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In Vitro Phagocytosis of Myelin Debris by Bone Marrow-Derived Macrophages
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Published on: December 30, 2017

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Human IgM antibody rHIgM22 promotes phagocytic clearance of myelin debris by microglia

Yana Zorina1, Jason Stricker2, Anthony O Caggiano3

  • 1Gene Editing and Screening Core Facility, Memorial Sloan Kettering Cancer Center, New York, NY, USA.

Scientific Reports
|June 22, 2018
PubMed

Insights

The experimental antibody rHIgM22 enhances microglial clearance of myelin debris, a key step in promoting remyelination in multiple sclerosis (MS). This antibody aids in clearing debris that inhibits oligodendrocyte precursor cell maturation.

Area of Science:

  • Neuroscience
  • Immunology
  • Cell Biology

Background:

  • Multiple sclerosis (MS) is characterized by demyelinated lesions in the central nervous system (CNS) that resist remyelination.
  • Damaged myelin debris within MS lesions impedes oligodendrocyte precursor cell (OPC) maturation and repair.
  • The experimental antibody rHIgM22 shows potential for promoting remyelination in animal models and is under investigation for MS treatment.

Purpose of the Study:

  • To investigate the mechanism by which rHIgM22 promotes remyelination.
  • To determine if rHIgM22 enhances microglial phagocytosis of myelin debris.
  • To elucidate the cellular pathways involved in rHIgM22-mediated myelin clearance.

Main Methods:

  • Utilized a mouse microglial cell line and primary rat microglia.
  • Treated microglial cells with myelin and rHIgM22.
  • Assayed for myelin phagocytosis, actin polymerization, Fc domain activity, and Complement Receptor 3 activation.

Main Results:

  • rHIgM22 dose-dependently stimulated myelin phagocytosis by microglia.
  • rHIgM22-mediated phagocytosis required actin polymerization.
  • The Fc domain of rHIgM22 and Complement Receptor 3 activation were essential for this process.

Conclusions:

  • rHIgM22 enhances the clearance of inhibitory myelin debris by microglia.
  • Stimulating phagocytic clearance of myelin debris is a potential therapeutic strategy for promoting remyelination in MS.
  • rHIgM22 may promote remyelination by facilitating the removal of myelin debris that hinders OPC differentiation.

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