The role of Galectin-3/MAC-2 in the activation of the innate-immune function of phagocytosis in microglia in injury and disease

  • Rotshenker S
  • 44


    Mendeley users who have this article in their library.
  • 62


    Citations of this article.


Microglia are a self-sustained population of immune/myeloid cells present throughout the central nervous system (CNS). Microglia are in a "resting" state in the normal adult CNS. They turn "active" in injury and disease (e.g., trauma, neurodegeneration, and infection). Activated microglia can be beneficial as well as detrimental/neurotoxic. The innate-immune function of phagocytosis of tissue debris, neurotoxic factor, and pathogens is a beneficial function of microglia. The current manuscript reviews the role of Galectin-3 (known also as MAC-2; Galectin-3/MAC-2) in the activation of the phagocytosis of degenerated myelin that is mediated by complement receptor-3 (known also as MAC-1; CD11b/CD18; alphaMbeta2 integrin) and SRA (scavenger receptor-AI/II). Observations suggest that Galectin-3/MAC-2 may act as a molecular switch that activates phagocytosis by up-regulating and prolonging KRas-GTP-dependent PI3K (phosphatidylinositol 3-kinase) activity. A similar mechanism may regulate the phagocytosis of other tissue debris, neurotoxic factors and pathogens in neurodegenerative and infectious diseases.

Author-supplied keywords

  • Galectin-3
  • MAC-2
  • Myelin
  • Neurodegenetation
  • Phagocytosis
  • Wallerian degeneration

Get free article suggestions today

Mendeley saves you time finding and organizing research

Sign up here
Already have an account ?Sign in

Find this document

Cite this document

Choose a citation style from the tabs below

Save time finding and organizing research with Mendeley

Sign up for free