Other Blood Group Systems
By
Dr. Christina Thompson
Texas A&M UniversityCorpus Christi
LEWIS SYSTEM
A serum antigen secondarily absorbed
to the red cells
 Le gene produces Lea
 Secretors change the Lea to Leb
 Le may also modify the A antigen
review the relationship to ABO
precursors

Lewis Red Cell Phenotypes
Genes
Lewis Red Cell Phenotype
Le
Se
Lea- Leb+
Le
se
Lea+ LebLea- Leb-
lele
le
se
Lea- Leb- Lec+
le
Se
Lea- Leb- Lec- Led+
Development of Antigens
Newborns born Le a-b If Le and Se

– 2 weeks to 6 months Le a+
– then Le a+b+
– then Le a-b+
During pregnancy, antigens become weaker
Phenotype Frequencies
Phenotype
White
Black
Le a+b-
22%
---
Le a-b+
72%
----
Le a-b-
6%
20%
Lewis Antibodies
Anti-Le a, Anti-Le b, Anti-Lex
 Most react at room temperature or
below  Often fix complement
 Some in vitro hemolysis
 Le a may cause HTR

Lewis Antibodies
Anti-Le a
 Found in Lea-b- secretors
 best room temperature or below - some
at ICT and enzymes
 Often fix complement
 Some in vitro hemolysis
 Le a may cause HTR

Lewis Antibodies
Anti-Le b
 Often found with Anti-Lea
 Most react at room temperature or
below
 Two types - Anti-LebH and Anti-LebL
 Rare cause of HTR

Lewis Antibodies
Anti-Lex
 Most react at room temperature or
below  Reacts with both Lea and Leb as a
single antibody

Lewis Antibodies

Special Problems in the Blood Bank
– Lewis antigens may be weaker during
pregnancy and women produce antibodies
– Can neutralize Lewis antibodies with Lewis
plasma
– Pregnant woman with room temperature
antibodies, neutralize with Lewis antigen
when testing for HDN antibodies
I Blood Group
Two antigens I and i
 I antigen present on almost all healthy
adults
 Rare adults that are I negative spectrum on page 175
 I antigen varies in strength on adult cells

I Blood Group
Newborns do not have much I antigen
 Newborns have i antigen
 At about 18 months the i is replaced
with I
 Some transitional antigens

I Blood Group
I substance can be found in saliva and
human milk and on lymphocytes and
platelets
 During disease, the I antigens may
alter

I Blood Group

Antibodies
Anti-I
anti-i
– Anti-I





usually reacts at room temperature, saline or
below
often attaches complement
doesn’t cause hemolysis unless it reacts at
37oC
Can be found in almost all sera in low titers and
titers increase during some diseases (viral
infections - syphilis - atypical pneumonia)
COLD AUTOAGGLUTIN
I Blood Group

Antibodies
Anti-I
anti-i
– Anti-i

rare antibody occurs in patients with infectious
mononucleosis, cirrhosis, myeloid leukemia,
reticulosis
I Blood Group

Antibodies
– Other combination antibodies have been
found (IA, IH, IP1, etc.) pp. 176 - 177
– ENZYMES ENHANCE ACTIVITY
– ABSORBTION IS USED TO TEST FOR
OTHER MORE IMPORTANT ANTIBODIES
Autoabsorption
P Blood Group
Discovered in 1927 by Landsteiner
 Antigens P1
P
p
pk Luke

– Luke antigen and disease association
- page 173
P Blood Group

Antibodies Anti-P1
Anti- P + P1 + pk
Anti-P Anti-pk
– Anti-P1




Usually IgM reacts at room temperature and
saline
May attach complement
rarely a problem with transfusion
easily inhibited with P1 substance
P Blood Group

Antibodies Anti-P1
Anti- P + P1 + pk
Anti-P Anti-pk
– Anti-P


found 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 DonathLandsteiner antibody
P Blood Group

Antibodies Anti-P1
Anti- P + P1 + pk
Anti-P Anti-pk
– Anti-pk and Anti P + P1 + pk


Anti-pk has only been found as part of other
antibodies
Anti-P + P1 + pk found in p individuals formerly called Anti-Tja and very hemolytic
Duffy Blood Group
Discovered in early 1950’s
 Fy antigen locus on chromosome 1 with
Rh locus
 Antigens
codominant inheritance

– Fya
Fyb
– Others Fy3
(page 185)
Fyx
Fy 4 Fy5
Fy6
Fs -
Duffy Blood Group

Duffy Blood Group
Fya-b- appear to provide some
protection from P.vivax infection
 Antibodies Anti-Fya Anti-Fyb

– Usually AHG reaction - IgG
– destroyed by enzymes
– Rare examples of antibodies to other
antigens (Anti-Fy 3, Anti-Fy4, Anti-Fy5)
and those reactions are not destroyed by
enzymes
– Cause HTR and HDN
Kell Blood Group
Many antigens in this system and has
been given a numerical nomenclature
Refer to table 8-8
 Six most important

Numeric
KEL 1
KEL 2
KEL 3
KEL 4
KEL 6
KEL 7
Alpha
K
k
Kpa
Kpb
Jsa
Jsb
Name
Kell
Cellano
Penny
Rautenberg
Sutter
Matthews
Incidence
10%
99.8%
2%
99.9
Rare (19% Blacks)
99.9%(99.8% Blacks
Kell Blood Group

Most common gene complexes
Kell Blood Group

Mc Leod syndrome
– Reduced expression of Kell antigens
– association with hemolytic anemia and
chronic granulomatous disease
– genetics and antigen page 181
Kell Blood Group

Antibodies
– Usually IgG and require AHG
– rare reaction in saline
– common antibodies
– implicated in HTR and HDN
– Anti-K is a very common antibody
MNSs Blood Group
Many antigens in this system and some
are alleles to the four common antigens
 M
N
S s




Association with GPA and GPB
Four gene complexes
MS Ms NS Ns
Other alleles Mg, Mk, Mc, Mr, Mz, Mv, Na,
T1m, Sj, S2, some quantitative differences
MNSs Blood Group

Phenotypes
MNSs Blood Group





U antigen is absent or reduced on S-sOther antigens - page 165
Mi - abnormal forms of Ss glycoprotein
En(a-) absence of MN glycoprotein
Disease association Page 170
MNSs Blood Group
Antibodies
 Anti-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
MNSs Blood Group
Antibodies
 Anti-S

– Usually igM and room temperature
although some at AHG
– destroyed by enzymes
– Rare HTR and HDN
MNSs Blood Group
Antibodies
 Anti-s and anti-U

– Usually IgG and AHG
– Not destroyed by enzymes
– HTR and HDN
– Anti-U found as warm autoantibody and
does not react well with Rh null cells
– Other antibodies rarely detected but not
uncommon (ex. anti-Mg common antibody)
Kidd Blood Group


Discovered in the 1950s
Two antigens Jka
Jkb
Kidd Blood Group

Antibodies - Anti-Jka and Anti-Jkb
– Usually IgG and require AHG
– bind complement
– enhanced by enzymes
– implicated in HDN and HTR
– Seldom potent and deteriorate rapidly
– Classic delayed HTR
Kidd Blood Group
Antibodies
 Anti-Jk3

– found in some Jka-b- individuals
– reacts with Jka and Jkb
Lutheran Blood Group

Two antigens Lua (8%)
Lub (99%)
– Other antigens Table 8-12


Important blood group that demonstrates
multiple methods for inheritance of the null
cell type
Lu a-b- inheritance
– InLu dominate inhibitor gene
– lulu recessive lack of Lu gene
– sex linked inhibitor gene
Lutheran Blood Group

Antibodies
– Anti-Lua - not common - reacts in saline but
can be IgG and require AHG - gives a (mf)
agglutination - unclear about HTR & HDN
– Anti-Lub - rare - mostly IgG and requires
AHG - probable HTR and HDN
– Anti-Luab (Anti-Lu3 ) - reacts with all but
Lu a-b- of the recessive type
– Other antibodies react with rare Lu
phenotypes found on Lua-b- (page 192/3)
Other Blood Groups

Diego - Dia
Dib
Wra Wrb 3 others
– Dia found in Chippawah Native Americans
and Japanese and Chinese
– uncommon antibodies - AHG reaction and
important in HTR and HDN
– Wra is a low incidence antigen and Wrb is
a high incidence antigen
– anti-Wra is a fairly common antibody - IgM
or IgG
Other Blood Groups

Chido/Rogers
– Nine antigens - all normal individuals are
either Rg + or Ch +
– HTLA - use plasma inhibition
– Determinants on C4 molecule and linked to
HLA -
Other Blood Groups

Xg
– sex-linked inheritance

Xga positive
Male - 66%
Female - 89%
– uncommon antibody - AHG reaction and
destroyed by enzymes - HTR and HDN?
Other Blood Groups

Gerbich
– system with at least 3 high incidence
antigens and 4 low incidence antigens
– Antibodies usually IgG which require AHG
and clinically significant

Scianna
– Sc:1 - 100%
Sc:2 - 0.3% Sc:3 - 100%
– Antibodies are rare
Other Blood Groups

Colton
– antigens: Coa -99.7% Cob -10.7% Co3 -100%
– the null phenotype has been found and
associated with genetic abnormality and
anemia
– antibodies IgG and clinically significant

Cromer
– consists of 7 high incidence antigens and
three low incidence antigens
– antibodies probably clinically significant
Other Blood Groups

Cartwright
– antigens Yta - 99.8%
Ytb - 0.2%
– Usually IgG and AHG ?HDN and HTR?

Dombrock
– antigens Doa - 57%
Dob - 83%
– additional antigens added Holly, Gregory,
and Joseph
– Uncommon antibodies HTR and ?HDN?
Other Blood Groups

IN
– Ina
Inb
– Ina Iranian and Arabs
– Enzyme destroyed - Ina HTR

Knops
– five antigens
– depressed in some diseases
– HTLA
Other Antigens

High incidence
– Vel, Lan, August, Jacobs, Sid, Wra

Low incidence
– too numerous to mention

Bg - HLA antigens that coat red cells
Other Blood Group Systems
By
Dr. Christina Thompson
Texas A&M UniversityCorpus Christi