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The Diego system antigens are located on a major RBC protein, Band 3, also known as the RBC anion exchange
(AE1).
Anti-Dia, anti-Dib, and anti-Wra are generally considered to be clinically significant; all have caused severe HTRs
and HDFN. Anti-Wra is a relatively common antibody.
Wrb expression requires the presence of a normal GPA (MNS system); alloanti-Wr b is extremely rare.
Anti-Yta is a fairly common antibody to a high-prevalence antigen that is sometimes clinically significant and
sometime insignificant.
The Xga antigen is found on the short arm of the X chromosome and is of higher prevalence in females (89%)
than in males (66%). Although it is usually IgG, anti-Xg a has not been implicated in HDFN or is a cause of HTRs.
Antibodies to Scianna system antigens are rare and little is known about their clinical significance. The rare null
phenotype, Sc: -1, -2, -3, has been observed in the Marshall Islands and New Guinea.
In addition to the Doa and Dob antigens, the Gya, Hy, Joa antigens are assigned to the Dombrock system. Anti-Do a
and anti-Dob have caused HTRs but no clinical HDFN; these antibodies are usually weak and difficult to identify.
The Colton system is composed of the antithetical Co a and Cob antigens as well as the high-prevalence Co3
antigen; the antigens are carried on aquaporin 1, a red cell water channel. The Colton antibodies have caused
HTRs and HDFN.
LW has a phenotypic relationship with the D antigen; Rh null RBCs type LW (a-b-).
Anti-LW reacts strongly with D+ RBCs and can look like anti-D. DTT treatment of test RBCs will distinguish
between these two antibodies because the LW antigen is denatured by DTT, but the D antigen is not. In other
words, anti-LW does not react with DTT-treated D+ RBCs but anti-D does.
The antigens in the Chido/Rodgers system are located on the complement fragments C4b and C4a, respectively,
that are adsorbed onto RBCs from plasma.
The clinically insignificant anti-Ch and anti-Rg react weakly, often to moderate or high-titer endpoints in the
antiglobulin test and may be tentatively identified by plasma inhibition methods.
Gerbich antibodies are sometimes clinically significant for transfusion and sometimes insignificant. Only 3 cases
of serious HDFN due to anti-Ge3 have been reported.
The Cromer antigens are carried on the decay accelerating factor and are distributed in body fluids and on RBCs,
WBCs, platelets, and placental tissue.
The rare anti-Cra and anti-Tca have been found only in black individuals; some examples have caused HTRs.
The Knops antigens are located on complement receptor 1 (CR1). Knops antibodies are clinically insignificant
and have weak and “nebulous” reactivity at the antiglobulin phase; they are not inhibited by plasma.
The Ina antigen is more prevalent in Arab and Iranian populations, with In a and Inb antigen expression being
depressed on the dominant type Lu(a-b-) RBCs.
JMH antibodies most often occur in individuals with acquired JMH-status. Anti-JMH in these individuals is not
clinically significant.
Anti-Vel is most often IgG but can be IgM, and has caused severe immediate HTRs and HDFN. When serum is
tested, anti-Vel characteristically causes in vitro hemolysis.
Anti-Ata has been found only in blacks; the antibody is usually IgG and has caused severe HTRs.
Anti-Jra is found more commonly in Japanese, but clinical significance is not well established, since it is a rare
antibody; it has caused HTRs and a fatal case of HDFN.
Anti-Sda has characteristic shiny and refractile agglutinates under the microscope and is inhibited with urine
from Sd(a+) individuals.