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2334 Part XIII: Transfusion Medicine Chapter 136: Erythrocyte Antigens and Antibodies 2335

TABLE 136–2. Summary of Common Blood Group Systems or Collections and Their Antigens (Continued)
Antigen
Blood No. Antigen Distribution
Group Frequency Copies on in Blood,
(Year Common White/ Adult RBC Dosage (See Cord Cell Fluids, and
Reported) Phenotypes Black (%) × 10 3 Text) Expression Biochemistry Tissues Comments
Kp /Js : K+k+ 8.8/2 K/k Met 193 Kx: RBC plus Common
a
a
(1957) K+k– 0.2/rare Thr skeletal/ phenotype: k,
b
b
b
a
Kp(a–b+) 97.7/100 Kp /Kp : Trp heart muscle, Kp , Js
neurologic
281 Arg
Kell antigen
Kp(a+b+) 2.3/rare a b tissues expression
Kp(a+b–) Rare/0 Js /Js : Pro depends on both
597 Leu
Js(a–b+) 100/80 Kell and Xk genes
Js(a+b+) Rare/19 K lacks Kell anti-
null
Js(a+b–) 0/1 gens, has Kx
Kx lacks Kx,
null
has poor Kell
antigen expres-
sion (McLeod
phenotype)
Other causes of
poor Kell expres-
sion: cis Kp , Ge-,
a
K , autoantibody
mod
Duffy Fy(a+b–) 17/9 Fy : 6–13 Yes, but not Normal: Multipass RBC plus Fy(a–b–) blacks
a
(1950) Fy(a+b+) 49/1 always evi- adult levels glycoprotein: brain, colon, do not express
b
Fy(a–b+) 34/22 dent because at 12 weeks 35–45 kDa, lung, spleen, Fy on their RBC,
thyroid, thy-
but express it on
of Fy gene
338 aa
Fy(a–b–) Rare/68 Fy /Fy Gly mus, kidney, other tissues and
b
a
42Asp endothelium; seldom make
not in liver anti-Fy b
or placenta
tissue
Kidd (1951) Jk(a+b–) 28/57 Jk : ~14 Yes Normal adult Multipass RBC specific Important cause
a
Jk(a+b+) 49/34 protein: ~43 of DHTR
Jk(a–b+) 23/9 kDa, 391 aa Nulls are unable
1 potential
Jk(a–b–) <1% N-glycan Jk / to fully concen-
a
trate urine; dom-
Polynesians Jk : Asp284 inant inhibitor
b
Asn In(Jk) has weak Jk
antigen
Lutheran Lu(a+b–) 0.15/– Lu : 1.5–4 Yes, but fam- Weak: adult Single-pass RBC plus System of high-
b
(1951) Lu(a+b+) 7.5/0 ily variations level at glycoprotein brain, heart, and low-
Lu(a–b+) 92.3/– exist 15 years type I: kidney, lung, frequency
85 kDa, 597
pancreas,
antigens
Lu(a–b–) Very rare aa 78 kDa placenta, Dominant inhib-
5 Ig super- skeletal itor In(Lu) and
family muscle X-linked inhibitor
domains: (XS2) cause greatly
two vari- reduced Lu
able, three expression
constant First known auto-
B-CAM somal linkage
Lu /Lu : to Se
b
a
His77Arg
aa, amino acids; B-CAM, B-cell adhesion molecule; DHTR, delayed hemolytic transfusion reactions; GPA, glycophorin A; GPB, glycophorin B;
granulos, granulocytes; Ig, immunoglobulin; ISBT, International Society of Blood Transfusion; lymphs, lymphocytes; monos, monocytes; plts,
platelets; RBC, red blood cell.

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