ABO Grouping 01

BLOOD GROUPS

Mansyur ArifBag. Patologi Klinik FK UNHAS / RSUP Dr. Wahidin Sudirohusodo

DefinitionsBlood groups are determined by antigens structures on the surfaces or red cells and are detected by reactions with specific antibodies.A blood group system is defined by antigens that are regulated either by allelic genes or closely linked genes.

Table 1. Survey of major Red Cell Blood Group SystemSystem Important antigensABOA1,A2,B,H,A3,Am,AxMNSsM,N,S,s,U,Mg,Mia,Hu,HeMta,Vw,M2,N2,S2PP1,pk,P2,(Tja)Rh D,C,E,c,e,Cw,Ew,ce,Ce,G,CE,cE,Du,Cu,Eu,LWLutheranLua,LubKellK,k,Kpa,Kpb,Jsa,JsbLewisLea,LebWrightWra,WrbDiegoDia,DibCartwrightYta,YtbXgXgaDombrockDoa,DobColtonCoa,Cob

Antibodies : sources & properties1. Normal humansA.bodies to some blood group a.g occur in the serum of individuals who lack the a.g and have had no prior exposure to it natural isohemagglutinins.

2. Immunized animals If animals are immunized with human red cells may form a.bodies to certain of the xenogeneic blood group a.g important source of blood group anti sera carefully absorbed with human red cells to establish specificity.Recently developed a.g specific monoclonal a.bodies do not require such absorption.

3. Immunized humansThe third major source of the blood group anti bodies are donors who have been allogenically immunized either by (1) prior blood transfusions or (2) previous pregnancies immune antibodies elicited by prior exposure to red cell a.g are commonly IgGs

ABO SYSTEMHistorical notesIn subsequent work Landsteiner recognized that the pattern of reactions could be explained by two a.g, which designated A and B. O signified the state of not having A or B. Table 3. The Landsteiner scheme

Table 3. The ABO system defined by Anti-A and Anti B

Blood GroupsAntigens on RCAntibodies in serumOABABNoneABA and BAnti-A and Anti-BAnti-BAnti-ANone

GeneticsDetermining the blood group : genotype and phenotype. A child receives one of four genes from each parent : A1, A2, B, or O. Six phenotypes are possible because the A a.g associated with group A2 and also A1.There are ten possible genotypes. Group A1 may have 3 genotypes (A1 A1, A1 O, A1A2). Group A2 can have either A2A2 or A2 O genotypes. Group B can have either BB or BO genotypes

Genotype :- specific genes that person carries- determined by family studies- AA, AO, BB, BO, AB and OO

Phenotype : Four phenotypes : A, B, AB and OAlthough there are ten possible genotypes, the absence of a specific anti-O prevents the serological recognition of more than four phenotypes. (table 5)

H antigen The surfaces oligosaccharides that constitutes the H a.g is the precursor of the A and B a.g Gene A & B responsible for converting H substance into A & B substanceThe O gene is an amorph and doesnt transform the H substance

Rare variant Bombay, the H precursor cannot be converted to H lack H ag & hence A or B phenotype cant be expressed.A terminal sugar molecules determine a.g specificity : A a.g : N acetylgalactosamine B a.g : galactosa

Rhesus System

Nomenclature : relation to genetic models

Fischer-Race theory (table 6) : Postulates 3 closely linked genes Cc, Dd and Ee. Rhesus a.g is renamed D. Rhesus positive presence of the D antigen, also called Rh or Rh factorRhesus negative absence of D but doesnt denote absence of other a.g of the Rh system (C,c,E or e)

2. Weiner system3. Rosenfield systemB.Compound antigensC.Weakened antigens : - weakly reactive ag Du - formal terminology : Rh +, Du variant- for transfusion : Du is equivalent to Rh + D.Deleted antigens : Rh null cells.E.Rh antigens structure

Table 6. Rh gene complexes Fischer-Race Wiener

CDeR1cdercDER2cDeRoCwDeR1WcdEruCder1CDERz

Other clinically significant systemsKell systemThe Kell a.g system rivals the Rh system in its complexity and clinical importance. Appearing in response to prior immunization, anti-Kell a.b have caused hemolytic transfusion reactions and HDN. The main a.g pairs : K-k, Kpa-Kpb and Jsa-JsbDuffy systemDouble negative phenotype red cells, Fy (a-b-) are totally resistant to invasion by Plasmodium vivax. Transfusion of incompatible blood into Duffy-sensitive individuals can cause severe hemolysis.

Kidd systemImmunization to Kidd is caused mainly by transfusions. Kidd a.b are evanescent warm-active incomplete a.b that may not be detected in red cell a.b screens. Consequently they often cause delayed transfusions rx, which may be severe. Lutheran systemThere are 2 common alleles, Lua and Lub and a silent one. The double-negative phenotype caused by either dominant inhibitor gene or a recessive silent allele.

5. Xga blood groupThis a.g is controlled by a gene on the X chromosome. Its not clinically significant but is of interest as a marker for X chromosome that appear to escape inactivation by the Lyon mechanism.

The ABO and Rhesus (Rh) groups are of major clinical significance. Some other systems of less overall importance are listed in table 7. Systems Frequency of a.body Cause of HDN

ABOVery commonYesRhCommonYesKellOccasionalYesDuffyOccasionalYesKiddOccasionalYesLutheranRareNoLewisOccasionalNoPOccasionalYes (rare)MNRareYes (rare)IiRareNo

Uses of blood grouping dataIn clinical medicine Pretransfusion testing : Prior to transfusion, blood is typed and crossmatched to establish ABO and D compatibility2. Hemolytic disease of the newborn

B. In genetics chromosome mappingC. In forensic medicine :1. Identification studies2. Paternity testing

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