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Daniels G.,International Blood Group Reference Laboratory | Daniels G.,Bristol Institute for Transfusion science
Human Blood Groups: 3rd edition | Year: 2013

Human Blood Groups is a comprehensive and fully referenced text covering both the scientific and clinical aspects of red cell surface antigens, including: serology, inheritance, biochemistry, molecular genetics, biological functions and clinical significance in transfusion medicine. Since the last edition, seven new blood group systems and over 60 new blood group antigens have been identified. All of the genes representing those systems have now been cloned and sequenced. This essential new information has made the launch of a third edition of Human Blood Groups, now in four colour, particularly timely. This book continues to be an essential reference source for all those who require clinical information on blood groups and antibodies in transfusion medicine and blood banking. © 2013 Geoff Daniels.

Anstee D.J.,Bristol Institute for Transfusion science
Vox Sanguinis | Year: 2011

Antigens of 23 of the 30 human blood group systems are defined by the amino acid sequence of red cell membrane proteins. The antigens of DI, RH, RHAG, MNS, GE and CO systems are carried on blood group-active proteins (Band 3, D and CE polypeptides, RhAG, Glycophorins A and B, Glycophorins C and D and Aquaporin 1, respectively) which are expressed at high levels (>-200-000 copies/red cell). These major proteins contribute to essential red cell functions either directly as membrane transporters and by providing linkage to the underlying red cell skeleton or by facilitating the membrane assembly of the protein complexes involved in these processes. The proteins expressing antigens of the remaining 17 blood group systems are much less abundant (<-20-000 copies/red cell) and their functional importance for the circulating red cell is largely unknown. Human gene knock-outs (null phenotypes) have been described for many of these minor blood group-active proteins, but only absence of Kx glycoprotein has been clearly linked with pathology directly related to the function of circulating red cells. Recent evidence suggesting the normal quality control system for glycoprotein synthesis is altered during the latter stages of red cell production raises the possibility that many of these low abundance blood group-active proteins are vestigial. In sickle cell disease and polycythaemia vera, elevated Lutheran glycoprotein expression may contribute to pathology. Dyserythropoiesis with reduced antigen expression can result from mutations in the erythroid transcription factors GATA-1 and EKLF. © 2010 The Author(s). Vox Sanguinis © 2010 International Society of Blood Transfusion.

Kumpel B.M.,Bristol Institute for Transfusion science | Manoussaka M.S.,St Georges, University of London
Vox Sanguinis | Year: 2012

During pregnancy, women are tolerant of their semi-allogeneic fetus whilst not being immunosuppressed and indeed readily form alloantibodies. This 'Immunological Paradox of Pregnancy' may be explained by an understanding of placental anatomy and immunology. Trophoblast cells form the interface between the fetus and maternal tissues and blood and escape allorecognition because they lack classical human leucocyte antigen (HLA) class I and II molecules. Local immunoregulation, or tolerance, in the decidua is mediated partly by HLA-G+ extravillous trophoblasts (EVT) that invade the tissue and prevent killing by maternal natural killer cells, cytotoxic T cells and macrophages. Placental hormones orchestrate the composition and regulatory function of maternal immune cells. In contrast, syncytiotrophoblast cells at the surface of chorionic villi, in contact with maternal blood, maintain a state of mild maternal systemic immunity via activation of innate immunity and skewing towards humoral immunity. This enables maintenance of a healthy immune system in pregnant women and robust protective antibody responses to pathogens whilst enabling survival of the fetus. However, this has the unfortunate consequence that pregnant women readily form alloantibodies to incompatible alloantigens on fetal red cells, platelets and leucocytes if fetomaternal haemorrhage (FMH) occurs. The antibodies are initially low affinity but after re-immunization with further FMH become functionally effective, high-titre IgG. © 2011 The Author(s). Vox Sanguinis © 2011 International Society of Blood Transfusion.

Daniels G.,Bristol Institute for Transfusion science | van der Schoot C.E.,Sanquin Research at CLB | Olsson M.L.,Lund University
Vox Sanguinis | Year: 2011

The fourth International Society of Blood Transfusion (ISBT) workshop on molecular blood group genotyping was held in 2010, with a feedback meeting at the ISBT Congress in Berlin, Germany. Fifty laboratories participated, 17 more than in 2008. Six samples were distributed. Samples 1-3 were DNA samples for all red cell blood group tests available to the participants. Of the 46 laboratories that tested these samples, 37 obtained completely correct results, although the extent of testing varied considerably. Sample 4, also a DNA sample, was an Rh problem in which RHDΨ and RHCE*ceCF were present, but the participants were only informed that the donor's red cells typed as positive with some monoclonal anti-D. Of the 42 laboratories that participated in this exercise, seven performed the sequencing necessary to obtain the correct result. Samples 5 and 6 were plasma samples from RhD-negative pregnant women, for foetal RhD testing. These were sent to 25 laboratories, and two incorrect results were reported. Overall, the level of accuracy was about equal to that of the previous workshop. The main conclusion for the last two workshops can be reiterated: with greater care and attention to detail, very high standards could be set for molecular blood group genotyping. © 2011 The Author(s). Vox Sanguinis © 2011 International Society of Blood Transfusion.

Anstee D.J.,Bristol Institute for Transfusion science
Blood | Year: 2010

The relative contribution of founder effects and natural selection to the observed distribution of human blood groups has been debated since blood group frequencies were shown to differ between populations almost a century ago. Advances in our understanding of the migration patterns of early humans from Africa to populate the rest of the world obtained through the use of Y chromosome and mtDNA markers do much to inform this debate. There are clear examples of protection against infectious diseases from inheritance of polymorphisms in genes encoding and regulating the expression of ABH and Lewis antigens in bodily secretions particularly in respect of Helicobacter pylori, norovirus, and cholera infections. However, available evidence suggests surviving malaria is the most significant selective force affecting the expression of blood groups. Red cells lacking or having altered forms of blood group-active molecules are commonly found in regions of the world in which malaria is endemic, notably the Fy(a-b-) phenotype and the S-s- phenotype in Africa and the Ge- and SAO phenotypes in South East Asia. Founder effects provide a more convincing explanation for the distribution of the D- phenotype and the occurrence of hemolytic disease of the fetus and newborn in Europe and Central Asia.© 2010 by The American Society of Hematology.

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