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B Bother Blood Group Systems
B Bother Blood Group Systems
B Bother 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 Le a
Secretors change the Le a to Leb
Le may also modify the A antigen
review the relationship to ABO
precursors
Le
Se
Lea- Leb+
Le
se
Lea+ Leb-
lele
Lea- Leb-
le
se
le
Se
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
Le a+b-
White
22%
Le a-b+
72%
Le a-b-
6%
Black
-----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-Le a
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
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
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
I Blood Group
Antibodies
Anti-I
anti-i
Anti-i
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
P Blood Group
P Blood Group
P Blood Group
Fya
Fyb
Others Fy3
Fyx
Fy 4 Fy5
Fy6
Fs -
(page 185)
Incidence
10%
99.8%
2%
99.9
Rare (19% Blacks)
99.9%(99.8% Blacks
Mc Leod syndrome
Reduced expression of Kell antigens
association with hemolytic anemia and
chronic granulomatous disease
genetics and antigen page 181
Antibodies
Usually IgG and require AHG
rare reaction in saline
common antibodies
implicated in HTR and HDN
Anti-K is a very common antibody
Phenotypes
Lub (99%)
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)
Diego - Dia
Dib
Chido/Rogers
Nine antigens - all normal individuals are
either Rg + or Ch +
HTLA - use plasma inhibition
Determinants on C4 molecule and linked to
HLA -
Xg
sex-linked inheritance
Xga positive
Male - 66%
Female - 89%
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
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
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?
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