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ePoster
CD33 IGV-SPECIFIC NANOBODIES TO MODULATE AMYLOID-Β UPTAKE IN HUMAN MICROGLIAL CELLS
Denisa R. Contand 3 co-authors
Karl Landsteiner University
FENS Forum 2026 (2026)
Barcelona, Spain
Board PS03-08AM-117
Presentation
Date TBA
Board: PS03-08AM-117
Event Information
Poster Board
PS03-08AM-117
Poster
View posterAbstract
Microglial dysfunction is increasingly recognized as a key contributor to impaired amyloid-β (Aβ) clearance in Alzheimer’s disease (AD). Among microglial immune receptors, CD33 acts as an inhibitory regulator of phagocytosis and is strongly associated with increased AD risk. Emerging evidence suggests that this inhibitory function is primarily mediated through the extracellular IgV domain of CD33, which interferes with pro-phagocytic signaling pathways. In this project, we hypothesize that selective targeting of the CD33 IgV domain using specific nanobodies can modulate CD33-dependent inhibitory signaling and thereby alter microglial handling of Aβ. To test this hypothesis, we use human HMC3 microglial cells as an in vitro model system. CD33 expression and IgV accessibility are first validated using biochemical and fluorescence-based approaches. IgV-specific nanobodies are then applied to assess their impact on microglial Aβ uptake using quantitative uptake assays. By dissecting the role of IgV-mediated CD33 regulation in human microglia, this study aims to establish a mechanistic framework for nanobody-based modulation of microglial Aβ clearance. These findings may provide a foundation for the development of targeted immunomodulatory strategies addressing microglial dysfunction in AD.
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