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The article presents questions and answers related to the prevention of transfusion related acute lung injury (TRALI). One question on the transfusion of blood from a donor suffering from TRALI to a another patient and another question on the policies adopted by physicians when such antibodies are detected in the donors or patient's serum are presented.

Subsets of human lymphocytes were isolated from peripheral blood using magnetic beads coated with anti-CD4, -CD8 -CD19 or -CD56 antibodies to yield T4, T8. B and natural killer (NK) cell suspensions with greater than 95% purity. The functional activity of Fcγ receptor II (FcγRII) and Fcγ receptor III (FcγRIII) on these subsets was assessed by measuring rosette formation with red cells sensitized with known levels of either rabbit IgG or human (monoclonal or polyclonal) IgG1 anti-D, IgG3 anti-D or IgG3 anti-c (E-IgG). Lysis of red cells by K cells (mediated by FcγRIII) in antibody- dependent cell-mediated cytotoxicity (ADCC) assays was promoted by polyclonal and some monoclonal antibodies. Using these `ADCC+' antibodies, minimum red cell sensitization levels required to promote rosette formation with NK cells were 2000 IgG1 or IgG3 molecules/red cell compared to 15,000 IgG1 or 4000 IgG3 molecules/red cell with `ADCC-' monoclonal antibodies. The greater efficiency of ADCC+ antibodies is consistent with their previously reported ability to bind FcγRIII via CH2 and CH3 domains whereas ADCC antibodies bind only via CH3 domains. B cells formed rosettes only at high levels of sensitization: approximately 60,000 IgG1 or 20,000 IgG3 anti-D molecules/cell. These data reflect the low affinity of FcγRII for monomeric human IgG. Although over 90% of NK cells bound anti-CD16, and 70% formed rosettes with red cells sensitized with rabbit IgG (30,000 molecules/cell), only 25% of NK cells formed rosettes with E-IgG3 at 100,000 IgG molecules/cell. Approximately 35% of B cells, 10% of 18 cells but no T4 cells formed rosettes with E-IgG (100,000 IgG3 molecules/cell). With T8, B and NK cells, IgG3 anti-D promoted greater rosette formation than IgG1 anti-D at comparable levels of sensitization. Presumably the longer hinge region of IgG3 enabled it to bridge the gap between negatively charged lymphocytes and red cells more efficiently than IgG1. [ABSTRACT FROM AUTHOR]

Investigates the frequency of the human platelet antigens (HPA1-5) in the Polish population using polymerase chain reaction (PCR) with sequence primers. Differences of HPA2 and HPA5 observed in other European populations; Description of the HPA5 alleles frequency similarities observed in the Finnish population.

The Colton (Coa) antigen is of high frequency; its incidence in Caucasians is about 99.8%. Reports on haemolytic transfusion reactions and haemolytic disease of the foetus/newborn (HDFN) due to anti-Coa are rare. We report a severe HDFN due to anti-Coa. The first child of the mother was healthy. The second died a few hours after delivery because of hydrops fetalis, likely due to HDFN; anti-Coa in the maternal serum, the father typed as Co(a+). The third pregnancy was followed up by the measurements of anti-Coa titre (additional antibodies were excluded), its functional activity by the chemiluminescence test (CLT) and the Doppler flow in the middle cerebral artery of the foetus. Increased values of antibody titre up to 128, the CLT to 30% and multiplex of median of the peak systolic velocity to 1·71 indicated haemolytic disease and the necessity for an intrauterine transfusion. The foetus received the maternal red blood cells (RBCs). Delivery had to be by Caesarean section for obstetrical reasons at 34-week gestation. The newborn (anti-Coa on red cells and in plasma, the rise of the bilirubin concentration up to 333 μmol L−1) had four exchange transfusions: the first of maternal RBCs, the remaining of donor’s Co(a+) cells and one top-up transfusion. The baby was discharged in good health. Anti-Coa was responsible for severe HDFN. Proper monitoring during pregnancy and antenatal and post-natal therapy were successful. This is the second severe published HDFN due to anti-Coa. [ABSTRACT FROM AUTHOR]

Presents a case study of isoimmune neonatal neutropenia (NAIN) due to anti-Fe [sub gamma] RIIIb antibody. Effect of maternal neutrophil-specific antibodies on NAIN; Detection of pancreatic granulocyte alloantibodies in maternal serum; Increase in the neutrophil count through intravenous immunoglobulin.