IMMUNO-HEMATOLOGY. - ocw.usu.ac.idocw.usu.ac.id/.../his127_slide_immuno_-_hematology.pdf · IMMUNO-HEMATOLOGY. P f Adi K A S PK(KH)Prof. Adi Koesoema Aman SpPK(KH) Dr. Zulfikar Lubis

IMMUNOIMMUNO--HEMATOLOGY.HEMATOLOGY.IMMUNOIMMUNO HEMATOLOGY.HEMATOLOGY.

P f Adi K A S PK(KH)P f Adi K A S PK(KH)Prof. Adi Koesoema Aman SpPK(KH)Prof. Adi Koesoema Aman SpPK(KH)Dr. Zulfikar Lubis SpPK(K)Dr. Zulfikar Lubis SpPK(K)

DIVISI HEMATOLOGI DEPARTEMENT PATOLOGY KLINIK DIVISI HEMATOLOGI DEPARTEMENT PATOLOGY KLINIK FK USU/RSUP.H.ADAM MALIK MEDAN .FK USU/RSUP.H.ADAM MALIK MEDAN .

IMMUNO IMMUNO –– HEMATOLOGI .HEMATOLOGI .

Mengandung arti reaksi Mengandung arti reaksi i l ik b k iti l ik b k itimmunologik yg berkaitanimmunologik yg berkaitandengan sel darah merah .dengan sel darah merah .Tidak saja mencakup Tidak saja mencakup Immunologi , hematologiImmunologi , hematologig gg gtapi juga genetika &tapi juga genetika &biokimia biokimia biokimia biokimia

The ABO SystemThe ABO SystemThe ABO SystemThe ABO System

Discovered in 1901 by Dr. KarlDiscovered in 1901 by Dr. KarlDiscovered in 1901 by Dr. Karl Discovered in 1901 by Dr. Karl LandsteinerLandsteiner4 Main Phenotypes (A, B, AB, O)4 Main Phenotypes (A, B, AB, O)yp ( , , , )yp ( , , , )ABOABO gene located on long arm of gene located on long arm of chromosome 9chromosome 9

The ABO AntigensThe ABO AntigensThe ABO AntigensThe ABO Antigens

Added to Proteins or Lipids in Red CellsAdded to Proteins or Lipids in Red CellsSubstrate Molecule is H (fucose)Substrate Molecule is H (fucose)Substrate Molecule is H (fucose)Substrate Molecule is H (fucose)A antigen is NA antigen is N--acetylacetyl--galactosamine galactosamine (GalNAc)(GalNAc)(GalNAc)(GalNAc)B antigen is Galactose (Gal)B antigen is Galactose (Gal)A and B genes code for transferase A and B genes code for transferase enzymesenzymesenzymesenzymes

ABO AntibodiesABO AntibodiesABO AntibodiesABO Antibodies

A and B substances very commonA and B substances very commonA and B substances very commonA and B substances very commonAntibodies produced to “nonAntibodies produced to “non--self”self”P d d ft fi t f th f lifP d d ft fi t f th f lifProduced after first few months of lifeProduced after first few months of lifeA & B people have mainly IgMA & B people have mainly IgMO people have IgGO people have IgGMay fade in old ageMay fade in old ageMay fade in old ageMay fade in old age

Antigens & AntibodiesAntigens & AntibodiesAntigens & AntibodiesAntigens & Antibodies

Blood Group Antigens on RBCs Antibodies in Serum Genotypes

A A Anti-B AA or AO

B B Anti-A BB or BO

AB A and B Neither AB

O Neither Anti-A and anti-B OO

Inheritance of ABO GroupsInheritance of ABO Groups

Allele from the mother

Allele from the father

Genotype ofoffspring

Blood types ofoffspring the mother the father offspring offspring

A A AA A

A B AB AB

A O AO A

B A AB AB

B B BB B

B O BO B

O O OO OO O OO O

ABO TypingABO TypingABO TypingABO Typing

Cell GroupCell Group Reverse GroupReverse GroupCell GroupCell Group–– Test Washed Cells Test Washed Cells

With:With:

pp–– Test plasma/serum Test plasma/serum

with:with:Known AKnown A cellscells–– Monoclonal AntiMonoclonal Anti--AA

–– Monoclonal AntiMonoclonal Anti--BBI t t lI t t l

–– Known AKnown A11 cellscells–– Known B cellsKnown B cells–– Known O cellsKnown O cells

–– Inert controlInert controlAgglutination is a Agglutination is a positive resultpositive result

–– ? Known A? Known A22 cellscellsReactions may be Reactions may be

k th llk th llpositive resultpositive result weaker than cell weaker than cell groupgroup

Distribution of ABO GroupsDistribution of ABO GroupsDistribution of ABO GroupsDistribution of ABO Groups

Population O A B AB

Aborigines 61 39 0 0Basques 51 44 4 1Basques 51 44 4 1Blackfoot (N. Am. Indian) 17 82 0 1Bororo 100 0 0 0Chinese-Canton 46 23 25 6Chinese Peking 29 27 32 13Chinese-Peking 29 27 32 13English 47 42 8 3Hawaiians 37 61 2 1Irish 52 35 10 3M 98 1 1 1Mayas 98 1 1 1Navajo (N. Am. Indian) 73 27 0 0Peru (Indians) 100 0 0 0United Kingdom (GB) 47 42 8 3g ( )USA (blacks) 49 27 20 4USA (whites) 45 40 11 4

Distribution of theDistribution of the AA allelealleleDistribution of the Distribution of the AA alleleallele

Distribution of the Distribution of the BB AlleleAllele

Distribution of the Distribution of the OO AlleleAllele

Significance of ABO GroupSignificance of ABO GroupSignificance of ABO GroupSignificance of ABO Group

ABO mismatched transfusions:ABO mismatched transfusions:ABO mismatched transfusions:ABO mismatched transfusions:–– RareRare

May be life threateningMay be life threatening–– May be life threateningMay be life threatening–– Can be caused by technical or clerical errorCan be caused by technical or clerical error

Intra asc lar haemol sisIntra asc lar haemol sis–– Intravascular haemolysisIntravascular haemolysis–– More severe in group O patientsMore severe in group O patients

Universal Donor and RecipientUniversal Donor and RecipientUniversal Donor and RecipientUniversal Donor and Recipient

Universal DonorUniversal Donor Universal RecipientUniversal RecipientUniversal DonorUniversal DonorGroup OGroup O–– Carries no A or BCarries no A or B

Universal RecipientUniversal RecipientGroup ABGroup AB–– Patient has no antiPatient has no anti--AACarries no A or B Carries no A or B

antigensantigens–– Packed and processed Packed and processed

it h littlit h littl

Patient has no antiPatient has no anti A A or antior anti--B presentB present

–– Cannot lyse any Cannot lyse any t f d llt f d llunits have little units have little

antibodyantibodytransfused cellstransfused cells

–– Beware: otherBeware: otherantibodies may beantibodies may be–– antibodies may be antibodies may be presentpresent

Using the patient’s own group ASAP will conserve resources

The Rh(D) AntigenThe Rh(D) AntigenThe Rh(D) AntigenThe Rh(D) Antigen

RH is the most complex system, withRH is the most complex system, withRH is the most complex system, with RH is the most complex system, with over 45 antigens over 45 antigens Discovered in 1940 after work on Discovered in 1940 after work on Rhesus monkeysRhesus monkeysSubsequently discovered to be Subsequently discovered to be q yq yunrelated to monkeysunrelated to monkeysRHRH gene located on short arm of gene located on short arm of chromosome 1chromosome 1

Simple Genetics of Rh(D)Simple Genetics of Rh(D)Simple Genetics of Rh(D)Simple Genetics of Rh(D)

86% of caucasians are Rh(D) pos86% of caucasians are Rh(D) pos86% of caucasians are Rh(D) pos86% of caucasians are Rh(D) posThe antithetical antigen d has not been The antithetical antigen d has not been foundfoundfoundfoundThe The dd gene is recessive:gene is recessive:–– Dd, dD, DDDd, dD, DD, persons are Rh(D) pos, persons are Rh(D) pos–– Only Only dd dd persons are Rh(D) negpersons are Rh(D) neg

Distribution of Rh(D) TypesDistribution of Rh(D) TypesDistribution of Rh(D) TypesDistribution of Rh(D) Types

PopulationPopulation Rh(D) posRh(D) pos Rh(D) negRh(D) negPopulationPopulation Rh(D) posRh(D) pos Rh(D) negRh(D) neg

CaucasianCaucasian 86%86% 14%14%CaucasianCaucasian 86%86% 14%14%

AfricanAfrican 95%95% 5%5%AfricanAfrican--AmericanAmerican

95%95% 5%5%

OrientalOriental >99%>99% <1%<1%OrientalOriental >99%>99% <1%<1%

Significance of Rh(D)Significance of Rh(D)Significance of Rh(D)Significance of Rh(D)

80% of Rh(D) neg persons exposed to Rh(D)80% of Rh(D) neg persons exposed to Rh(D)80% of Rh(D) neg persons exposed to Rh(D) 80% of Rh(D) neg persons exposed to Rh(D) pos blood will develop antipos blood will develop anti--DDAntiAnti--D can also be stimulated by pregnancy with D can also be stimulated by pregnancy with y p g yy p g yan Rh(D) positive babyan Rh(D) positive baby–– Sensitisation can be prevented by the use of antiSensitisation can be prevented by the use of anti--D D

immunoglobulin, antenatally and post natallyimmunoglobulin, antenatally and post natallyRh(D) neg females of childbearing potential Rh(D) neg females of childbearing potential h ld b i Rh(D) iti bl dh ld b i Rh(D) iti bl dshould never be given Rh(D) positive blood should never be given Rh(D) positive blood

productsproducts

Significance of Rh(D)Significance of Rh(D)Significance of Rh(D)Significance of Rh(D)

80% of Rh(D) neg persons exposed to Rh(D)80% of Rh(D) neg persons exposed to Rh(D)80% of Rh(D) neg persons exposed to Rh(D) 80% of Rh(D) neg persons exposed to Rh(D) pos blood will develop antipos blood will develop anti--DDAntiAnti--D can also be stimulated by pregnancy with D can also be stimulated by pregnancy with y p g yy p g yan Rh(D) positive babyan Rh(D) positive baby–– Sensitisation can be prevented by the use of antiSensitisation can be prevented by the use of anti--D D

immunoglobulin, antenatally and post natallyimmunoglobulin, antenatally and post natallyRh(D) neg females of childbearing potential Rh(D) neg females of childbearing potential h ld b i Rh(D) iti bl dh ld b i Rh(D) iti bl dshould never be given Rh(D) positive blood should never be given Rh(D) positive blood

productsproducts

InheritanceInheritanceInheritanceInheritance

ABOABO && RHRH genes are not linkedgenes are not linkedABOABO & & RHRH genes are not linkedgenes are not linkedABO & Rh(D) type are inherited ABO & Rh(D) type are inherited independentlyindependentlyindependentlyindependentlyFor example:For example:An A Rh(D) pos mother An A Rh(D) pos mother and a B Rh(D) pos father and a B Rh(D) pos father could have an O Rh(D) neg childcould have an O Rh(D) neg child

Inheritance of ABO and Rh(D)Inheritance of ABO and Rh(D)Inheritance of ABO and Rh(D)Inheritance of ABO and Rh(D)

Mother FatherGroup A AO

Rh(D) pos Dd

Group B BO

Rh(D) pos Dd

Group A AO

Rh(D) pos Dd

Group B BO

Rh(D) pos Dd

Group O OO

Rh(D) neg dd

Clinical significance of Rh Clinical significance of Rh –– antigenantigeng f fg f f gg11-- Blood transfusionBlood transfusion::

If Rh If Rh ––ve person is transfused with Rh + ve blood, anti ve person is transfused with Rh + ve blood, anti –– Rh antibodies will develop in his Rh antibodies will develop in his If Rh If Rh ve person is transfused with Rh ve blood, anti ve person is transfused with Rh ve blood, anti Rh antibodies will develop in his Rh antibodies will develop in his plasma.plasma.Latter on if he needs a second blood transfusion and is given Rh +ve blood, agglutination Latter on if he needs a second blood transfusion and is given Rh +ve blood, agglutination of donor's R.B.Cs would occur inside the blood vessels of the recipient haemolysis.of donor's R.B.Cs would occur inside the blood vessels of the recipient haemolysis.of donor s R.B.Cs would occur inside the blood vessels of the recipient haemolysis.of donor s R.B.Cs would occur inside the blood vessels of the recipient haemolysis.

22-- In marriage : ( erythroblastosis foetalis )In marriage : ( erythroblastosis foetalis )If Rh + ve male person married Rh If Rh + ve male person married Rh –– ve female, the fetus will be Rh + ve in most cases.ve female, the fetus will be Rh + ve in most cases.During delivery ( i.e. separation of the placenta ), some fetal blood containing Rh During delivery ( i.e. separation of the placenta ), some fetal blood containing Rh agglutinogen may cross the placenta and reach the mother's blood.agglutinogen may cross the placenta and reach the mother's blood.So, sensitization of mother's blood will occur with formation of antibodies (So, sensitization of mother's blood will occur with formation of antibodies (anti anti –– RhRh. Or . Or , f f f (, f f f ( RRanti anti –– DD) in her plasma, (usually first baby saved).) in her plasma, (usually first baby saved).In the second pregnancy with Rh + ve fetus, antibodies already present cross the placenta In the second pregnancy with Rh + ve fetus, antibodies already present cross the placenta to the foetus and cause haemolysis of his R.B.Cs (to the foetus and cause haemolysis of his R.B.Cs (erythroblastosisFoetaliserythroblastosisFoetalis). ). f y f R (f y f R ( yy ))

LEWIS SYSTEMLEWIS SYSTEM

A serum antigen secondarily absorbed to th d llthe red cellsLe gene produces Lea

Secretors change the Lea to Leb

Le may also modify the A antigenLe may also modify the A antigen review the relationship to ABO precursors

Lewis Red Cell PhenotypesLewis Red Cell Phenotypes

Genes Lewis Red Cell Phenotype

Le Se Lea- Leb+Le Se Lea Leb+

Le se Lea+ Leb-

lele Lea- Leb-

le se Lea- Leb- Lec+

le Se Lea- Leb- Lec- Led+

Development of AntigensDevelopment of Antigens

Newborns born Le a-b-Newborns born Le If Le and Se

2 k t 6 th L a+– 2 weeks to 6 months Le a+

– then Le a+b+

b– then Le a-b+

During pregnancy antigens become weakerDuring pregnancy, antigens become weaker

Phenotype FrequenciesPhenotype Frequencies

Phenotype White Black yp

Le a+b- 22% ---

Le a-b+ 72% ----

Le a-b- 6% 20%

Lewis AntibodiesLewis Antibodies

Anti-Le a, Anti-Le b, Anti-Lex

Most react at room temperature or below -Most react at room temperature or below Often fix complementS i it h l iSome in vitro hemolysisLe a may cause HTR

I Blood GroupI Blood Group

Two antigens I and iI antigen present on almost all healthy g p yadults Rare adults that are I negative - spectrumRare adults that are I negative spectrum on page 175I antigen varies in strength on adult cellsI antigen varies in strength on adult cells


Newborns do not have much I antigenNewborns do not have much I antigen Newborns have i antigen At about 18 months the i is replaced with ISome transitional antigens


Antibodies Anti-I anti-i– Anti-I

usually reacts at room temperature, saline or belowft tt h l toften attaches complement

doesn’t cause hemolysis unless it reacts at 37oC37 C Can be found in almost all sera in low titers and titers increase during some diseases (viral infections - syphilis - atypical pneumonia)COLD AUTOAGGLUTIN


Antibodies Anti-I anti-i– Anti-i

rare antibody occurs in patients with infectious mononucleosis, cirrhosis, myeloid leukemia,

ti l ireticulosis

P Blood GroupP Blood Group

Discovered in 1927 by LandsteinerAntigens P1 P p pk Luke g 1– Luke antigen and disease association

- page 173


Antibodies Anti-P1 Anti-P Anti-pk

Anti- P + P1 + pk

– Anti-P11Usually IgM reacts at room temperature and salineMay attach complementrarely a problem with transfusioneasily inhibited with P substanceeasily inhibited with P1 substance



Anti- P + P1 + pk

– Anti-Pfound in sera from pk individuals - an IgM hemolytic antibody that is clinically significant also found as an IgG biphasic antibody in parozysmal cold hemoglobinuria called Donath-Landsteiner antibody y



Anti- P + P1 + pk

– Anti-pk and Anti P + P1 + pk

Anti-pk has only been found as part of other antibodiesantibodiesAnti-P + P1 + pk found in p individuals -formerly called Anti-Tja and very hemolytic

Duffy Blood GroupDuffy Blood Group

Discovered in early 1950’s Fy antigen locus on chromosome 1 withFy antigen locus on chromosome 1 with Rh locusAntigensAntigens codominant inheritance– Fya Fyb Fyx

– Others Fy3 Fy 4 Fy5 Fy6 Fs - (page 185)

Kell Blood GroupKell Blood Group

Many antigens in this system and hasMany antigens in this system and has been given a numerical nomenclature Refer to table 8 8Refer to table 8-8Six most important

Numeric Alpha Name IncidenceKEL 1 K Kell 10%KEL 2 k Cellano 99 8%KEL 2 k Cellano 99.8%KEL 3 Kpa Penny 2%KEL 4 Kpb Rautenberg 99.9KEL 6 Jsa Sutter Rare (19% Blacks)KEL 6 Jsa Sutter Rare (19% Blacks)KEL 7 Jsb Matthews 99.9%(99.8% Blacks

Kell Blood Gro pKell Blood Group

Most common gene complexes

MNSs Blood GroupMNSs Blood Group

M ti i thi t dMany antigens in this system and some are alleles to the four common antigensM N S s

Association with GPA and GPB Four gene complexes

MS Ms NS NsMS Ms NS Ns Other alleles Mg, Mk, Mc, Mr, Mz, Mv, Na, T1m, Sj, S2, some quantitative differences j, 2, q


Ph tPhenotypes


A tib diAntibodiesAnti-M and Anti-N– Usually room temperature– IgM saline reaction– Dosage (antibodies react better with

homozygous cells)– Destroyed by enzymes – Possible HDN and HTR if reaction at AHG– Anti-Nf found in dialysis patients


AntibodiesAnti-SAnti S– Usually igM and room temperature although

some at AHG– destroyed by enzymes– Rare HTR and HDNRare HTR and HDN


A tib diAntibodiesAnti-s and anti-U – Usually IgG and AHG– Not destroyed by enzymes– HTR and HDN– Anti-U found as warm autoantibody and y

does not react well with Rh null cells– Other antibodies rarely detected but not

uncommon (ex. anti-Mg common antibody)

Kidd Blood GroupKidd Blood Group

Di d i th 1950Discovered in the 1950sTwo antigens Jka Jkb


Antibodies - Anti-Jka and Anti-Jkb

Usually IgG and require AHG– Usually IgG and require AHG– bind complement

enhanced by enzymes– enhanced by enzymes– implicated in HDN and HTR

S ld t t d d t i t idl– Seldom potent and deteriorate rapidly– Classic delayed HTR


Antibodies Anti Jk3Anti-Jk3

– found in some Jka-b- individualsi h Jk d Jkb– reacts with Jka and Jkb

Lutheran Blood GroupLutheran Blood Group

T ti L a (8%) L b (99%)Two antigens Lua (8%) Lub (99%)– Other antigens Table 8-12

Important blood group that demonstratesImportant blood group that demonstrates multiple methods for inheritance of the null cell typetypeLu a-b- inheritance– InLu dominate inhibitor geneInLu dominate inhibitor gene– lulu recessive lack of Lu gene– sex linked inhibitor gene

Lutheran Blood GroupLutheran Blood Group

AntibodiesAntibodies– Anti-Lua - not common - reacts in saline but

can be IgG and require AHG gives a (mf)can be IgG and require AHG - gives a (mf) agglutination - unclear about HTR & HDN

– Anti-Lub - rare - mostly IgG and requires– Anti-Lu - rare - mostly IgG and requires AHG - probable HTR and HDN

– Anti-Luab (Anti-Lu3 ) - reacts with all butAnti Lu (Anti Lu ) reacts with all but Lu a-b- of the recessive type

– Other antibodies react with rare Lu– Other antibodies react with rare Lu phenotypes found on Lua-b- (page 192/3)

Other Blood GroupsOther Blood Groups

Diego - Dia Dib Wra Wrb 3 othersDiego Di Di Wr Wr 3 others– Dia found in Chippawah Native Americans

and Japanese and Chineseand Japanese and Chinese– uncommon antibodies - AHG reaction and

important in HTR and HDNimportant in HTR and HDN– Wra is a low incidence antigen and Wrb is

a high incidence antigeng g– anti-Wra is a fairly common antibody - IgM

or IgGg


Chido/Rogers– Nine antigens - all normal individuals are g

either Rg + or Ch +– HTLA - use plasma inhibition– Determinants on C4 molecule and linked to

HLA -


Gerbich– system with at least 3 high incidence y g

antigens and 4 low incidence antigens– Antibodies usually IgG which require AHG

and clinically significantScianna– Sc:1 - 100% Sc:2 - 0.3% Sc:3 - 100%– Antibodies are rare


ColtonColton– antigens: Coa -99.7% Cob -10.7% Co3 -100%

the null phenotype has been found and– the null phenotype has been found and associated with genetic abnormality and anemiaanemia

– antibodies IgG and clinically significantCromerCromer– consists of 7 high incidence antigens and

three low incidence antigensthree low incidence antigens– antibodies probably clinically significant


Cartwright– antigens Yta - 99.8% Ytb - 0.2%g– Usually IgG and AHG ?HDN and HTR?

DombrockDombrock– antigens Doa - 57% Dob - 83%– additional antigens added Holly Gregory– additional antigens added Holly, Gregory,

and Joseph – Uncommon antibodies HTR and ?HDN?Uncommon antibodies HTR and ?HDN?


IN– Ina Inb

– Ina Iranian and Arabs– Enzyme destroyed - Ina HTR y y

Knops– five antigens– five antigens– depressed in some diseases

HTLA– HTLA

Other AntigensOther Antigens

High incidenceHigh incidence– Vel, Lan, August, Jacobs, Sid, Wra

L i idLow incidence– too numerous to mention

Bg - HLA antigens that coat red cells

IgM AntibodyIgG Antibody IgM Antibody(Pentamer Structure)(Monomer Structure)

I id d b t tb k Fi 14 3 97 K bImages provided by textbook: Figure 14.3, page 97, KubyImmunology, 4th Edition, W.H. Freeman and Company

Immune ResponseImmune ResponseDefinition: Physiological mechanism to fight Definition: Physiological mechanism to fight

Immune ResponseImmune Responsey g gy g g

disease or clear foreign substances.disease or clear foreign substances.Primary immune response: First exposure of a Primary immune response: First exposure of a f i I M i h d i ib df i I M i h d i ib dforeign agent. IgM is the predominant antibody foreign agent. IgM is the predominant antibody produced that attaches to and fights the foreign produced that attaches to and fights the foreign agent In our case a foreign red blood cellagent In our case a foreign red blood cellagent. In our case a foreign red blood cell agent. In our case a foreign red blood cell antigen.antigen.Secondary immune response: Subsequent Secondary immune response: Subsequent exposure of the same foreign agent. Rapid exposure of the same foreign agent. Rapid response in which IgG is the predominant response in which IgG is the predominant antibody producedantibody producedantibody produced.antibody produced.

Concentration of Ag and Ab also affects agglutination reactions both also affects agglutination reactions, both the first and second stages.

KEGUNAANNYA .KEGUNAANNYA .KEGUNAANNYA .KEGUNAANNYA .

1.1. Menyesuaikan donor dan resipien utk Menyesuaikan donor dan resipien utk y py ptransfusi dn trasnplantasi organ .transfusi dn trasnplantasi organ .

2.2. Identifikasi dan pencegahan thd Identifikasi dan pencegahan thd ll i i i it h il l h ti ll i i i it h il l h ti alloimmunisasi wanita hamil oleh antigen alloimmunisasi wanita hamil oleh antigen

Rh .Rh .3.3. Menentukan diagnosis , prognosis , terapi Menentukan diagnosis , prognosis , terapi g , p g , pg , p g , p

HDN .HDN .4.4. Diagnosis dan pemeriksaan destruksi Diagnosis dan pemeriksaan destruksi

it it di b bk t tib di t it it di b bk t tib di t eritrosit yg disebabkan autoantibodi atau eritrosit yg disebabkan autoantibodi atau alloantibodi . alloantibodi .

ANTIGEN ERITROSIT .ANTIGEN ERITROSIT .ANTIGEN ERITROSIT .ANTIGEN ERITROSIT .

1.1. ANTIGEN H ANTIGEN H 1.1. ANTIGEN H ANTIGEN H Komponen dasar Ag eritrosit , Komponen dasar Ag eritrosit , Diatur oleh gen H , ada pada semua eritrosit , Diatur oleh gen H , ada pada semua eritrosit , K d dit t k l h A &B K d dit t k l h A &B Kadarnya ditentukan oleh gen A &B Kadarnya ditentukan oleh gen A &B Subtansi H oleh gen A & gen B → antigen A dan B Subtansi H oleh gen A & gen B → antigen A dan B Gen O tdk merubah substansi H → substansi H >>>Gen O tdk merubah substansi H → substansi H >>>

1.1. ANTIGEN A .ANTIGEN A .

2.2. ANTIGEN BANTIGEN B

STRUKTUR ANTIGEN ERITROSIT .STRUKTUR ANTIGEN ERITROSIT .STRUKTUR ANTIGEN ERITROSIT .STRUKTUR ANTIGEN ERITROSIT .

ABO BLOOD GROUP SYSTEMABO BLOOD GROUP SYSTEMABO BLOOD GROUP SYSTEMABO BLOOD GROUP SYSTEM

GOLONGAN DARAH O BAMBAYGOLONGAN DARAH O BAMBAYGOLONGAN DARAH O BAMBAYGOLONGAN DARAH O BAMBAY

Orang gol O tanpa gen H ( genotype hh ) → Orang gol O tanpa gen H ( genotype hh ) → g g p g ( g yp )g g p g ( g yp )tidak mampu membentuk Antigen A dan B tidak mampu membentuk Antigen A dan B walau gen A & B normal → tidak memiliki anti walau gen A & B normal → tidak memiliki anti gen A B dan H pada eritrisit tapi anti bodi A gen A B dan H pada eritrisit tapi anti bodi A gen A , B dan H pada eritrisit tapi anti bodi A , gen A , B dan H pada eritrisit tapi anti bodi A , B, H dalam serumnya sangat kuat → fenotipe B, H dalam serumnya sangat kuat → fenotipe Bombay ( Oh ) .Bombay ( Oh ) .

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IMMUNO-HEMATOLOGY. - ocw.usu.ac.idocw.usu.ac.id/.../his127_slide_immuno_-_hematology.pdf · IMMUNO-HEMATOLOGY. P f Adi K A S PK(KH)Prof. Adi Koesoema Aman SpPK(KH) Dr. Zulfikar Lubis