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17.Rhesus Blood Groups. RhD-incompatibility between mother andchild

Rhesus Blood Groups

·Genetically determined by 6 important antigens (among 50 Ags): c-C, d-D, e-E

·Presence of antigen D (strong Ag) on erythrocyte Membrane determines positivity (Rh+) – 85 % of European Population

oGenotype: CDE, CDe, cDe, cDE

·Rh negativity (Rh-) by d antigen (weak Ag)

oGenotype: Cde, Cde, cde, cdE

·Sometimes presence of E shows a weak positivity

·Antibodies in Rh system "normally notpresent

oHowever: D Is a strong antigen which can induce the production of antibodies in Rh- Persons

Biochemical structure & Inheritance:

·Proteins which carry the Rh antigens are transmembrane proteins (seem to be ion Channels)

·Main antigens are encoded by two adjacent gene loci:

oRHD Gene: expresses D-Ag on chromosome 1 (p36-p34) with various Alleles; (lack of gene " Rh negativity Rh-) ; RHD-polymorphism

oRHCE Gene: expresses the Next 4 most common antigens C,c,E and e on chromosome 1

·A child will be Rh negative If both parents are Rh negative

Haemolytic disease of the Newborn

·Haemolytic disease of a newborn develops when Maternal IgG antibodies specific for foetal- blood group antigens cross the Placenta and destroy foetal red blood cells

·Most commonly develops in RH negative (dd) Mother and Rh* (D) positive foetus 1stPregnancy:

·Rh- negative mother is usually not exposed to Sufficient quantity of foetal RBC to activate immune response

·At the time of delivery: separation of the ther Placenta from uterine walls allows larger amounts of foetal umbilical cord Blood to enter mothers circulation " Foetal RBCsactivate the Rh(D)- specific B-cells " production of Anti-D antibodies and appearance of memory B-cells

·Secreted IgM antibodies clears the Rh(D) foetal RBCs; BUT memory B-cells remain (Rh- isoimmunisations)

2nd Pregnancy:

·Rh(D) positive foetal RBCs cross the placenta and Activate the memory B-cells"

production of anti-D Antibodies

·IgG class from  Secondary immune response  cross The placenta and bind to Rh(D) antigens

·"Complement Activation system: Destruction of foetal red bloodcells

Result of cell lysis:

ØHaemolytic anaemia

ØErythroblastosis foetalis (more Severe) Diagnostics for development of haemolytic disease:

·Coomb’s test:

oDetermines the presence of maternal IgG on the Surface of foetal erythrocytes

oIsolated RBCs are incubated with coomb’s reagent (antibody to human IgG antibody)

oIf maternal IgG is bound to foetal RBCs "Agglutination Preventive procedures:

·All Rh-negative women are given anti-Rh antibodies Within 72 after delivery Therapy for haemolytic disease:

·Severe form: intrauterine blood exchange transfusion For the foetus (replace Rh* with Rh- cells) evry 10-21 till delivery

·Less severe cases: transfusion not given until Birth; Exposure to UV light to remove bilirubin

·Mother is treated during pregnancy by plasmapherisis:

oCell-separation machine is used to separate the Mother’s blood into cell and plasma

oPlasma containing Anti D- antibodies are discarded; Cells are re-infused

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