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An Engulfment Assay: A Protocol to Assess Interactions Between CNS Phagocytes and Neurons
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Microglia C-lectin/selectin' neurons to eat

Yike Jiang1, Mari L Shinohara2

  • 1Department of Immunology, Duke University School of Medicine, Durham, NC, USA; Division of Pediatric Rheumatology, Department of Pediatrics, Duke University School of Medicine, Durham, NC, USA.

Immunity
|February 15, 2023
PubMed

Insights

Gaucher disease involves beta-glucosylceramide buildup. This study shows Mincle-activated microglia phagocytose neurons, causing neuroinflammation and neurological symptoms.

Area of Science:

  • Neuroscience
  • Immunology
  • Metabolic Disorders

Background:

  • Beta-glucosylceramide (β-GlcCer) accumulation is a hallmark of Gaucher disease.
  • The mechanisms linking β-GlcCer to neuroinflammation and neuronopathy remain unclear.
  • Beta-glucosylceramide is a known ligand for the Mincle receptor.

Purpose of the Study:

  • To elucidate the role of β-GlcCer in Gaucher disease-associated neuroinflammation.
  • To investigate the involvement of the Mincle receptor in the pathogenesis of neurodegeneration.

Main Methods:

  • Utilized mouse models of Gaucher disease.
  • Investigated microglial activation pathways.
  • Assessed neuronal phagocytosis and neurological outcomes.

Main Results:

  • Mincle receptor activation on microglia was observed in response to β-GlcCer.
  • Mincle-dependent microglial activation led to the phagocytosis of neurons.
  • This process correlated with the development of neurological symptoms.

Conclusions:

  • Mincle-mediated microglial activation is a key driver of neuroinflammation and neuron loss in Gaucher disease.
  • Targeting the Mincle pathway may offer therapeutic strategies for Gaucher disease.
  • Understanding β-GlcCer's role in Mincle activation is crucial for neuroprotection.

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