| 41. |
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| 42. |
- Halverson, Gregory R, et al.
(författare)
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Murine monoclonal anti-s and other anti-glycophorin B antibodies resulting from immunizations with a GPB.s peptide.
- 2009
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Ingår i: Transfusion. - : Wiley. - 1537-2995 .- 0041-1132. ; 49, s. 485-494
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: The blood group antigens S and s are defined by amino acids Met or Thr at position 29, respectively, on glycophorin B (GPB). Commercial anti-s reagents are expensive to produce because of the scarcity of human anti-s serum. Our aim was to develop hybridoma cell lines that secrete reagent-grade anti-s monoclonal antibodies (MoAbs) to supplement the supply of human anti-s reagents. STUDY DESIGN AND METHODS: Mice were immunized with the GPB(s) peptide sequence TKSTISSQTNGETGQLVHRF. Hybridomas were produced by fusing mouse splenocytes with mouse myeloma cells (X63.Ag8.653). Screening for antibody production was done on microtiter plates by hemagglutination. Characterization of the MoAbs was done by hemagglutination, immunoblotting, and epitope mapping. RESULTS: Eight immunoglobulin G MoAbs were identified. Five antibodies are specific by hemagglutination for s and two MoAbs, when diluted, are anti-S-like, but additional analyses shows a broad range of reactivity for GPB. Typing red blood cells (RBCs) for s from 35 donors was concordant with molecular analyses as were tests on RBCs with a positive direct antiglobulin test (DAT) from 15 patients. The anti-s MoAbs are most reactive with peptides containing the (31)QLVHRF(36) motif, with (29)Thr. By Pepscan analyses, the anti-S-like MoAbs reacted within the same regions as did anti-s, but independently of (29)Met. One antibody was defined serologically as anti-U; however, its epitope was identified as (21)ISSQT(25), a sequence common for both GPA and GPB. CONCLUSION: In addition to their value as typing reagents, these MoAbs can be used to phenotype RBCs with a positive DAT without pre-test chemical modification.
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| 43. |
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| 44. |
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| 45. |
- Hellberg, Åsa, et al.
(författare)
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A novel RHCE*02 allele, containing the single-nucleotide change c.460A>G, encodes weakened expression of C and e antigens
- 2016
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Ingår i: Transfusion. - : Wiley. - 0041-1132 .- 1537-2995. ; 56:9, s. 2391-2392
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Tidskriftsartikel (refereegranskat)abstract
- We report a novel RHCE*02 allele in a Swedish blood donor that is characterized by the change c.460A>G (Arg154Gly). The blood donor's red blood cells showed variable reactivity with different monoclonal anti-C and anti-e and antigen strength was markedly weakened. We believe that these changes represent both a quantitative and qualitative alteration of the antigens encoded by this allele.
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| 46. |
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| 47. |
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| 48. |
- Hellberg, Åsa, et al.
(författare)
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Expression of a novel missense mutation found in the A4GALT gene of Amish individuals with the p phenotype.
- 2008
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Ingår i: Transfusion. - : Wiley. - 1537-2995 .- 0041-1132. ; 48:3, s. 479-487
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: The rare p phenotype is found at a higher frequency in Amish people than in other populations. Different mutations in the 4-alpha-galactosyltransferase gene (A4GALT), responsible for synthesis of P(k) (Gb(3)) antigen, have been found to cause the P(k)-deficient p phenotype. The aim of this study was to explore the molecular background of the p phenotype in people of Amish origin. STUDY DESIGN AND METHODS: Twenty blood samples with the p phenotype, 19 of them from Amish individuals and 1 Pakistani, were investigated. Amplification of genomic DNA by polymerase chain reaction (PCR) and sequencing by capillary electrophoresis were performed. Blood donors of different geographic origin were screened with PCR-allele-specific primer to investigate whether the novel mutation occurs among individuals with common phenotypes. The mutation was also cloned into an expression vector and transfected to Namalwa cells, which do not normally express P(k). P(k) expression on the transfected cells and P/P(k) on red blood cells (RBCs), both with p and with common phenotypes, were analyzed by flow cytometry. RESULTS: All 20 samples were homozygous for 299C>T changing serine to leucine in a region that is highly conserved in homologous genes across species borders. The mutation was not found in any of the 500 alleles of blood donors investigated. P(k) expression was neither observed by serology and flow cytometry on p RBCs from Amish individuals nor following transfection of cells with constructs containing the novel missense mutation. CONCLUSION: A novel A4GALT missense mutation causes the p phenotype in Amish individuals.
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| 49. |
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| 50. |
- Holmqvist, Jacob, et al.
(författare)
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No evidence of transfusion transmitted sporadic Creutzfeldt-Jakob disease: results from a bi-national cohort study
- 2020
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Ingår i: Transfusion. - : Wiley. - 0041-1132 .- 1537-2995. ; 60:4, s. 694-697
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND Creutzfeldt-Jakob disease (CJD) is an uncommon, invariably fatal, neurodegenerative disorder that presents as progressive dementia with concurrent motor symptoms and myoclonia. The pathophysiology involves prion protein misfolding and spreading in a self-catalyzed manner. It has been shown to be transmissible through tissue transplants. Variant CJD (vCJD), a subtype of the disease is also transmissible through transfusion of blood products. This study aims to corroborate the scarce data that suggest that sporadic CJD (sCJD) is not transmitted via blood transfusion. METHODS AND STUDY DESIGN A retrospective cohort study was performed, using data from the bi-national Scandinavian Donations and Transfusions (SCANDAT2) database containing data on blood donors, donations, transfusions, and transfused patients in Sweden and Denmark since 1968 and 1982, respectively. Mortality and medical data were collected from nationwide health care and population registries. Donors with subsequent CJD were identified, as well as recipients of blood products from these donors. A second analysis was performed, screening for clustering of CJD cases from donors without a CJD diagnosis. RESULTS We identified 39 donors with a subsequent diagnosis of sCJD. No cases of CJD occurred among the 883 recipients of blood products from these donors. A total of 89 CJD cases were identified among recipients of transfusions. No clustering of cases from the same donor occurred. DISCUSSION Using data from a large, bi-national database of transfused patients, we find no evidence of sCJD transmission. Our data adds to the growing body of evidence indicating that sCJD is not transfusion transmitted.
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