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Related Experiment Videos

Galectin-3/MAC-2 in experimental allergic encephalomyelitis.

F Reichert1, S Rotshenker

  • 1Department of Anatomy and Cell Biology, Hebrew University-Hadassah Medical School, Jerusalem, Israel.

Experimental Neurology
|January 5, 2000
PubMed
Summary

Galectin-3/MAC-2 marks activated microglia and macrophages involved in myelin removal during central nervous system autoimmune disease. This activation state, along with myelin phagocytosis, is suppressed by Copolymer 1 in experimental autoimmune encephalomyelitis.

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Area of Science:

  • Neuroscience
  • Immunology
  • Cell Biology

Background:

  • Phagocytosis of myelin is crucial for nervous system repair and disease pathogenesis.
  • Galectin-3/MAC-2 is a marker for activated monocytes, macrophages, and microglia.
  • Myelin phagocytosis in peripheral nerves involves MAC-1-expressing macrophages, unlike the slow degeneration in the central nervous system (CNS).

Purpose of the Study:

  • To investigate the presence of Galectin-3/MAC-2 activation in the CNS during experimental autoimmune encephalomyelitis (EAE).
  • To determine if Galectin-3/MAC-2 expression correlates with autoimmune-induced myelin degeneration and phagocytosis in EAE.
  • To assess the effect of Copolymer 1 on EAE, demyelination, and Galectin-3/MAC-2 expression.

Main Methods:

  • Induction of EAE in mice using mouse spinal cord homogenate.

Related Experiment Videos

  • Assessment of demyelination via light microscopy.
  • Immunocytochemical analysis of Galectin-3/MAC-2, MAC-1, and F4/80 expression in spinal cords and optic nerves.

    • Main Results:

    • Galectin-3/MAC-2, MAC-1, and F4/80 expression were upregulated in demyelinated areas of the CNS in EAE mice.
    • These markers were found on microglia and macrophages actively phagocytosing myelin.
    • Copolymer 1 treatment reduced EAE severity, demyelination, and Galectin-3/MAC-2 expression.

    Conclusions:

    • EAE pathogenesis involves microglia and macrophage activation, characterized by Galectin-3/MAC-2 and MAC-1 expression, correlating with myelin degeneration and phagocytosis.
    • CNS responses to injury and autoimmune challenges differ in microglia/macrophage activation patterns, specifically regarding Galectin-3/MAC-2 expression and myelin phagocytosis.
    • Galectin-3/MAC-2 serves as a key marker for identifying activated phagocytic cells in the CNS during autoimmune demyelinating diseases.