Immunologic Consequences of Blood Transfusion and Their Clinical Manifestations

Abstract

Aspects of clinical immunology, in the context of transfusion medicine, became highlighted in the last decade as a consequence of the accelerating expansion of basic immunology, immunogenetics and molecular biology. In addition sophisticated new technologies, which were capable of producing pure and safe blood products, attracted more attention to research and monitor the consequences of transfusion. These technologies also had obvious effects on supportive hematological therapy. The transfusion of blood components follows the rules of organ transplantation: when there is a mismatch between the donor and the recipient, the transfusion has the potential to induce various kinds of immune response against alloantigens. Antigen-compatible transfusions that involve major and rare blood groups are in almost all cases mismatched with respect to various polymorphic systems expressed on the cellular blood components. These include histocompatibility leukocyte antigens (HLA), tissue-specific and differentiation alloantigens, and, in the case of plasma, immunoglobulins, complement components, heat shock proteins, and shedded soluble membrane alloantigens. Clinical manifestations of alloimmune responses are typically deleterious. For example, immediate antigen-antibody binding and its consequences as secondary activations are paralleled by the nonhaemolytic febrile reaction, HLA sensitization can lead to a state of platelet refractoriness and inconvenient clinical symptoms. In certain immunogenetic situations and in immunodeficient patients graft-versus-host disease can be induced by blood products that contain live lymphocytes. Leukocyte filtration techniques are widely used to avoid most but not all of these harmful side effects of blood component therapy. In contrast to these harmful side effects in certain immunogenetic conditions, alloantigens that are expressed on various blood products can elicit an advantageous suppression of the immune response in the recipient. In the context of kidney transplantation this is termed the ‘beneficial transfusion effect’, and typically results in the prolongation of the graft’s survival. In cases of recurrent habitual abortion and IgG therapy associated with certain autoimmune diseases, immunization with leukocytes specifically takes advantage of this phenomenon. To date the beneficial transfusion effect is not fully understood. In certain cases of malignancies or gastrointestinal surgeries this suppression of immune regulation that is induced by transfusion can worsen the clinical state either by permitting the spread of the tumor or by allowing severe infections to proceed unchecked. In conclusion it is imperative to monitor the immunological consequences of transfusion in order to deter the disadvantageous side effects. Taking advantage of the ‘beneficial transfusion effect’ may also provide a new means for immune therapy using the various blood products.

Ventricular assist device-associated anti-human leukocyte antigen antibody sensitization in pediatric patients bridged to heart transplantation

“…4,5,7,10,18 A wide range of sensitization has been reported, with 17% to 66% of patients showing evidence of PRA Ն 10%. Factors that have been implicated include multiple blood product exposures in patients requiring mechanical support, 6,19 prior sternotomy, 20 and the immune-activating properties of the VAD circuit material. 21 VAD use was associated with new-onset sensitization in 35% of VAD recipients in our series, a value consistent with prior reports.…”

The sensitized pediatric heart transplant candidate: Causes, consequences, and treatment options

“…*p < 0.01 compared with control patients and compared with allograft patients before surgery. Reprinted with permission (8).…”

Recent advances in laboratory assays for nonhemolytic transfusion reactions

“…Thus, the precise mechanisms for the high incidence of NHTRs in PC transfusion remain largely unknown. Finally, febrile reactions are often associated with the HLA Class I Ab in patients 41,42 . However, the association of HLA Class I Abs in patients to other NHTRs has not been established.…”