title: The role of Rh antibodies in haemolytic disease of the newborn.
abstract: Recent insights into the structure-function relationship of IgG, the nature of Fc receptors and their interactions with antibodies, and the cellular mechanisms involved in the immune destruction of IgG-sensitized cells have all contributed to a fuller understanding of the role of Rh antibodies in HDN. As this understanding has increased, so different diagnostic and therapeutic approaches have been developed and evaluated in order either to predict or ameliorate disease severity. The role of Rh antibodies in HDN can be considered in three contexts: maternal anti-D, monoclonal anti-D and prophylactic anti-D. Anti-D formed after maternal alloimmunization may be transported across the placenta, resulting in destruction of sensitized red cells by mononuclear phagocytes in the fetus and infant. The use of monoclonal anti-D has given an insight into the cellular and molecular mechanisms involved in red cell destruction, and has facilitated the development and evaluation of assays which use maternal anti-D to predict the severity of HDN. Polyclonal anti-D, given prophylactically, can prevent maternal alloimmunization to D-positive fetal red cells. Future developments are likely in several areas. Prophylactic polyclonal anti-D may be replaced, wholly or partially, with monoclonal anti-D. The development and introduction of cellular assays as non-invasive tests for predicting disease severity is likely to continue as preliminary results are encouraging. Finally, new strategies for ameliorating disease severity may be assessed including the role of ivIgG and Fc gamma R-blocking antibodies.
authors.affiliation: International Blood Group Reference Laboratory, Bristol, UK.
authors.forename: A G
authors.initials: AG
authors.lastname: Hadley
authors.forename: B M
authors.initials: BM
authors.lastname: Kumpel
mesh_terms: D000017:ABO Blood-Group System / Q000276:immunology; D001803:Blood Transfusion; D004899:Erythroblastosis, Fetal / Q000453:epidemiology / Q000235:genetics* / Q000517:prevention & control; D005260:Female; D006801:Humans; D007112:Immunity, Maternally-Acquired; D007116:Immunization, Passive; D007074:Immunoglobulin G / Q000276:immunology; D007075:Immunoglobulin M / Q000276:immunology; D016756:Immunoglobulins, Intravenous; D007231:Infant, Newborn; D008431:Maternal-Fetal Exchange; D009000:Monocytes / Q000502:physiology; D010587:Phagocytosis; D010956:Plasmapheresis; D011247:Pregnancy; D011248:Pregnancy Complications / Q000276:immunology / Q000628:therapy; D011446:Prospective Studies; D011961:Receptors, Fc / Q000276:immunology; D012203:Rh Isoimmunization / Q000276:immunology* / Q000628:therapy; D012204:Rh-Hr Blood-Group System / Q000737:chemistry / Q000235:genetics / Q000276:immunology*; D018029:Rho(D) Immune Globulin / Q000097:blood / Q000276:immunology
chemical_list: D000017:ABO Blood-Group System; D007074:Immunoglobulin G; D007075:Immunoglobulin M; D016756:Immunoglobulins, Intravenous; D011961:Receptors, Fc; D012204:Rh-Hr Blood-Group System; D018029:Rho(D) Immune Globulin