In 1950, the Duffy blood group was named for the multiply transfused hemophiliac whose
serum contained the first example of anti-Fya. In 1951, the
antibody to the antithetical antigen, Fyb, was discovered in the
serum of a woman who had been pregnant three times. Using these antibodies three common
phenotypes were defined: Fy(a+b+), Fy(a+b-), and Fy(a-b+). Differences in the racial
distribution of the Duffy antigens were discovered four years later when it was reported
that the majority of Blacks had the erythrocyte phenotype Fy(a-b-). This phenotype is
exceedingly rare in Whites. The frequency of the Fy(a-b-) phenotype is 68 percent in
American Blacks and 88-100 percent in African Blacks. The molecular basis for the Fy(c-b-) phenotype
is the result of a point mutation in the erythroid specific promoter. The absence of Duffy antigens on
erythrocytes results in their resistance to invasion by two malaria parasites, Plasmodium
vivax and Plasmodium knowlesi. This racial variation in distribution of the
Duffy system antigens provides one of the few known examples of selective advantage
conferred by a blood group phenotype.
The Duffy genes, located on chromosome one at position 1922-23, have recently
been cloned and sequenced. The difference between Fya and Fyb
is a change in the amino acid at position 43 from aspartic acid (Fya)
to glycine (Fyb). Studies have shown that blacks whose
erythrocytes express Fyb antigen also have the antigen on the
cells of their kidney, heart, muscle, brain and placenta. The Duffy gene codes for a
protein known as a chemokine receptor, which is important in the inflammatory process.
Accordingly, the Fy protein is also known as DARC (Duffy Antigen Receptor for Chenokines).