Platelets are small, disc-shaped cell fragments in the blood that play a role in hemostasis, the process of stopping bleeding. When a blood vessel is injured, platelets aggregate at the site of damage, forming a plug that initiates the blood clotting cascade. Because platelets have a limited shelf life, blood banks must maintain a constant, readily available supply. However, safe and effective platelet transfusion requires navigating complex compatibility factors that prevent a single “universal” donor type.
Correcting the Universal Donor Misconception
The concept of a “universal donor” is commonly associated with red blood cells (RBCs). Group O negative blood is often used in emergencies because Group O RBCs lack the A and B antigens that trigger an immune response. Similarly, Group AB plasma is the universal donor for plasma because it lacks the anti-A and anti-B antibodies that could attack a recipient’s native RBCs. This simplicity does not translate to platelets, which follow different immunological rules.
Platelets express ABO antigens on their surface, though the expression level is generally lower than on red cells. Transfusing ABO-incompatible platelets can cause problems in two ways. First, the recipient’s anti-A or anti-B antibodies can attack and clear the transfused platelets. Second, the donor plasma accompanying the platelets can contain antibodies that attack the recipient’s red cells, leading to hemolysis. While blood banks prioritize using ABO-identical products, some degree of ABO mismatching is a common, managed practice necessary to maintain supply.
The Unique Compatibility Challenges of Platelets
The most significant barrier to a universal platelet product is Human Leukocyte Antigens (HLA). HLA are protein structures found on the surface of most cells, including platelets and white blood cells, that help the immune system distinguish between “self” and “non-self.” These antigens are highly polymorphic, meaning there are many different combinations, which makes matching a donor to a recipient extremely difficult.
Exposure to foreign HLA antigens, such as through a prior transfusion, organ transplant, or pregnancy, can cause an individual to develop alloantibodies. When a patient with these antibodies receives platelets from a random donor, their immune system may rapidly destroy the transfused platelets. This condition, known as platelet refractoriness, renders the transfusion ineffective and can be life-threatening for patients with severe bleeding risk.
Patients who are frequently transfused often require HLA-matched platelets. HLA Class I antigens (specifically HLA-A and HLA-B) are the most clinically significant markers on platelets. Matching these markers is complex due to the wide genetic variation in the human population. Finding a perfectly matched donor is challenging, especially for highly immunized patients, which prevents the existence of a single universal type based on HLA.
Preparation Methods for Safe Platelet Transfusion
Several standard blood bank procedures make platelet products safer and broaden the pool of usable donations.
Leukoreduction
Leukoreduction is a process where the majority of white blood cells (leukocytes) are removed from the platelet product. This step is performed because white blood cells carry a high concentration of HLA antigens. Their removal significantly reduces the recipient’s exposure to foreign HLA, lowering the risk of alloimmunization and subsequent refractoriness.
Pathogen Inactivation
Pathogen inactivation treats the platelet product to neutralize a wide range of viruses, bacteria, and parasites. This is important because platelets are stored at room temperature, which allows for potential bacterial growth. Inactivation systems use methods like adding a photoactive compound followed by ultraviolet (UV) light exposure. This damages the nucleic acids of contaminating organisms, preventing their replication.
Gamma Irradiation
Platelets may also undergo gamma irradiation to prevent transfusion-associated graft-versus-host disease (TA-GVHD). The irradiation inactivates the residual donor lymphocytes within the product. This ensures the lymphocytes cannot multiply and attack the recipient’s tissues. These preparation methods maximize the safety and efficacy of the platelet supply, mitigating risks associated with imperfect compatibility.