KODE technology not only enables the creation of artificial transfusion reactions in animal models, but also has the potential to be used clinically in man to determine 24-hour cell survival. The ability to recover the kodecytes for further analysis has valuable research and diagnostic potential.
FSL constructs have the potential to neutralize circulating antibodies and allow for, or mitigate, the consequences of ABO-incompatible red blood cell transfusion.
Background KODE technology uses Function‐Spacer‐Lipid (FSL) constructs for artificial attachment of blood group antigens onto live cells (kodecytes) and visualisation, thus making it potentially suitable to model both transfusion reactions and determine in vivo cell survival. Additionally, as some FSL constructs are glycolipid‐like, the possibility exists that they may also neutralise circulating antibodies, in the same way Lewis glycolipids were historically used to allow Lewis incompatible transfusions.
Aims To determine if kodecytes can be used to both mimic and monitor transfusion reactions in an animal model, and also to determine if FSL construct infusions can neutralise circulating antibodies and allow for an incompatible transfusion.
Methods Naïve, anti‐A positive (immunised), and anti‐A positive/FSL‐A neutralised mice were given transfusions of murine kodecytes created with FSL‐biotin and FSL‐A. Levels of surviving kodecytes were determined at multiple time‐points via their biotin label. Analysis for anti‐A was performed with inkjet printed FSL‐A constructs in a micro immunoassay.
Results Normal kodecyte survival was observed in control animals. Mice with anti‐A predominantly cleared their incompatible A‐kodecyte transfusions within 6 min. Mice with anti‐A that had been neutralised with an FSL‐A infusion had normal survival of their incompatible A‐kodecyte transfusions. Re‐challenge transfusions of A‐kodecytes into mice previously given FSL‐A (once the FSL‐A had cleared from their circulation) gave two different results. One group cleared the incompatible A‐kodecytes within minutes while the other had normal survival, suggesting potential induction of tolerance.
Conclusions Kodecytes can be used to model blood group A incompatible transfusions in animals. FSL‐A can neutralise anti‐A and allow for incompatible A‐kodecyte transfusion. The potential exists to extend these research observations into clinical use to allow for transfusion and transplantation across the ABO barrier, or at least mitigate the consequences of accidental ABO incompatibilities.
A new high-frequency red cell antigen has been identified and named GIL. GIL differs from all high-frequency antigens included in the International Society of Blood Transfusion classification. There is very little family information and GIL has not been shown to be an inherited character. Five women with anti-GIL have been found. All had been pregnant at least twice. Red blood cells of two of the babies gave positive direct antiglobulin tests, but there were no clinical signs of hemolytic disease. Anti-GIL may have been responsible for a hemolytic transfusion reaction and results of monocyte monolayer assays of two of the anti-GIL suggested a potential to cause destruction of trans-
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