BB mdtrms exam

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REMINDERS for Blood Group Systems

• Antigens are designated by letters, such as A and B.
• It is important to include the symbol of the blood group system when writing the phenotype or antigen, for clarity.
  • Example: For a person with the Duffy A antigen, write Fya.
  • Example: Phenotype is Fy(a+b-).

COMMON BLOOD GROUPS

• Kell
• Duffy
• Kidd
• Lutheran
• Antibodies released by these blood groups are usually IgG, can cross the placenta, and cause Hemolytic Disease of the Fetus and Newborn (HDFN) and Hemolytic Transfusion Reactions (HTR).

Kell System 006 (KEL) & Kx Systems 019 (XK)

• Named after Mrs. Kelleher (1946), a patient whose anti-Kell antibodies resulted in hemolytic disease of her newborn.
• Similar to Rh, it has high and low incidence antigens.
  • High prevalence antigens are commonly found in the majority of the population.
  • Low incidence antigens are less common.
• KEL Gene is located on chromosome 7.
• Kellnull individuals show no expression of ALL Kell antigens except the related antigen Kx.
  • Kx antigen is embedded in the cell membrane; if there is no Kell antigen, the only exposed antigen is Kx.
  • The RBC membrane is normal because of the transmembrane protein Kx.

Kell Antibodies

• Produced by individuals with the small "k" antigens, Kell(K-k+) phenotype.
• IgG (reacts well at the AHG phase).
• Can cross the placenta.
• May react at the Immediate Spin (IS) phase; red blood cells are mixed with antiserum and centrifuged to observe for agglutination reactions.
• An immune antibody (transfusion, pregnancy).
  • Anti-K antibodies are not naturally occurring; they are only produced during transfusion or pregnancy.
• Structure includes disulfide bonds formed from 2 Cysteine AA.

Kell Antigens

• Well-developed at birth, with K antigen present at 10 weeks of gestation (9%) and k antigen at 7 weeks of gestation (99.8%).
• The K antigen is VERY IMMUNOGENIC (2nd to D Antigen) at stimulating antibody production, and can cause severe hemolytic disease.
• Have disulfide-bonded regions on the glycoproteins, connecting it with the XK protein.
• Sensitive to SULFHYDRYL REAGENTS which easily break disulfide bonds.
  • 2-mercaptoethanol (2-ME).
  • Dithiothreitol (DTT).
  • 2-aminoethylisothiouronium bromide (AET).
  • ZZAP (DTT + enzyme).
• K is <9% of the population (low incidence), k is >90% of the population (high prevalence).
• Antigens are only found in RBCs.
• Kell antigens are highly abundant in the testes.

More Kell Antigens

• Kpa is a low frequency antigen found in 2% of the population, also known as Penney and Antibody produced is Anti-Kpb
  • Together with Kpb are the low prevalence mutation of the Kpb gene
• Kpb is a high frequency antigen found in 99.9% of the population
  • Also known as Rautenberg and Antibody Produced is Anti-Kpa.
• Jsa is found in 20% of blacks; 0.1% in whites. Also known as Sutter and Antibody produced is Anti-Jsb
• Jsb is found in high frequency; 80-100% in blacks. Also known as Matthews and Antibody produced is Anti-Jsa

Anti-K vs Anti-D

• Anti-K destroys the erythroid precursor cells of the fetus. "k" antigens can be identified as early as 7 or 10 weeks of gestation, so most likely these antigens are present in the erythroid precursor cells.
• Anti-D does not harm erythroid precursor cells, only hemolysis leads to reticulocyte production, hyperbilirubinemia, and anemia.

Suppressed erythropoiesis due to anti-K

• Reticulocytopenia
• Anemia

Hemolysis due to anti-D

• Reticulocytosis
• Hyperbilirubinemia
• Anemia
• Anti-Ku (KEL5) recognizes all RBCs except Kellnull. Produced by Kellnull individuals, it can cause HDFN and HTR; rare Kell negative units should be given. k, Kpb and Jsb antibodies are rare because many individuals have these antigens. Kpa and Jsa are low prevalence antigens and also rare; few donors have the antigen and rare exposure leads to low incidence.

XK1 Gene & McLeod syndrome

• Located on the X chromosome.
• Not part of the Kell system, related, acts as a transport protein, spans the membrane 10 times.
• Kx antigens are increased in those who are K0
• Present in all RBCs except McLeod phenotype.
• Kell antigen expression depends on the presence of the XK protein; without XK, Kell antigens are not expressed.

Kx antigen expression

• Kx antigen is present in small amounts in individuals with normal kell antigens
• When Kell antigens are denatured, the expression of Kx antigens are INCREASED

McLeod Syndrome

• Absence of Kx & Km antigen (almost exclusive in white males; X-linked inheritance; Mother is the Carrier)
• McLeod has no Kx antigen expressed, while Kellnull has Kx antigen to be expressed.
• Mutated in the XK locus.
• McLeod phenotypes are written with superscript "W" (weak kell antigens).
• Causes abnormal red cell morphologies and decreased red cell survival because the Kx antigen transmembrane protein deletion disrupts the RBC structure.
  • Acanthocytic – spikey/ thorny RBC
  • Decrease RBC survival (decreased deformability)
• Often compensated despite chronic Hemolytic anemia
  • Reticulocytosis
  • Bilirubinemia
  • Splenomegaly
  • Decreased Haptoglobin
• Associated with CHRONIC GRANULOMATOUS DISEASE
  • WBCs can engulf but cannot kill.
• Also inability of the phagocyte to produce NADPH oxidase which is needed to produce hydrogen peroxide, responsible in killing the phagocytosed organism
  • Die at an early age due to overwhelming infection
• Not all males with McLeod syndrome has CGD and not all CGD patients have McLeod phenotype.
• Antibodies produced are Anti-Kx and Anti-Km, which strongly react with the K0 phenotype RBCs due to abundant Kx antigens. - Normal vs K0 vs Kmod (CGD) comparison: - Kell antigens - Normal: Normal - K0: Absent - Kmod: Very weak - Kx - Normal: Weak is - K0: Increased - Kmod: Mildly increased - Km - Normal: Normal - K0: Absent - Kmod: Weak - Antibodies against missing antigens - Normal: Anti-Ku - K0: Anti-Ku-like - Kmod: Anti-Kx + Anti-Km

K. Antigen 019 (XK)

• ISBT 019; membrane transport protein

Duffy Blood Group System 008 (FY)

• Transmembrane proteins that traverse the cell membrane 7 times.
• Discovered in 1950 from a Mr. Duffy, who had hemophilia and had undergone blood transfusions, and Anti-Fya was observed in his plasma
• A year later the antithetical antigen discovered on a woman who has 3 pregnancies known as Anti-Fyb discovered a year later.
• The Duffy genes are formerly known as DARC and located on chromosome 1.

Duffy genes (ACKR1)

• Fya and Fyb code for antigens
• Fy is a silent allele and major allele in Blacks

Duffy Antigens Characteristics

• Identified at 6 weeks gestation
• Well developed at birth
• Are destroyed by enzymes
  • Such as: Ficin, Papain, Bromelin, Chymotrypsin, and ZZAP
  • NOT destroyed by Dithiothreitol (DTT) (ALONE), AET, Glycine acid EDTA treatment
• Shows dosage
• Not found on other cells only in RBCs, but can be seen in other TISSUES such as Brain, Colon, Endothelium, Lungs, etc.
• At the 42nd position is the differentiation of Fya and Fyb comes from
  • Fya -42nd position – Glycine
  • Fyb: 42nd position – Aspartate

###Fy3 antigens

• Antigenic precursor to both Fya and Fyb antigens - required for expression of Fya and Fyb
• Anti-Fy3 = inseparable anti-FyaFyb, discovered in a Fynull individual. - this creates aAntibodies against normal Duffy antigens Will react to other RBCs except the null phenotype RBC because null phenotype individuals have no Fy3 in their RBC.

Fyx antigens

• Inherited weak form of Fyb and does not produce a distinct antigen
• May type as Fy(b-), but reacts with some anti-Fyb because it expresses weak Fyb
• No anti-FyX since it does not produce a distinct antigen.

Fy phenotypes:

• Fy (a+b-) 9% in blacks and 17% in whites
• Fy (a+b+) 1% in blacks and 49% in whites
• Fy (a-b+) is 22% in blacks and is 35% in whites
• Fy (a-b-) is 68% in blacks and very rare in whites

More Fy phenotypes assignments

• Assigned numbers include Fy3, Fy4, Fy5, Fy6 & Fyx
• The silent allele is responsible for Fy(a-b-) - The Fy gene is a MUTATED variant of the Fyb gene.
• Fynull individuals do not usually possess Fyb antigens on their red cells but expresses it on other tissues and don't create Anti-Fyb antibody, since Fyb is considered NOT FOREIGN because it is found in other tissues of the body

Duffy antibodies

• IgG exhibit dosage and react best in the AHG phase.
• Rarely bind complement.
• Clinically significant and cause delayed and acute HTR and HDFN.
• DO NOT react with enzyme treated RBCs by Papain, Ficin, Chloroquine, DTT, AET, Glycine-acid EDTA - Useful in antibody screening because it does not react with RBCs which has been treated with enzymes.

Duffy and Malaria

• A connection that involves Most African-Americans as Fy (a-b-) due to Evolutionary adaptation
• Fya and Fyb are receptors for the malaria parasite (P. vivax & P. knowlesi).

Receptors for Chemokine

• The duffy antigens are receptors membranes of the chemokine known as ATYPICAL CHEMOKINE RECEPTOR 1 (ACKR1)
  • This protein is a receptor for proinflammatory chemokines and a malarial parasite P. Vivax. This blocks access of the parasite to cells.
• This mean thar Fy-null individuals are are protected from parasitic infections such as Malaria. Meaning more people with African Decent possess Fy-null

Kidd Blood Group System 009

• The serum in the anti-Mrs Kidd who also had antibody that caused hemolytic disease of thee fetus and neewborn
• Jka - react with 77% of the bostonians (england)

Kidd genes

Jka and Jkb (codominant alleles)

• Silent gene and found in chromosome 18
• Kidd antigens:
  • Only present in RBCs; not found on any other tissues.
  • Show dosage.
• Not very immunogenic + Enhanced by enzymes.

###Kidd Antigens

• Are not very accessible of RBC memory

Kidd genotypes-

• Jka:Jka is 26.3% among whites and 51.1% among blacks.
• Akakb is 50.3% for whites and is 40.8% for blacks.
• JkbJkb is 23.4% present for whites and is 8.1% present for blacks.
• Jk- Null is very rare for both.

Kidd Antignes formation

• Jka detected at 11- weeks of gestation and Jkb has at week 7. and both are well developed at birth ####Kidd antibodies:
• Igg; can cross placenta. clinically significant; they are heavily implicated in HTR and HDN.
• Known for notorious detection is very hard to find. Detection requires LISS/PEG.
• Dosage- non -IgG-ang enhanced when bounded. Always check blood cards because they might have been previous transfusion. anti j3 will also react against kidd. ####### Kidd phenotypes: With other antibodies Kidd are complement binding. Reagent reaction of ANti-JK 3 will cause anti controll reagents

Kidd antibodies

Ig3: looks like unseparable antigen jk. Reating all RBC with autocontrol.

Lutheran System 005

• Lutheran bloods are are uncommon antigen system for blood bank handling; they are low incidince but are more immune. This happens due to the discovery after SLE with the anitbodies present caused luatrin antibody in the patient.

Anti LUA -

antigens are from Lua

• Poorly expressed until 15yrs old
• Ficin papain and glycine EDTA Resistant
• Trypsin and alpha chymotrypsin destroys DTT and AET/ RBC - Blood banks seldomly deal with this group cuz they are hard to handle and most have poor immunogenicity

Lutheran Antibodies

(anti lu a): Created by those Lub and most are Naturally occurring, with both IGM/ G, will respond quickly at room temperature. They have poor clinicality / mild

• ANTI LUB*
• high incidents antigen, so it's uncommon(usually) and they occur from blood transfusion pregnancy ( IgG/IgA). Reactive / Warm at 37 dgC)

Looks are only created by a recessive form of Luab.

Lutheran types

1 Expression is always suppress during dominant stages due to the inhibitor - In(Lu) which is called ""Inhibotor of Luteran"" gene This mean that LU have their Lua / Lub antigens but during inheritce, Lu inhibits

###Luthran Genes types

• Trace amounts always exist which mean they cannot cause Lu3. Silent recessive lutheran allelies; 2 silent lu will lack it. recessive will always inhibit
• Linked with Australian type.

In conclusion for Lu they aren't used often cuz of high and low levels.

#######

• Additional information:
• Kell antiges are for the tested
• K- k antignes are similar to E- facicium/ proteus and so on to them. This can cause the reactive nature of kid

reactivity to be stored always with anti-bodys and if theres a Lu lack, u will have cell abnormalities

Diego System (010)

• 22 antigens
  • High/low prevalence antigens
  • Reside on red cell protein BAND 3
    • RBC Anion Exchanger I (AE1).
  • AE1 is responsible for the entry and exit of bicarbonate and chloride ions.
• The third loop of Band 3 (AE1) carries antigens from the ABH and I blood groups.
• IgG, sometimes IgM, causes HTR and HDFN
• Identified in 1955 from a Venezuelan baby suffering from Hemolytic Disease of the Fetus and Newborn (HDFN) where the mother produced Anti-Dia antibodies, leading to the condition.
• Most of the population has the Dib antigen (99% of the population).
  • The Dia antigen is most common in Mongolians, so detection of the Dia antigen is vital to determine Mongolian ancestry
• For Wright antigens (Wra and Wrb) to be expressed, BAND 3 must interact with GLYCOPHORIN A
  • Glycophorin A also houses MNS antigens.
  • Wr(a-b-) represents the null phenotype of Wright antigens for individuals without Glycophorin A.

Phenotype Classification of Diego Blood Group System:

- Majority of the population: Di(a-b+).
- Other possible phenotypes: Di(a+b-), Di(a+b+), Di(a-b-).
    - Di(a-b-) which is the null phenotype, has not been reported

• Discovery of Dia and Dib antigens led to identifying other low-prevalence antigens assigned to the Di system, including Wda and Rba.

Diego Antigens expression

• Diego antigens are expressed on newborns RBC's
• Resistant to enzyme treatments (ficin and papain), sulfhydryl reagents (DTT, glycine-acid EDTA)
  • EXCEPT, Bpa is sensitive to papain

Diego Antibodies

• Could occur in IgM or IgG form

  • Anti-Dia, Anti-Dib cause HTR and HDFN
  • Anti-Wra causes severe HTR
  • Anti-Wrb is an autoantibody commonly found in the serum of px with warm autoimmune hemolytic anemia
  • Anti-ELO causes severe HDFN

• Little data is available on the clinical significance for the other antibodies with the exception to Anti-ELO

YT System 011

• The first individual found to have associated abs was the Cartwrights
• The new BGS that was discovered was named after T and would become the ISBT name YT.
• AChE gene is responsible for encoding acetylcholinesterase, which is important in nerve-nerve impulses/neurotransmission
• Acetylcholinesterase: the enzyme bound in RBC membranes.
  • The function of AChE bound to RBC membrane is unknown.
  • Discovered to be housing YT antigens
• The Yta (high prevalence) has an antigens found in most population, except only 8% of whites
  • It is much more common in the Israeli population showing 21-26%
• YT antigens are weakly expresses in cord blood cells
  • BUT not present when PX have paroxysmal nocturnal hemoglobinuria
• YTa antigens are immunogenic vs. YTb
  • Stimulated by pregnancy or transfusion.
  • Not found to cause HDFN but is clinically significant for transfusion.
  • Enhanced by enzymes: ficin, papain, and DTT
  • EXCEPT Resistant to glycine-acid EDTA
• YT antibodies are mostly IgG and and very not found to be IgM.

YT SYSTEM

• YT phenotypes YT(a+b+) YT(a+b-) YT(a-b+)

Rare YT Null Phenotype

• The absence phenotype (a-b-) has not been shown
• Are based on amino acid substitution on glycosylphosphatidylinositol

Xg System 012

• The gene for for that produces are is from XG and MIC2Genes on chromosome
• Antigens present : Xga, CD39 (respectfully)
  • 89% in omen and 66% in males sensitive to ficin and papain
  • And Resistant to DTT

Antidies:

• Anti-: Xga

Additional facts

• Now belongs to Xg blood group system
  • Xga was also know as Xg1 AND CD99 is Xg2
  • Majoritivey of women are X linked for antigen if the their father passed it down to them
• X antigens cause mile HTR an slight HDFN
  • EXCEPTED Anti- RB COULD CAUSED SEVERE HDFN

XG

• Mores from females have x and can be homo/herto zyogours

Scianna System 013

• 7 antigens
  • Expressed on CRBC
  • Names according to order of discovery
  • can be weakeaned by DDTT AND RESISITNAT TO enzymes but ficin / facpian

Dombrock System 014

• The genes of DOMBRAK has ART4 that resid on chromosome 12

• The produce ART4 for ADT transfe

• can have high and low antigen prevalence They contain high (Gy/Hy /Low Doa,Dob,Joa

• Hstory

  • the antigens was formed to dombrack and the other one later on

• Antibodys* 1: not immuohenic 2: small but are usually weak

• Similarities with KIDS as tittles lower This mean that DR WILL HAVE HTRS TOO

COTTON SYSTEM (105)

• This has AQUA 1 geness / is high/ low to prevent the colton antigens to go back to their origin.
• Antigoa is is highly effective to cause heart cell problem by causing mild HDR HTRS
• Resistant to other enzyme but not hte DTT and has AQUAti

LUTHERAN (landSteinerWeiner 106

• Are very weird
• is from CAMS high n low agin
• High are weak cuz ot hreat are destroyed by DDTT / but are resistant to ficcinn
• Has ANTI and high A
• This is not found cuz thtese aren't a lot of Lu antigens because most ppl inherit Inlu to have high

Ok System 024

• Basigin - A high/low molecule in super high and high/resistant / DTT , EDTA

GY stem O20 (GE) IS HIGH AND LOW AS FOK

• This has two parts (Gy / Gp) 1: with GIC Most cases has that and is 3 hDFN causing death. 2: with 41 proteins

Kid - is not in a good area of RBC so we cants get in with the

this looks like is the opposite with GPYC

CHROMER 021

• HasDTT can affect/ are good proteins in placenta/ has chord cells toooo

RAPHS O25 is a

• A red membrane high n low to for the Kinde is for cAusing 80 htr because of renal faily. The rBC is is for the kidney for membranes to get in .

Jr- Abc4/ has ddit - to help or htr hfdn 22

Lan- abc3 is for 19

Jm - is a seama 11 genes

Gille- is for AQP / helps in for with CD44.

FORS

• has a high amount of code and EColi

RH assoc

• A high and 1 complex to help RH for C/E

Augu

• Is on gene an help

Bell system

• Helps is get ddt and good

High - for 903 + for 208 + all over and

Low for 7 23+700- is all under.1%.

All of which, has a lot of info on HTR

I have now added ISBT blood group collections

• blood group has tends to be biochem related

ISB 700

• Founds in random samples

I have now added a lot of info is a 902 series

And much much more.