A Complement-Mediated Rat Xenotransfusion Model of Platelet Refractoriness
Posted by Adam Awdish on
Innovative Grade US Origin Rat Sprague Dawley Complement Serum from Innovative Research was used in the following study:
A Complement-Mediated Rat Xenotransfusion Model of Platelet Refractoriness
Adrianne I. Enos, Pamela S. Hair, Neel K. Krishna, Kenji M. Cunnion
Molecular Immunology
May 30, 2020
Platelet refractoriness, or the failure of transfused platelets to increase a patient’s platelet count that results in continued thrombocytopenia, is a concerning medical issue that has an urgent need for a solution. This continued state of thrombocytopenia can increase the risk of spontaneous bleeding in the patient and can result in increased medical expenses due to the need for additional treatments and procedures.
The most common cause for platelet refractoriness is related to immune mechanisms, however some cases can stem from non-immune mechanisms such as intravascular coagulopathy and splenomegaly. Regarding immune mechanisms, the most common factor contributing to platelet refractoriness is alloimmunization, or the phenomenon where patients develop anti-platelet antibodies after receiving multiple platelet transfusions. Further, recent studies have shown that anti-HLA antibodies are able to activate the complement pathway that initiates membrane attacks on platelets, thus suggesting that the complement system plays some role in immune-related platelet refractoriness.
Current attempts to counter platelet refractoriness focus transfusing only HLA-matched platelets, however it is often difficult to find readily available donors. In this study, researchers observed complement-mediated killing of platelets ex vivo to better understand how the complement system affects platelet viability. The findings suggest that platelet viability is decreased by complement activation, however this can be reversed with complement inhibitor PA-dPEG24.
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