Article

Journal of Molecular Neuroscience

, Volume 39, Issue 1, pp 99-103

First online:

The Role of Galectin-3/MAC-2 in the Activation of the Innate-Immune Function of Phagocytosis in Microglia in Injury and Disease

  • Shlomo RotshenkerAffiliated withDepartment of Medical Neurobiology, IMRIC, Hebrew University-Hadassah Medical School and the Eric Roland Center for Neurodegenerative Diseases Email author 

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Abstract

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; αMβ2 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.

Keywords

Galectin-3 MAC-2 Phagocytosis Wallerian degeneration Neurodegenetation Myelin