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Complement as an Immune Barrier in Platelet Transfusion Refractoriness
Stephan Meinke1, Cecilia Karlström2, Petter Höglund3
1Center for Hematology and Regenerative Medicine (HERM), Department of Medicine Huddinge, Karolinska Institutet, Sweden.
Patients with hematological cancers often have low platelet counts because of progressing bone marrow failure or cytostatic therapy. A large fraction of those patients need platelet transfusions, which can be life-saving if bleedings occur and also allow diagnostic and therapeutic interventions. The outcomes of platelet transfusions are not always easy to predict in terms of bleeding control or increase in platelet count. Reasons could be disease-specific factors, fever, or infections leading to platelet consumption, but the immune system may also be involved, in particular, in patients previously immunized against foreign human leukocyte antigens (HLA). Mechanisms underlying immune-mediated platelet destruction in the presence of antibodies again HLA are not well understood in clinical situations. This review discusses the role of complement in platelet refractoriness, with a focus on HLA antibody-mediated platelet refractoriness. We summarize recent work in this area, discuss complement-platelet interactions in general terms, and a suggest a possible role of complement in platelet transfusion in general.
Patients with hematological cancers often have low platelet counts because of progressing bone marrow failure or cytostatic therapy. A large fraction of those patients need platelet transfusions, which can be life-saving if bleedings occur and also allow diagnostic and therapeutic interventions. The outcomes of platelet transfusions are not always easy to predict in terms of bleeding control or increase in platelet count. Reasons could be disease-specific factors, fever, or infections leading to platelet consumption, but the immune system may also be involved, in particular, in patients previously immunized against foreign human leukocyte antigens (HLA). Mechanisms underlying immune-mediated platelet destruction in the presence of antibodies again HLA are not well understood in clinical situations. This review discusses the role of complement in platelet refractoriness, with a focus on HLA antibody-mediated platelet refractoriness. We summarize recent work in this area, discuss complement-platelet interactions in general terms, and a suggest a possible role of complement in platelet transfusion in general.
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