Utility of acid citrate dextrose-acidification for platelet volume reduction protocols in the transfusion service.

Background: Volume-reduced platelets can minimize circulatory overload, allergic transfusion reactions, or out-of-group plasma infusion. Our center adopted a volume reduction protocol that includes acidification with acid citrate dextrose solution A (ACD-A) before centrifugation and without any rest period prior to resuspension allowing a better turnaround time for platelet issue.

Study Design And Methods: This report compares corrected count increments (CCIs) from full-volume and ACD-A acidified volume-reduced human platelets in a retrospective study at a single hospital and in a mouse model.

Evaluating stored platelet shape change using imaging flow cytometry.

Platelets are routinely stored at room temperature for 5-7 days before transfusion. Stored platelet quality is traditionally assessed by Kunicki's morphology score. This method requires extensive training, experience, and is highly subjective.

Effect of bedside filtration on aggregates from cold-stored whole blood-derived platelet-rich plasma and apheresis platelet concentrates.

Background: The current approach to manufacture cold-stored platelets (CSP) replicates that of room temperature-stored platelets (RSP). However, this production method is associated with aggregate formation in CSP, a major pitfall that leads to significant wastage. We hypothesized that isolating platelets from whole blood as platelet-rich plasma (PRP) and storing them at a lower concentration reduces aggregates and that conventional bedside transfusion filtration removes CSP aggregates.

Storage temperature determines platelet GPVI levels and function in mice and humans.

Platelets are currently stored at room temperature before transfusion to maximize circulation time. This approach has numerous downsides, including limited storage duration, bacterial growth risk, and increased costs. Cold storage could alleviate these problems.

Antibodies to Low-Copy Number RBC Alloantigen Convert a Tolerogenic Stimulus to an Immunogenic Stimulus in Mice.

Red blood cells expressing alloantigens are well known to be capable of inducing robust humoral alloantibody responses both in transfusion and pregnancy. However, the majority of transfusion recipients and pregnant women never make alloantibodies, even after repeat exposure to foreign RBCs. More recently, RBCs have been used as a cellular therapeutic-very much like transfusion, engineered RBCs are highly immunogenic in some cases but not others.

In utero exposure to alloantigens primes alloimmunization to platelet transfusion in mice.

Background: Platelet transfusions remain a mainstay of treatment for many patients with thrombocytopenia, but can lead to alloantibodies to Human Leukocyte Antigens (anti-HLA) resulting in inadequate responses to subsequent platelet transfusions (refractoriness), as well as complicate transplantation. Despite substantial decreases in alloimmunization with the implementation of leukoreduction, a significant percentage of patients still become alloimmunized following platelet transfusions. It remains unclear why some patients make anti-HLA antibodies, but others do not make anti-HLA antibodies even with chronic transfusion.

Autoantigen presentation by splenic dendritic cells is required for RBC-specific autoimmunity.

Background: Failure of humoral tolerance to red blood cell (RBC) antigens may lead to autoimmune hemolytic anemia (AIHA), a severe and sometimes fatal disease. Previous studies have shown that although tolerance is robust in HOD mice, autoantibodies are generated upon adoptive transfer of OTII CD4 T cells, which are specific for an epitope contained within the HOD antigen. These data imply that antigen-presenting cells (APCs) are presenting RBC-derived autoantigen(s) and are capable of driving T-cell activation.