Evidence map›Paper›PMID 28500071›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2017

Activated Microglia Desialylate and Phagocytose Cells via Neuraminidase, Galectin-3, and Mer Tyrosine Kinase.

Koji Nomura, Anna Vilalta, David H Allendorf, Tamara C Hornik, Guy C Brown

Open access · hybridAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
72citing papers in PubMed, 1 pooled it
4.2field-weighted citation impact, top 5% 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

72 citing papers in PubMed, 1 synthesis or guideline pooled it, 109 citations in OpenAlex.

  1. Pooled it
  2. Synthetic viral RNA mimetics induce neuronal loss through microglial phagocytosis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Article
  3. Review
  4. Review
  5. Article
  6. Review
  7. Microglial phagocytosis in Alzheimer disease.Nature reviews. Neurology · 2026
    Review
  8. Review
  9. Article
  10. Review
  11. Microglial galectin-3 increases with aging in the mouse hippocampus.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2025
    Article
  12. Review
  13. Article
  14. Article
  15. Article
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  17. Article
  18. Article
  19. Review
  20. Review

12 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

5 authors at 1 institution in 2 countries.

Koji NomuraDepartment of Biochemistry, University of Cambridge, Cambridge CB2 1QW, United Kingdom.ORCID 0000-0002-5912-074X
Anna VilaltaDepartment of Biochemistry, University of Cambridge, Cambridge CB2 1QW, United Kingdom.ORCID 0000-0003-1430-6337
David H AllendorfDepartment of Biochemistry, University of Cambridge, Cambridge CB2 1QW, United Kingdom.
Tamara C HornikDepartment of Biochemistry, University of Cambridge, Cambridge CB2 1QW, United Kingdom.
Guy C BrownDepartment of Biochemistry, University of Cambridge, Cambridge CB2 1QW, United Kingdom gcb3@cam.ac.uk.ORCID 0000-0002-3610-1730
University of Cambridge · GB

Funding

Medical Research Council MR/L010593/1
6 · The paper itself

Abstract

Activated microglia can phagocytose dying, stressed, or excess neurons and synapses via the phagocytic receptor Mer tyrosine kinase (MerTK). Galectin-3 (Gal-3) can cross-link surface glycoproteins by binding galactose residues that are normally hidden below terminal sialic acid residues. Gal-3 was recently reported to opsonize cells via activating MerTK. We found that LPS-activated BV-2 microglia rapidly released Gal-3, which was blocked by calcineurin inhibitors. Gal-3 bound to MerTK on microglia and to stressed PC12 (neuron-like) cells, and it increased microglial phagocytosis of PC12 cells or primary neurons, which was blocked by inhibition of MerTK. LPS-activated microglia exhibited a sialidase activity that desialylated PC12 cells and could be inhibited by Tamiflu, a neuraminidase (sialidase) inhibitor. Sialidase treatment of PC12 cells enabled Gal-3 to bind and opsonize the live cells for phagocytosis by microglia. LPS-induced microglial phagocytosis of PC12 was prevented by small interfering RNA knockdown of Gal-3 in microglia, lactose inhibition of Gal-3 binding, inhibition of neuraminidase with Tamiflu, or inhibition of MerTK by UNC569. LPS-induced phagocytosis of primary neurons by primary microglia was also blocked by inhibition of MerTK. We conclude that activated microglia release Gal-3 and a neuraminidase that desialylates microglial and PC12 surfaces, enabling Gal-3 binding to PC12 cells and their phagocytosis via MerTK. Thus, Gal-3 acts as an opsonin of desialylated surfaces, and inflammatory loss of neurons or synapses may potentially be blocked by inhibiting neuraminidases, Gal-3, or MerTK.

Indexed as

PhagocytosisAnimalsc-Mer Tyrosine KinaseGalactoseGalectin 3LipopolysaccharidesMacrophagesMicrogliaNeuraminidaseNeuronsOpsonin ProteinsOseltamivirPC12 CellsProto-Oncogene ProteinsPyrazolesPyrimidinesc-Mer Tyrosine KinaseGalactoseGalectin 3LipopolysaccharidesMertk protein, ratNeuraminidaseOpsonin ProteinsOseltamivirProto-Oncogene ProteinsPyrazolesPyrimidinesReceptor Protein-Tyrosine KinasesUNC569

Identifiers

PMID28500071
PMCPMC5458330
OpenAlexW2612664982

What OpenQuestion holds

Textmetadata
LicenceTDM
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.