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RhD alloimmunization from platelet transfusions have been documented in the literature. However, non-RhD platelet alloimmunization is much less frequent and the risk for non-RhD alloimmunization from platelets is thought to be extremely low and most associated with buffy coat pooled platelets. A 22-month-old male with acute myeloid leukemia received 99 mL apheresis platelets for thrombocytopenia. Three months later, an antibody screen, the direct antiglobulin test (DAT), and red blood cell (RBC) genotype were sent for laboratory evaluation. The antibody screen was positive, with anti-E identified. The DAT was negative and the RBC genotype of the patient was predicted to be negative for the E antigen whereas the platelet donor was predicted to be positive for E antigen. There is a risk of alloimmunization of non-RhD antigen from platelet pheresis transfusion even in a patient less than 2 years old. [ABSTRACT FROM AUTHOR]

BACKGROUND AND OBJECTIVE: A number of glycophorin variant phenotypes or hybrid glycophorin variants of the MNS blood group system bear multiple immunogenic antigens such as Mia, Mur, and MUT. In the East and Southeast Asian populations, glycoprotein (GP.) Mur is the most common glycophorin variant phenotype expressing those three immunogens. The aim of this study was to detect MNS system glycophorin variant phenotypes (GP. Mur, GP. Hop, GP. Bun, GP. HF, and GP. Hut) among Malaysian blood donors. MATERIALS AND METHODS: In this cross-sectional study, 144 blood donors were selected under stratified random sampling. The deoxyribonucleic acid was extracted from whole blood samples, followed by a polymerase chain reaction assay. Sanger sequencing was used to identify the specific MNS variants and then validated by a serological crossmatch with known anti-Mur and anti-MUT. RESULTS: GP. Mur was identified among Malaysian blood donors with a prevalence of 6.94%, and no other variants of the MNS system were found. CONCLUSION: The present study substantiates that GP. Mur is the main variant of the MNS system glycophorin (B-A-B) hybrid in Malaysian blood donors. GP. Mur-negative red blood cells must therefore be considered in the current transfusion policy in order to prevent alloimmunization and immune-mediated transfusion reactions, particularly in transfusion-dependent patients. [ABSTRACT FROM AUTHOR]

Background and Objectives: The RHAG blood group system contains five antigens: Duclos (RHAG001), Ola (RHAG002), DSLK (RHAG003), Kg (RHAG005) and SHER (RHAG006). Individuals who are DSLK‐negative and Kg‐positive have the same allele RHAG*01.–3, with a single‐nucleotide variation (rs144305805), c.490A>C (p.Lys164Gln), in exon 3 of the RHAG gene. We aimed to confirm whether DSLK and Kg are antithetical antigens. Materials and Methods: Blood samples of the original DSLK‐negative proband with anti‐DSLK, her son and another DSLK‐negative individual were examined. The RHAG gene was analysed by polymerase chain reaction and Sanger sequencing. Immunocomplex capture fluorescence assays (ICFAs) and monocyte phagocytosis assays were performed to characterize the anti‐DSLK antibody. Cross‐testing of alloanti‐DSLK and monoclonal anti‐Kg (OSK46) was performed using transduced HEK293 cells by inducing the construct of expression vectors encoding wild‐type RHAG*01 or the variant RHAG*01.–3. Results: ICFA using monoclonal anti‐RHAG (LA18.18) revealed that the anti‐DSLK and anti‐Kg antibodies reacted with the wild‐type and variant RhAG (Rh‐associated glycoprotein), respectively. The proband and a DSLK‐negative individual appeared to be homozygous for variant RHAG*01.–3, and the proband's son was typed as RHAG*01/RHAG*01.–3 heterozygote. HEK293 cells with wild‐type RhAG reacted with the anti‐DSLK but not anti‐Kg antibody, whereas HEK293 cells expressing the variant RhAG reacted with the anti‐Kg but not anti‐DSLK antibody. Monocyte phagocytosis assays indicated that 64% of red cells sensitized with anti‐DSLK were phagocytosed by monocytes. Conclusion: Our results demonstrate that DSLK and Kg are antithetical antigens in the RHAG blood group system. Anti‐DSLK may be a clinically significant antibody. [ABSTRACT FROM AUTHOR]

Objective: To assess the clinicohaematological presentation and outcome of patients with antibodies to high frequency antigen (HFA) in our setup. Study Design: Cross sectional study. Place and Duration of Study: Armed Forces Institute of Transfusion, Rawalpindi, from Jan 2016 to Jan 2018. Methodology: We diagnosed 29 cases of uncommon red cell antibodies including antibodies to HFA, in a span of two years (2016-2018). Information regarding patient's age, diagnosis, transfusion history, incompatible cross match and history of pregnancy was obtained. Venous blood sample of 3ml was taken in EDTA for grouping, red cell phenotyping and Direct Anti-Globulin Test (DAT) and 5 ml venous blood was taken for Indirect Antiglobulin Test (IAT), antibody screening and identification. Tube method was used for forward and reverse blood grouping, DAT and IAT. Column Agglutination Technique (CAT) was used for antibody screening, identification and red cell phenotyping. Results: Out of a total of 29 cases, 24 (83%) were of anti H antibody (Bombay blood group). Rest of 5 (17%) included one each of anti Rh 17, anti Rh 29 (Rh null), anti P1Pk, anti-ENA/WRB and anti P antibodies. Anti H Lectin (Ulexeuropaeus) was used for confirmation of H antigen absence, while rest of antibodies were confirmed by IBGRL Bristol, UK. Conclusion: The sources of antigen negative blood are family members, rare donor registry, autologous donations and frozen blood banks. Finding compatible blood for patients with an antibody to HFA may be a challenge. [ABSTRACT FROM AUTHOR]

Background: Despite the significant adverse clinical consequences of RBC alloimmunization, our understanding of the signals that induce immune responses to transfused RBCs remains incomplete. Though RBC storage has been shown to enhance alloimmunization in the hen egg lysozyme, ovalbumin, and human Duffy (HOD) RBC alloantigen mouse model, the molecular signals leading to immune activation in this system remain unclear. Given that the nonclassical major histocompatibility complex (MHC) Class I molecule CD1D can bind to multiple different lysophospholipids and direct immune activation, we hypothesized that storage of RBCs increases lysophospholipids known to bind CD1D, and further that recipient CD1D recognition of these altered lipids mediates storage-induced alloimmunization responses.Study Design and Methods: We used a mass spectrometry-based approach to analyze the changes in lysophospholipids that are induced during storage of mouse RBCs. CD1D knockout (CD1D-KO) and wild-type (WT) control mice were transfused with stored HOD RBCs to measure the impact of CD1D deficiency on RBC alloimmunization.Results: RBC storage results in alterations in multiple lysophospholipid species known to bind to CD1D and activate the immune system. Prior to transfusion, CD1D-deficient mice had lower baseline levels of polyclonal immunoglobulin (IgG) relative to WT mice. In response to stored RBC transfusion, CD1D-deficient mice generated similar levels of anti-HOD IgM and anti-HOD IgG.Conclusion: Although storage of RBCs leads to alteration of several lysophospholipids known to be capable of binding CD1D, storage-induced RBC alloimmunization responses are not impacted by recipient CD1D deficiency. [ABSTRACT FROM AUTHOR]