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- Alattar, Abdul Ghani, et al.
(författare)
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Evidence that CD36 is expressed on red blood cells and constitutes a novel blood group system of clinical importance
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Ingår i: Vox Sanguinis. - 1423-0410. ; , s. 1-9
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND AND OBJECTIVES: Polymorphic molecules expressed on the surface of certain blood cells are traditionally categorized as blood groups and human platelet or neutrophil antigens. CD36 is widely considered a platelet antigen (Nak a ) and anti-CD36 can cause foetal/neonatal alloimmune thrombocytopenia (FNAIT) in CD36-negative pregnant women. CD36 is used as a marker of differentiation in early erythroid culture. During the experimental culture of CD34+ cells from random blood donors, we observed that one individual lacked CD36. We sought to investigate this observation further and determine if CD36 fulfils the International Society of Blood Transfusion criteria for becoming a blood group. MATERIALS AND METHODS: Surface markers were monitored by flow cytometry on developing cells during the erythroid culture of CD34+ cells. Genetic and flow cytometric analyses on peripheral blood cells were performed. Proteomic datasets were analysed, and clinical case reports involving anti-CD36 and foetal anaemia were scrutinized.RESULTS: Sequencing of CD36-cDNA identified homozygosity for c.1133G>T/p.Gly378Val in the CD36-negative donor. The minor allele frequency of rs146027667:T is 0.1% globally and results in abolished CD36 expression. CD36 has been considered absent from mature red blood cells (RBCs); however, we detected CD36 expression on RBCs and reticulocytes from 20 blood donors. By mining reticulocyte and RBC datasets, we found evidence for CD36-derived peptides enriched in the membrane fractions. Finally, our literature review revealed severe cases of foetal anaemia attributed to anti-CD36.CONCLUSIONS: Based on these findings, we conclude that CD36 fulfils the criteria for becoming a new blood group system and that anti-CD36 is implicated not only in FNAIT but also foetal anaemia.
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- Araujo, F, et al.
(författare)
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Weak D type 2 is the most prevalent weak D type in Portugal
- 2006
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Ingår i: Transfusion Medicine. - : Wiley. - 0958-7578 .- 1365-3148. ; 16:1, s. 63-67
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Tidskriftsartikel (refereegranskat)abstract
- The weak D phenotype is the most common D variant, with a frequency of 0.2-1% in Caucasian individuals. There are several weak D types, with different frequencies in European countries, which may pose serologic problems and have the potential for alloimmunization. Samples from Portuguese individuals were tested for RhD by two or three distinct monoclonal and oligoclonal antisera, in direct agglutination tests. When discrepant results were observed, samples were tested with panels of monoclonal anti-D by LISS-indirect antigobulin test. Cases that reacted weakly with IgM but positive with IgG anti-D were analysed by PCR-sequence-specific primers and real-time PCR. Ninety-nine samples were referred after being characterized as weak D. This genotype was recognized, with a preponderance of weak D type 2 (63.6%) over type 1 (16.2%) and 3 (14.1%). The high incidence of weak D type 2 in our population is in marked contrast to studies performed in other European populations and might be due to our sample selection criteria or ethnic variation. There are advantages in genotyping serologically depressed D samples to avoid the waste of D-negative RBC units and the use of immunoglobulin in pregnant women, who have no risk of alloimmunization.
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- Arvidsson, Ida, et al.
(författare)
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Shiga toxin-induced complement-mediated hemolysis and release of complement-coated red blood cell-derived microvesicles in hemolytic uremic syndrome.
- 2015
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Ingår i: Journal of Immunology. - : The American Association of Immunologists. - 1550-6606 .- 0022-1767. ; 194:5, s. 2309-2318
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Tidskriftsartikel (refereegranskat)abstract
- Shiga toxin (Stx)-producing Escherichia coli (STEC) cause hemolytic uremic syndrome (HUS). This study investigated whether Stx2 induces hemolysis and whether complement is involved in the hemolytic process. RBCs and/or RBC-derived microvesicles from patients with STEC-HUS (n = 25) were investigated for the presence of C3 and C9 by flow cytometry. Patients exhibited increased C3 deposition on RBCs compared with controls (p < 0.001), as well as high levels of C3- and C9-bearing RBC-derived microvesicles during the acute phase, which decreased after recovery. Stx2 bound to P1 (k) and P2 (k) phenotype RBCs, expressing high levels of the P(k) Ag (globotriaosylceramide), the known Stx receptor. Stx2 induced the release of hemoglobin and lactate dehydrogenase in whole blood, indicating hemolysis. Stx2-induced hemolysis was not demonstrated in the absence of plasma and was inhibited by heat inactivation, as well as by the terminal complement pathway Ab eculizumab, the purinergic P2 receptor antagonist suramin, and EDTA. In the presence of whole blood or plasma/serum, Stx2 induced the release of RBC-derived microvesicles coated with C5b-9, a process that was inhibited by EDTA, in the absence of factor B, and by purinergic P2 receptor antagonists. Thus, complement-coated RBC-derived microvesicles are elevated in HUS patients and induced in vitro by incubation of RBCs with Stx2, which also induced hemolysis. The role of complement in Stx2-mediated hemolysis was demonstrated by its occurrence only in the presence of plasma and its abrogation by heat inactivation, EDTA, and eculizumab. Complement activation on RBCs could play a role in the hemolytic process occurring during STEC-HUS.
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| 7. |
- Avent, Neil D., et al.
(författare)
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The Bloodgen Project of the European Union, 2003-2009
- 2009
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Ingår i: Transfusion Medicine and Hemotherapy. - : S. Karger AG. - 1660-3818 .- 1660-3796. ; 36:3, s. 162-167
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Forskningsöversikt (refereegranskat)abstract
- The Bloodgen project was funded by the European Commission between 2003 and 2006, and involved academic blood centres, universities, and Progenika Biopharma S. A., a commercial supplier of genotyping platforms that incorporate glass arrays. The project has led to the development of a commercially available product, BLOODchip, that can be used to comprehensively genotype an individual for all clinically significant blood groups. The intention of making this system available is that blood services and perhaps even hospital blood banks would be able to obtain extended information concerning the blood group of routine blood donors and vulnerable patient groups. This may be of significant use in the current management of multi-transfused patients who become alloimmunised due to incomplete matching of blood groups. In the future it can be envisaged that better matching of donor-patient blood could be achieved by comprehensive genotyping of every blood donor, especially regular ones. This situation could even be extended to genotyping every individual at birth, which may prove to have significant long-term health economic benefits as it may be coupled with detection of inborn errors of metabolism.
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- Brumit, M C, et al.
(författare)
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Moderate hemolytic disease of the newborn (HDN) due to anti-Rh17 produced by a black female with an e variant phenotype
- 2002
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Ingår i: Immunohematology. - 0894-203X. ; 18:2, s. 40-42
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Tidskriftsartikel (refereegranskat)abstract
- The Rh blood group antigen e is of high incidence and has many epitopes. Partial expression may occur, more commonly in black persons. Individuals with e variant phenotypes can make antibodies to epitopes they lack. While some of these antibodies may be specific for an antigen, e.g., hrB, others, like anti-Rh17 (anti-Hro), show broader specificity, compatible only with D-- and Rhnull red blood cells (RBCs). Anti-Rh17 in persons of the D-- phenotype has been reported to cause mild to fatal HDN. We report an example of anti-Rh17 produced by a black female with an e variant RBC phenotype that caused moderate HDN. A panel of seven monoclonal anti-e demonstrated her RBCs carried a variant e antigen, and her genotype was RHD, RHce by PCR-RFLP analysis. Amniotic fluid with.OD450 values from 30 to 35 weeks' gestation predicted moderate HDN probability by the Liley method. At 38+ weeks, a viable 3165 g female infant was delivered. The infant's direct antiglobulin test was 2+ with anti-IgG. Total bilirubin rose to 14.2 mg/dL within 48 hours. Indirect bilirubin peaked at 14.7 mg/dL. The bilirubin responded to triple phototherapy. The infant was discharged on day 6. Potential for infant morbidity due to anti-Rh17- mediated HDN and the importance of specifying risks to women with this antibody if they contemplate pregnancy are discussed.
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