OTHERMAJOR BLOOD GROUPSYSTEM (LEWIS, I, P, MNSS, KELL, KIDD, DUFFY)

SYSTEM THAT PRODUCE COLD-REACTING ANTIBODIES Ii Collection (207) and I Blood Group (027)
Lewis Blood Group Ii and I
• I stands for “individuality”
• I and i antigens are not antithetical; they have reciprocal relationship
• Newborns are rich in i
• Adults are rich in I
• i antigen (linear) converts to I (branched) as the child matures
(precursor chain is more linear at birth) at about 18 months
• Some people do not change their i status. They become rare adult i
or the I negative phenotype.
• I is inversely proportional to i.
• Are expressed strongly if you remove your ABH Ags (in trace amount)
• Bombay phenotype has greatest I Ags than ABH.
2 kinds of i phenotype
u wan(1)t white • i1 has the least amount of I Ag and common among whites
pero nami mag i(2)t ang black • i2 has more I Ag; common among blacks
Lewis Antibodies
maubrahan
sulod palang
gleng 25 pa cia
mangyawix

Anti – I Pathogenic
• Strong, cold autoagglutinin that demonstrates high titer reactivity at
4OC and reacts over a wide thermal range (up to 30OC - 32OC)
• When the peripheral circulation cools, these Abs attach and cause
autoagglutination and vascular occlusion known as
• Reynaud’s phenomenon
• Production auto anti-I may be stimulated by microorganism carrying
I-like in their cell surface
• Mycoplasma pneumoniae is chemically similar to I Ag and infected
patients often develop strong cold agglutinins with I specificity as a
cross reactive response
• Associated as a cause of Cold Agglutinin Disease (similar to PCH)
tam-an ka dako • Anti – I is not associated with HDN rare IgM antibody that reacts
Anti-Lea optimally at 4OC
• most commonly encountered of the Lewis antibodies • occurs in patients with infectious mononucleosis, cirrhosis, myeloid
• Often detected at room temperature tests but sometimes reacts at leukemia, reticulosis
37°C and in the indirect antiglobulin test parehas bolbol aiai may pnemumonia
• Rare HTR have been reported in patients with anti-Lea who were
transfused with Le (a+) RBCs may sakit sa cold, sa init (hilanat, alcohol, chemo)
Anti-Leb
• Not as common or generally as strong as anti- Lea
• Usually an IgM agglutinin that can bind complement
• Can be classified into two categories: anti-LebL and anti-LebH
Lewis Antigens
• are not intrinsic to the RBC membrane and readily shed from
transfused RBCs within a few days of transfusion
• Lewis blood group system present in transfused plasma neutralizes
Lewis antibodies in the recipient – it is exceedingly rare for Lewis
antibodies to cause hemolysis of transfused RBCs.
 OTHERMAJOR BLOOD GROUPSYSTEM (LEWIS, I, P, MNSS, KELL, KIDD, DUFFY)

The P Blood Groups

Antigens:
• P1 : (003)
• P: (028)
• Pk and LKE : (209)
• Like the ABH Ags, are synthesized by sequential action of
glycosyltransferases

kay landsteiner rule gaming

U-nega ->

• produced by P1– individuals exposed to droppings of pigeons

and turtle doves or the eggwhite of turtle doves
• The P1 Ag in bird droppings may be attributed to certain gram
– bacteria rather than to the birds themselves
Anti- PP1Pk
• Discovered in 1927 by Landsteiner • Originally called anti-Tja
• Antigens : P1, P2, p, PkLuke • Tj : Tumor of Mrs. J (a p individual with adenocarcinoma of the
Phenotype Ag present PossibleAbs stomach) pp ni ms. ja
P1 P1 P None Landsteiner • Produced by all p individuals early in life without rbc
(Pk) rule sensitization same gdya galaw ABO
P2 P (Pk) Anti – P1 gaming • May be IgG or IgM; bind complement
• May demonstrate in vitro hemolysis
p None Anti -PP1Pk you always has pk,
gene pk = more • Are IgM and IgG kay anti sa tnan daan
P1 P1 Pk Anti – P
k • Bind complement and are potent hemolysin
P2 k Anti – P, anti -P1
Pk Cause severe HTR and HDN
• Asso. With increases incidence of spontaneous and early
P1 Ag
• Poorly developed at birth abortions
Luke Ag and Ab
• Found in fetal rbcs as early as 12 weeks but weakens at gestation
• Deteriorates rapidly on storage • It was thought to be phenotypically related to P blood group.
• The Ab reacted with all RBCs except 2% of P1, P2, p and Pk
• In(Lu) : inhibits expression of P1
• (Lutheran – P1 individuals who inhibit this modifier gene may be Disease association:
• Pyelonephritis
typed serologically as P1) nd gusto ni Leu, piso
o Caused by strains of E.coli
o Produces ladder-like infections
o The E.coli uses the P Ag as a point of adhesion

Antibodies
Anti-P1
• Naturally occurring IgM in sera of P– individuals
• Weak, cold reative saline agglutinin (4OC)
• Not seen in routine testing
• Some react at 37OC and bind complement and are considered
clinically significant
• Because P1 Ag expression on rbcs varies and deteriorates during
storage, Abs may react only with rbcs having the strongest
expression and give inconclusive patterns of reactivity when Ab
identification is performed
• Produced by P1– individuals infected with Echinococcus
granulosus
 OTHERMAJOR BLOOD GROUPSYSTEM (LEWIS, I, P, MNSS, KELL, KIDD, DUFFY)

MNSs (ISBT 002) ANTIGENS

M and N Ag
• M and N Ags are found on glycophorin A (GPA), the major RBC sialic
acid-rich glycoprotein.
• Because M and N are located at the outer end of GPA, they are
easily destroyed by the routine blood bank enzymes ficin,
i mi ss u papain, and bromelin.

Not a MaN kay nubo,

pero at least di
makapyutan

• GPA-deficient RBCs are more resistant to invasion by

Plasmodium falciparum merozoites because sialic acid appears
to be essential for adhesion of the parasite to the RBC.
S and s antigens
• are located on smaller GPB (glycophorin B), which is very similar to
GPA
• Well developed at birth
• Less easily degraded by enzyme (enzyme sensitive sites are less
accessible)
ops walang agaway • S and s are differentiated by the amino acids at
• position 29 on GPB
o S = has methionine
o s= has threonine
• Clinical Relevance
• Antibodies to antigens in the MNS blood group system are often
“naturally occurring” and if they do not react at 37°C can be ignored
in transfusion practice.
Can a person have NO MNSs antigens?
• Yes, the Mk allele produces no M, N, S, or s antigens MNSs Antibodies
• Frequency of 0.00064 or 0.064% Anti – M
• Naturally occuring, react below 37OC
MNSs • Anti-M is often cold-reacting IgG and is enhanced by testing in an
• The MNS blood group system is second only to the Rh blood group acidified environment
system in its complexity • 50-80% are IgG or have IgG component
• MNS antigens are found predominately on the red cells, with some • Do not bind complement
found on the renal endothelium and epithelium. • Do not react with enzyme-treated rbc’s (destroyed by enzymes)
• Antigens in the MNS system are fully developed at birth • More common in non-transfused children and in patients with burns.
• Because the antigens were clearly related but not exactly • Reacts better with M+N- cells than with M+N+ rbcs at pH 6.5
antithetical, they named them, respectively, after the second and • Some react only with rbcs exposed to glucose solutions
fifth letters of the word IMMUNE. • Not clinically significant in transfusion
Anti-N
• Cold reactive
• Do not bind complement
• Reacts better with M-N+ rbcs than M+N+ rbcs
Anti-Nf - are seen in renal patients who are dialyzed on
equipment sterilized with formaldehyde
 OTHERMAJOR BLOOD GROUPSYSTEM (LEWIS, I, P, MNSS, KELL, KIDD, DUFFY)

• Anti-Nf = are seen in renal patients who are dialyzed on

equipment sterilized with formaldehyde

Kell antigens
• Kpa and Kpc Ag are low frequency mutations of their high
Anti – S and anti – s frequency partner, Kpb
• IgG-reactive at 37OC and the antiglobulin test phase • Kpc is found in individuals in Japan produced from
• A few express optimal reactivity between 10OC and 22OC by consanguineous marriages
saline indirect AT test. • Kx is the backbone of Ke l Ags but not a part of Ke l blood
• If anti–S or anti–s specificity is suspected, incubating tests at group ex mo mu hahha
room temp and performing AT test without incubating at • Ko – also called Ke l null
37OC may help its identification
• Significant – have caused HTR and HDN
• Insignificant – its very rare

Anti – K (originally called Kell)

SYSTEM HAT PRODUC WARM REACTING ANTIBODIES • Was identified in 1946 in the serum of Mrs. Kellacher
The Kell (006) and Kx (019) Blood Group System • The Ab reacted with the rbcs of her newborn infant, her older
Kell System daughter, her husband and about 7%of population
• Similar to the Rh system • 1949 : anti-k (Cellano) was described
• 2 major antigens (over 20 exist) • Antithetical partner to K
peke nga k (small) is letter c
o K (Kell), <90% of population Numeric Alpha Name
o k (cellano), >90% of population most is peke nga tawo
KEL1 K Kell
• The K and k genes are codominant alleles on chromosome 7
that code for the antigens KEL2 k Cellano
ang kappa
• Well developed at birth KEL3 Kpa Penny pangwa kwarta
• The K antigen is very immunogenic (2nd to the D antigen) in KEL4 Kpb Rautenberg
stimulating antibody production JiLsa ga stuter
KEL6 Jsa Sutter w. bira
KEL7 Jsb Matthews

mighty cloud
sa xray -> TB
kappa nga big

Kp, may KJ
Jia LissA was into BLACKED
 OTHERMAJOR BLOOD GROUPSYSTEM (LEWIS, I, P, MNSS, KELL, KIDD, DUFFY)

Kidd (009) • (if the individual is Rh null or Duffy (a–b–), they produce anti-
Fy5)
my kid, jake
• Fy6– malarial receptor
# of wings
o Fy (a–b–) : lack Fy6
o Resistant (but not immune) to P. vivax

popular si JiaLissa(jkajka)
among blacks

Duffy antibodies
• Anti–Fya and Anti–Fyb
• usually IgG and react best at antiglobulin phase
• Bind complement
• Do not react with enzyme treated cells
• Have been asso.with acute and delayed HTR and HDN

Anti-Jka and anti-Jkb MINOR BLOOD GROUPS REPORTING

• Demonstrate dosage, weak and are found in combination with 1. Diego (010) System years old ni brother Dora
other Abs (difficult to detect) 2. Yt (011) System years old lantaw vid
• Clinically significant 3. Xg (012) System years old lantaw x vid
• Usually IgG and partly IgM 4. Scianna (013) System looks like boobs ni anna
• Bind complement 5. Dombrock (014) System years old nabalda cm mo
• Made in response to transfusion or pregnancy (immune); 6. Colton (015) System edad mo tilaw ka beer
most common cause of delayed HTR 7. Landsteiner-Wiener (016) System weener mo ginagamit sa?
pagkabata pa gntr
• No naturally occurring Abs exist no 18, 10 8. Chido/Rodgers (017) System edad enter military school.
• Enhanced by enzymes, LISS, PEG 9. Gerbich (020) System edad ga tuka2 na bik2
10. Cromer (021) System crammer ka sa amu ni edad
Anti-Jk3 11. Knops (022) System edad tak-an ka na
12. Indian (023) System edad kaalamon mo daw indiano
13. Ok (024) System ok ka na grad ka na edad
14. Raph (025) System edad you realized that life is now rougher
15. John Milton Hagen (026) System hamilton may sex scene
16. Gill (029) System G, lapit nalang..
antipodal ni jissa 17. Rh-associated Glycoprotein (030) System Rh bill applies now

Duffy (008) kung ano antigen ara sa ngalan,

ang antibody may anti lang

• Named after Mr. Duffy, a multiple transfused hemophiliac who

was found to have the first described example of anti-Fya
(1950)
• Fyb – described in the serum of a woman who had had three
pregnancies (1955)
• The first ever gene assigned to chromosome 1
Duffy antigens
• Fyx - Don’t produce Ag but produces Fybw (weak Fyb) wala2 gd kag babaw2 ex ko
• Fy3 – common Ag; found on both Fya and Fyb 1a 2b=
• Fy5 – the molecular interaction of Rh and duffy Ag high five ni Rh kag duffy