Evidence map›Paper›PMID 31248427›Full record

ArticleJournal of neuroinflammation2019

Macrophage galactose-type lectin (MGL) is induced on M2 microglia and participates in the resolution phase of autoimmune neuroinflammation.

Juan M Ilarregui, Gijs Kooij, Ernesto Rodríguez, Susanne M A van der Pol, Nathalie Koning, Hakan Kalay, Joost C van der Horst, Sandra J van Vliet, Juan J García-Vallejo, Helga E de Vries and 1 more

Abstract read
In one paragraph

Article in Journal of neuroinflammation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing 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

29 citing papers in PubMed.

  1. Article
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  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Implications of Mucin-TypeMolecules (Basel, Switzerland) · 2025
    Review
  10. O-GalNAc glycans are enriched in neuronal tracts and regulate nodes of Ranvier.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  11. Dual roles ofFrontiers in immunology · 2025
    Article
  12. Article
  13. Article
  14. Review
  15. Article
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  17. Article
  18. Article
  19. Review
  20. 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

11 authors.

Juan M IlarreguiDepartment of Molecular Cell Biology and Immunology, Amsterdam Infection and Immunity Institute, Amsterdam UMC, Vrije Universiteit Amsterdam, O|2 building, room 11 E 41, PO Box 7057, Amsterdam, 1007MB, Noord-Holland, The Netherlands. juanila@yahoo.com.ORCID http://orcid.org/0000-0002-6871-6764
Gijs KooijDepartment of Molecular Cell Biology and Immunology, Amsterdam Neuroscience, VUmc MS Center, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam, the Netherlands.
Ernesto RodríguezDepartment of Molecular Cell Biology and Immunology, Amsterdam Infection and Immunity Institute, Amsterdam UMC, Vrije Universiteit Amsterdam, O|2 building, room 11 E 41, PO Box 7057, Amsterdam, 1007MB, Noord-Holland, The Netherlands.
Susanne M A van der PolDepartment of Molecular Cell Biology and Immunology, Amsterdam Neuroscience, VUmc MS Center, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam, the Netherlands.
Nathalie KoningDepartment of Molecular Cell Biology and Immunology, Amsterdam Infection and Immunity Institute, Amsterdam UMC, Vrije Universiteit Amsterdam, O|2 building, room 11 E 41, PO Box 7057, Amsterdam, 1007MB, Noord-Holland, The Netherlands.
Hakan KalayDepartment of Molecular Cell Biology and Immunology, Amsterdam Infection and Immunity Institute, Amsterdam UMC, Vrije Universiteit Amsterdam, O|2 building, room 11 E 41, PO Box 7057, Amsterdam, 1007MB, Noord-Holland, The Netherlands.
Joost C van der HorstDepartment of Molecular Cell Biology and Immunology, Amsterdam Infection and Immunity Institute, Amsterdam UMC, Vrije Universiteit Amsterdam, O|2 building, room 11 E 41, PO Box 7057, Amsterdam, 1007MB, Noord-Holland, The Netherlands.
Sandra J van VlietDepartment of Molecular Cell Biology and Immunology, Amsterdam Infection and Immunity Institute, Amsterdam UMC, Vrije Universiteit Amsterdam, O|2 building, room 11 E 41, PO Box 7057, Amsterdam, 1007MB, Noord-Holland, The Netherlands.
Juan J García-VallejoDepartment of Molecular Cell Biology and Immunology, Amsterdam Infection and Immunity Institute, Amsterdam UMC, Vrije Universiteit Amsterdam, O|2 building, room 11 E 41, PO Box 7057, Amsterdam, 1007MB, Noord-Holland, The Netherlands.
Helga E de VriesDepartment of Molecular Cell Biology and Immunology, Amsterdam Neuroscience, VUmc MS Center, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam, the Netherlands.
Yvette van KooykDepartment of Molecular Cell Biology and Immunology, Amsterdam Infection and Immunity Institute, Amsterdam UMC, Vrije Universiteit Amsterdam, O|2 building, room 11 E 41, PO Box 7057, Amsterdam, 1007MB, Noord-Holland, The Netherlands. y.vankooyk@vumc.nl.

Funding

H2020 Marie Skłodowska-Curie Actions grant 642870, ETN ImmunoshapeStichting MS Research 14-865MSStichting MS Research 14-878MSStichting MS Research MS09-924ZonMw Veni 916.12.113
6 · The paper itself

Abstract

backgroundMultiple sclerosis (MS) involves a misdirected immune attack against myelin in the brain and spinal cord, leading to profound neuroinflammation and neurodegeneration. While the mechanisms of disease pathogenesis have been widely studied, the suppression mechanisms that lead to the resolution of the autoimmune response are still poorly understood. Here, we investigated the role of the C-type lectin receptor macrophage galactose-type lectin (MGL), usually expressed on tolerogenic antigen-presenting cells (APCs), as a negative regulator of autoimmune-driven neuroinflammation.

methodsWe used in silico, immunohistochemical, immunofluorescence, quantitative real-time polymerase chain reaction (qRT-PCR) and flow cytometry analysis to explore the expression and functionality of MGL in human macrophages and microglia, as well as in MS post-mortem tissue. In vitro, we studied the capacity of MGL to mediate apoptosis of experimental autoimmune encephalomyelitis (EAE)-derived T cells and mouse CD4

resultsMGL plays a critical role in the resolution phase of EAE as MGL1-deficient (Clec10a

conclusionsOur results show a new role of MGL-expressing APCs as an anti-inflammatory mechanism in autoimmune neuroinflammation by dampening pathogenic T and B cell responses, uncovering a novel clue for neuroprotective therapeutic strategies with relevance for in MS clinical applications.

Indexed as

AnimalsAsialoglycoproteinsCells, CulturedEncephalomyelitis, Autoimmune, ExperimentalFemaleHumansLectins, C-TypeMembrane ProteinsMiceMice, Inbred C57BLMice, KnockoutMicrogliaRatsAsialoglycoproteinsClec10a protein, mouseLectins, C-TypeMembrane ProteinsC-type lectin receptorsExperimental autoimmune encephalomyelitisInflammationMGLMicrogliaMultiple sclerosisTolerance

Identifiers

PMID31248427
PMCPMC6598247

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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.