.International journal of molecular sciences · 2026
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42 more citing papers are in PubMed but not listed here.

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

12 authors at 2 institutions in 2 countries.

Elien GrajchenDepartment of Immunology and Infection, Biomedical Research Institute, Hasselt University, Diepenbeek, Belgium.
Elien WoutersDepartment of Immunology and Infection, Biomedical Research Institute, Hasselt University, Diepenbeek, Belgium.
Britt van de HaterdDepartment of Immunology and Infection, Biomedical Research Institute, Hasselt University, Diepenbeek, Belgium.
Mansour HaidarDepartment of Immunology and Infection, Biomedical Research Institute, Hasselt University, Diepenbeek, Belgium.
Kévin HardonnièreInflammation, Microbiome and Immunosurveillance, INSERM UMR99, Université Paris-Saclay, Châtenay-Malabry, France.
Tess DierckxDepartment of Immunology and Infection, Biomedical Research Institute, Hasselt University, Diepenbeek, Belgium.
Jana Van BroeckhovenDepartment of Immunology and Infection, Biomedical Research Institute, Hasselt University, Diepenbeek, Belgium.
Celine ErensDepartment of Immunology and Infection, Biomedical Research Institute, Hasselt University, Diepenbeek, Belgium.
Sven HendrixDepartment of Immunology and Infection, Biomedical Research Institute, Hasselt University, Diepenbeek, Belgium.
Saadia Kerdine-RömerInflammation, Microbiome and Immunosurveillance, INSERM UMR99, Université Paris-Saclay, Châtenay-Malabry, France.
Jerome J A HendriksDepartment of Immunology and Infection, Biomedical Research Institute, Hasselt University, Diepenbeek, Belgium.
Jeroen F J BogieDepartment of Immunology and Infection, Biomedical Research Institute, Hasselt University, Diepenbeek, Belgium. Jeroen.bogie@uhasselt.be.ORCID http://orcid.org/0000-0002-0016-1926
Hasselt University · BEInserm · FR

Funding

Belgian Charcot Foundation FCS-2016-EG7, R-8676, and R-6832Fonds Wetenschappelijk Onderzoek 12J9116N, 12JG119N, 12U7718N, and G099618N
6 · The paper itself

Abstract

backgroundThe presence of foamy macrophages and microglia containing intracellular myelin remnants is a pathological hallmark of neurodegenerative disorders such as multiple sclerosis (MS). Despite the importance of myelin internalization in affecting both central nervous system repair and neuroinflammation, the receptors involved in myelin clearance and their impact on the phagocyte phenotype and lesion progression remain to be clarified.

methodsFlow cytometry, quantitative PCR, and immunohistochemistry were used to define the mRNA and protein abundance of CD36 in myelin-containing phagocytes. The impact of CD36 and nuclear factor erythroid 2-related factor 2 (NRF2) on the phagocytic and inflammatory features of macrophages and microglia was assessed using a pharmacological CD36 inhibitor (sulfo-N-succinimidyl oleate) and Nrf2

resultsHere, we show that the fatty acid translocase CD36 is required for the uptake of myelin debris by macrophages and microglia, and that myelin internalization increased CD36 expression through NRF2. Pharmacological inhibition of CD36 promoted the inflammatory properties of myelin-containing macrophages and microglia in vitro, which was paralleled by a reduced activity of the anti-inflammatory lipid-sensing liver X receptors and peroxisome proliferator-activated receptors. By using the EAE model, we provide evidence that CD36 is essential for myelin debris clearance in vivo. Importantly, CD36 inhibition markedly increased the neuroinflammatory burden and disease severity in the EAE model.

conclusionAltogether, we show for the first time that CD36 is crucial for clearing myelin debris and suppressing neuroinflammation in demyelinating disorders such as MS.

Indexed as

AnimalsCD36 AntigensEncephalomyelitis, Autoimmune, ExperimentalFemaleInflammationMacrophagesMiceMice, Inbred C57BLMicrogliaMyelin SheathPhagocytosisCD36 AntigensCD36Fatty acidMacrophagesMicrogliaMultiple sclerosisMyelinNeuroinflammation

Identifiers

PMID32718316
PMCPMC7384221
OpenAlexW3045877203

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.