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Purification of Platelets from Mouse Blood
Published on: May 7, 2019
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A complement-mediated rat xenotransfusion model of platelet refractoriness
Adrianne I Enos1, Pamela S Hair1, Neel K Krishna2
1Department of Pediatrics, Eastern Virginia Medical School, 700 West Olney Road, Norfolk, VA 23507, USA.
Molecular Immunology
|June 3, 2020
Summary
Antiplatelet antibodies cause complement-mediated platelet destruction, leading to platelet refractoriness. A new rat model demonstrates complement
Area of Science:
- Immunology
- Hematology
- Transfusion Medicine
Background:
- Immune-mediated platelet refractoriness is a clinical challenge.
- Antiplatelet antibodies are a primary cause of refractoriness.
- The role of complement in platelet destruction is not well understood.
Purpose of the Study:
- To investigate the role of complement in antibody-mediated platelet destruction.
- To develop and validate a new animal model for studying platelet refractoriness.
Main Methods:
- Ex vivo assays using antibody-sensitized human platelets and human sera.
- Assessment of complement activation and opsonization.
- Utilization of a classical pathway complement inhibitor (PA-dPEG24).
- Development of a Wistar rat model for platelet refractoriness.
Main Results:
- Antibody-sensitized platelets were rapidly opsonized with iC3b.
- Complement inhibition blocked opsonization and preserved platelet viability.
- Complement activation reduced platelet viability, which was reversible with inhibition.
- The rat model showed complement-mediated platelet removal.
Conclusions:
- Complement activation by antiplatelet antibodies leads to platelet opsonization and reduced viability.
- A novel rat model provides a new tool to study platelet refractoriness mechanisms.
