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Increasing phagocytosis of microglia through targeting CD33 with liposomes displaying glycan ligands

Abhishek Bhattacherjee, Gour Chand Daskhan, Arjun Bains, Adrianne E. S. Watson, Ghazaleh Eskandari-Sedighi, Chris D. St. Laurent, View ORCID ProfileAnastassia Voronova, View ORCID ProfileMatthew S. Macauley
doi: https://doi.org/10.1101/2021.05.08.443135
Abhishek Bhattacherjee
1Department of Chemistry, University of Alberta. Edmonton, Alberta, Canada
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Gour Chand Daskhan
1Department of Chemistry, University of Alberta. Edmonton, Alberta, Canada
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Arjun Bains
1Department of Chemistry, University of Alberta. Edmonton, Alberta, Canada
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Adrianne E. S. Watson
2Department of Medical Genetics, University of Alberta. Edmonton, Alberta, Canada
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Ghazaleh Eskandari-Sedighi
1Department of Chemistry, University of Alberta. Edmonton, Alberta, Canada
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Chris D. St. Laurent
1Department of Chemistry, University of Alberta. Edmonton, Alberta, Canada
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Anastassia Voronova
2Department of Medical Genetics, University of Alberta. Edmonton, Alberta, Canada
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  • ORCID record for Anastassia Voronova
Matthew S. Macauley
1Department of Chemistry, University of Alberta. Edmonton, Alberta, Canada
3Department of Medical Microbiology and Immunology, University of Alberta. Edmonton, Alberta, Canada
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  • For correspondence: macauley@ualberta.ca
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Abstract

CD33 is an immunomodulatory receptor expressed on microglia and genetically linked to Alzheimer’s disease (AD) susceptibility. While antibodies targeting CD33 have entered clinical trials to treat neurodegeneration, it is unknown whether the glycan-binding properties of CD33 can be exploited to modulate microglia. Here, we use liposomes that multivalently display glycan ligands of CD33 (CD33L liposomes) to engage CD33. We find that CD33L liposomes increase phagocytosis of cultured monocytic cells and microglia in a CD33-dependent manner. Enhanced phagocytosis strongly correlates with loss of CD33 from the cell surface and internalization of liposomes. Increased phagocytosis by treatment with CD33L liposomes is dependent on a key intracellular signaling motif on CD33 as well as the glycan-binding ability of CD33. These effects are specific to trans engagement of CD33 by CD33L liposomes, as cis engagement through insertion of lipid-linked CD33L into cells produces the opposite effect on phagocytosis. Moreover, intracerebroventricular injection of CD33L liposomes in mice enhances phagocytosis of microglia in a CD33-dependent manner. These results demonstrate that multivalent engagement of CD33 with glycan ligands can modulate microglial cell function.

Competing Interest Statement

The authors have declared no competing interest.

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The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY-NC-ND 4.0 International license.
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Posted May 09, 2021.
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Increasing phagocytosis of microglia through targeting CD33 with liposomes displaying glycan ligands
Abhishek Bhattacherjee, Gour Chand Daskhan, Arjun Bains, Adrianne E. S. Watson, Ghazaleh Eskandari-Sedighi, Chris D. St. Laurent, Anastassia Voronova, Matthew S. Macauley
bioRxiv 2021.05.08.443135; doi: https://doi.org/10.1101/2021.05.08.443135
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Increasing phagocytosis of microglia through targeting CD33 with liposomes displaying glycan ligands
Abhishek Bhattacherjee, Gour Chand Daskhan, Arjun Bains, Adrianne E. S. Watson, Ghazaleh Eskandari-Sedighi, Chris D. St. Laurent, Anastassia Voronova, Matthew S. Macauley
bioRxiv 2021.05.08.443135; doi: https://doi.org/10.1101/2021.05.08.443135

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