Prevention of platelet alloimmunization

Based on transfusion studies in patients and animal model systems, there are currently only two established methods of at least delaying platelet alloimmunization. These involve the administration of leukocyte-poor platelets and red cells or reducing a recipient's exposure to incompatible donor antigens by using single-donor pheresis products. The application of these approaches is limited by practical considerations of achieving sufficiently leukocyte-poor blood products to produce the desired effect, and by the availability and costs of pheresis products compared to pooled random donor platelet concentrates. Furthermore, in chronically transfused aplastic patients who are not receiving concurrent immunosuppressive chemotherapy, there is reason to believe that these transfusion programs may be less effective then in leukemic patients. Fortunately, newer insights into the pathways of antigen recognition have suggested other possible ways to prevent recipient recognition of transfused or transplanted donor tissues. Cyclosporin A specifically inhibits T cells that are central to immune recognition of foreign antigens, and thereby is a very effective immunosuppressive agent. Furthermore, a major pathway of immune recognition may involve direct stimulation of the recipient's T cells by APC in donor tissue; methods to eliminate these cells by physical removal, treatment with anti-Ia antisera, or inactivation with U-V light may represent major advances in preventing alloimmunization. In addition, there is evidence that HLA and B antigens may not be intrinsic to the platelet membrane, suggesting it may be possible to remove them before transfusion, thereby eliminating a major source of incompatability. Finally, as platelets do not express Class II MHC antigens on their surface, "pure" platelet transfusions may be not only non-immunogenic, but may actually induce tolerance to subsequent transfusions or transplants.