3. Transfusion is the first form of transplantationDonor – recipient from the same species = Allogeneic transfusions Autologoustransfusions using the patient's own stored blood.
28. Alloantigens represents the blood groups major barriers for transfusion On RBCs - 30 major blood group systems and over 200 minor group systems ABO molecules are glyco-sphingolipids (major histocompatibility antigens) A and B = terminal sugars (A = N-Acetyl-Dgalactosamine; B = alpha-D-galactose) Availability of blood donors – major limitation ABO matching is also important in solid organ transplantation.
29. Pre-Transfusion compatibility testing Cross-matching = donor cells with recipient serum/ plasma determines the blood group (ABO compatibility) Alloantibodies New methods: PCR with specific probes (DNA typing) Serological Typing CDC- Method or Hemmaglutination
30. ABO Blood Types The A Blood Type contains aprox. 20 subgroups (A1 =80% , A2 = 20%) are the most common (over 99%).
31. 30 major blood group systems and over 200 minor group systems Lewis I P MNSs Kell Kidd Duffy The cell surface is a jungle!
32. HLA -A and B are important in platelet transfusion; HLA class I and II in neutrophil transfusion N > 2400
56. Platelets transfusion- more susceptible due to RT storage (Staphylococcus aureus, coagulase-negative staphylococci, diphtheroid bacilli, streptococci, and other skin flora)
68. in patients without alternate risk factors for acute lung injuryIn 2006, TRALI was the leading cause of transfusion-related death reported to the FDA Underrecognition and underreporting All plasma-containing blood and blood compartments may induce TRALI
72. The antibody –dependent hypothesis Anti-HLA or human neutrophil antigen (HNA) antibodies in the transfused component reacts with neutrophil antigens in the recipient (ie, when antileukocyte antibodies are transfused passively in a plasma-containing blood component) The recipient's neutrophils lodge in the pulmonary capillaries and release mediators that cause pulmonary capillary leakage. As a consequence, many patients with TRALI will develop transient leukopenia. TRALI- pulmonary edema with neutrophilic aggregates in the pulmonary vasculature Cherry et al, Am J ClinPathol 2008;129:287-297
73. The antibody –independent hypothesis Occurs in patients with clinical conditions that predispose to neutrophil priming and endothelial activation: infection, surgery, or inflammation. Bioactive substances (lipids) in the transfused component activate the primed, sequestered neutrophils and pulmonary endothelial damage occurs.
99. EXAMPLE Donor HLA-A1,-; B8,-; Cw7,-.(homozygosity) Recipient HLA A1, A2; B8, B27; Cw7, Cw9. No mismatched HLA in Host versus Graft Direction (A1, B8 and Cw7 are self HLA) A2, B27 and Cw9 mismatches in GVH direction.
100. Roles of CD4+ and CD8+ T cells in graft rejection CD8 cells Recognition of class I MHC molecules expressed on all donor tissue cells Direct cytotoxic effects Release of TNF+IFN augments macrophage activation and non-specific destruction CD4 cells Recognition of class II MHC molecules on passenger leukocytes (direct allorecognition) or infiltrating host DC (indirect allorecognition) Help the activation of CD8 T cells Release of TNF+IFN induces macrophage activation and non-specific destruction
101. Types of Allorecognition Direct – activation of recipient T cells by donor-derived professional APCs (dendritic cells) Indirect – activation of recipient T cells by recipient-derived professional APCs. The professional APCs that present the alloantigens also provide co-stimulatory signals that activate helper T cells and cytotoxic T cells.
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