By Andrew Hadley, Peter Soothill
The powerful prevention, analysis, and administration of alloimmune cytopenias has turn into a staff attempt regarding hematologists, obstetricians, pediatricians, immunologists, laboratory technicians, midwives, and learn scientists. This publication has been written via specialists of their respective fields to assemble the problems of pathogenesis, epidemiology, prevention, prognosis, and medical administration. This accomplished yet obtainable account is greatly cross-referenced to stress the hyperlinks among pathogenesis and medical sequels, among epidemiology and the reason for screening courses, and among prognosis and healing intervention.
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Additional info for Alloimmune Disorders of Pregnancy: Anaemia, Thrombocytopenia and Neutropenia in the Fetus and Newborn
Most blood group polymorphisms are the result of one or more nucleotide changes encoding amino acid substitutions in an extracellular domain of a red cell surface protein. In null phenotypes, the whole protein is absent from the membrane, usually as a result of a gene deletion or an inactivating mutation. When immunized, women with null phenotypes may make antibodies to a variety of epitopes on the blood group protein and these antibodies often have the ability to cause HDFN. Carbohydrate antigens, such as those of the ABO system, provide a further complexity to the genetics of red cell surface antigens.
40 Ghetie V & Ward ES (1997). FcRn, the MHC class I-related receptor that is more than an IgG transporter. Immunology Today, 18, 592–8. 41 Kim J-K, Firan M, Radu CG, Kim C-H, Ghetie V & Ward ES (1999). Mapping the site on human IgG for binding of the MHC class I-related receptor, FcRn. European Journal of Immunology, 29, 2819–25 42 Jeﬀeris R, Lund J & Pound JD (1998). IgG-Fc-mediated eﬀector functions, molecular deﬁnition of interaction sites for eﬀector ligands and the role of glycosylation. Immunological Reviews, 163, 59–76.
The maturational speciﬁcity of blood group antigens may also aﬀect the pathogenesis of HDFN. 60,61 The second criterion is antigen density. Some antigens (for example, Rh antigens) are well expressed early in embryonic development. Other antigens (for example, Lutheran antigens) are poorly expressed on fetal cells. 62 A third criterion may be antigen structure. 64 However, the implications of these in vitro observations for the pathogenesis of HDFN remain to be elucidated. 5 Antigen density There is evidence that the density of blood group antigens on fetal red cells may aﬀect the severity of haemolysis.
Alloimmune Disorders of Pregnancy: Anaemia, Thrombocytopenia and Neutropenia in the Fetus and Newborn by Andrew Hadley, Peter Soothill